Marijuana use is much more common in US states that have legalized recreational cannabis use

Highest rates among Americans who smoke cigarettes

July 19, 2022

Science Daily/Columbia University's Mailman School of Public Health

A study at Columbia University Mailman School of Public Health and The City University of New York found that the rates of cannabis use and daily cannabis use have increased across the U.S., and that current cannabis use and daily use are substantially higher among individuals residing in states that have legalized recreational cannabis use, relative to those where cannabis use remains illegal. The study also found that rates of cannabis use are even higher among Americans 12 and older who smoke cigarettes, and who reside in states with recreational cannabis laws, compared to those who live in states where cannabis was illegal in 2017.

"Based upon over a decade of data, cannabis use was markedly more prevalent in states where recreational use is legal for adults, relative to states where it was not in 2017. Yet, the increases in cannabis use during this time period were as fast, or faster, in states where cannabis use is prohibited by law, relative to states that had legalized for recreational use by 2017," said Renee Goodwin, PhD, adjunct associate professor of epidemiology at Columbia Mailman School and professor of epidemiology at CUNY, and lead author. "It remains to be seen how increased lawful accessi and growing use of cannabis among adults in all states -- almost regardless of legal status -- will impact the adolescent population. Recent trends, however, outline a potential explosion in both of-age and under-age use," she noted.

The researchers used data from the 2004-2017 National Survey on Drug Use and Health, a representative survey of U.S. individuals aged 12 and older. State of residence was used to determine state-level medical and recreational cannabis laws. The total sample was 784,293 respondents and for 2017 was 56,276 respondents.

The study found that cannabis use and daily cannabis use increased in the U.S with little difference in the speed of increase by state-level legal status of cannabis use from 2004 through 2017. Cannabis use and daily cannabis were much more common in states with recreationally legal cannabis use, relative to those with legal medical cannabis and those with no legal cannabis use.

Cannabis use was even greater among Americans who also smoke cigarettes in states that had adopted recreational cannabis laws, relative to those where cannabis use was not legal. In 2017, one in three (33 percent) daily cigarette smokers reported cannabis use in the past month in recreationally legal states and almost one in five (18 percent) reported daily cannabis use. In contrast, among non-smokers, one in ten reported any cannabis use in recreationally legal states and 3 percent of non-cigarette smokers in these states reported daily use.

The study found that among adolescents ages 12-17 who used cigarettes daily, the majority (73 percent) had used cannabis in the past month and almost one in three (30 percent) used cannabis daily. Among adolescents who did not smoke cigarettes, 5 percent used cannabis in the past month and one percent used cannabis daily.

The study is published online in the journal Drug and Alcohol Dependence.

Goodwin observes, "U.S. states are rapidly passing legislation, yet what should be requisite public education on how cannabis can be used safely has not accompanied these changes. For instance, retail licenses are being issued and it is expected that recreational retail outlets will open within the year in New York State, yet New York has not provided evidence-based guidance outlining safe cannabis use practices or informing the public of potential health risks associated with various levels of cannabis use."

https://www.sciencedaily.com/releases/2022/07/220719162133.htm

Shift workers 'can't all adjust to a night shift'

July 20, 2022

Science Daily/University of Warwick

Scientists at the University of Warwick, jointly with those at Université Paris-Saclay, Inserm and Assistance Publique-Hôpitaux de Paris (France), have challenged the widespread belief that shift workers adjust to the night shift, using data drawn from wearable tech.

By monitoring groups of French hospital workers working day or night shifts during their working and free time, the researchers have not only shown that night work significantly disrupts both their sleep quality and their circadian rhythms, but also that workers can experience such disruption even after years of night shift work.

Their findings, reported in a study in the Lancet group journal eBioMedicine, are the most detailed analysis of the sleep and circadian rhythm profiles of shift workers yet attempted, and the first to also monitor body temperature. This key circadian rhythm is driven by the brain pacemaker clock, and coordinates the peripheral clocks in all organs.

The research demonstrates the value of telemonitoring technology for identifying early warning signs of disease risks associated with night-shift work opening up intervention opportunities to improve the health of workers.

The study compared 63 night-shift workers, working three or more nights of 10 hours each per week, and 77 day-shifters alternating morning and afternoon shifts at a single university hospital (Paul Brousse Hospital in Villejuif, near Paris). Both groups wore accelerometers with chest surface temperature sensors throughout the day and night for a full week, with the data collected by the research team at Université Paris-Saclay and Inserm.

The accelerometer measured movement intensity and allowed the researchers to estimate how much sleep the participants had, how regular were their circadian rhythms, and whether that sleep was disrupted by movement. Patterns in the chest surface temperature gave a further indication of the participants' circadian rhythm, the internal body clock that coordinates rest-activity phases, varying core body temperature, and an array of other bodily rhythms.

Analysis by the University of Warwick statisticians of interruptions to sleep and rhythmic variations in core body temperature showed that night-shift workers had less than half the median regularity and quality of sleep of their day-shift colleagues. 48% of the night-shift workers had a disrupted circadian temperature rhythm.

Using information from questionnaires on the participants' chronotypes, they also found that the centre of sleep for those working the night shift didn't correlate with their respective chronotype, i.e. their morningness or eveningness orientation. This meant they were not sleeping in synch with their internal clocks.

Importantly, even workers who had been on night shifts for many years still showed these negative effects on circadian and sleep health. The more years they had been on night work, the more severe the circadian disruption, contradicting widespread assumptions about adaptation to night work.

This helps explain why previous research has linked disrupted circadian rhythms with long term health risks, including the development of cancer and cardiovascular diseases, as well as metabolic and infectious diseases.

Professor Bärbel Finkenstädt from the University of Warwick Department of Statistics said: "There's still an assumption that if you do night work, you adjust at some stage. But you don't. We saw that most workers compensate in terms of quantity of sleep, but not in terms of quality during the work time."

Dr Julia Brettschneider of the University of Warwick Department of Statistics said: "I think there's a misunderstanding that night shift work is just an inconvenience, whereas it can be linked to serious health risks. We can't avoid shift work for many professions, like healthcare workers, so we should be thinking about what can be done in terms of real-world adjustments to improve working conditions and schedules of shift workers. A better understanding of the biological mechanisms helps to find answers to this question.

"Together with our PhD student Yiyuan Zhang, we have developed a statistical analysis framework that enables the discovery of patterns and predictive factors in the complex data sets created by wearable tech."

Professor Francis Lévi from Université Paris-Saclay further added: "Nearly 20% of the night workers could not even adjust their circadian rhythms during their free time, with the severity of impairment tending to increase with the number of years of night work. The telemonitoring technology, and analysis methods we have set up make it now possible to objectively evaluate circadian and sleep health in night workers in near real time, and design prevention measures for individual workers whenever necessary."

In addition, the team has the potential in future research to look at more long-term outcomes, such as particular diseases such as cancer that have been linked to disruption of the circadian clock.

https://www.sciencedaily.com/releases/2022/07/220720102504.htm

Brain imaging reveals how mindfulness program boosts pain regulation

July 28, 2022

Science Daily/University of Wisconsin-Madison

Research at the University of Wisconsin-Madison's Center for Healthy Minds has isolated the changes in pain-related brain activity that follow mindfulness training -- pointing a way toward more targeted and precise pain treatment.

The study, published today (July 27) in The American Journal of Psychiatry, identified pathways in the brain specific to pain regulation on which activity is altered by the center's eight-week Mindfulness Based Stress Reduction course.

These changes were not seen in participants who took a similar course without the mindfulness instruction -- important new evidence that the brain changes are due to the mindfulness training itself, according to Joseph Wielgosz, who led the work while he was a graduate student at UW-Madison and is now a postdoctoral researcher at Stanford University. The study is the first to demonstrate pain-related brain changes from a standardized mindfulness course that is widely offered in clinical settings.

Around one-third of Americans experience pain-related problems, but common treatments -- like medications and invasive procedures -- don't work for everyone and, according to Wielgosz, have contributed to an epidemic of addiction to prescription and illicit drugs.

Popular with patients and promising in its clinical outcomes, mindfulness training courses like MBSR have taken a central place in the drive for a more effective approach to pain management. By practicing nonjudgmental, "present-centered" awareness of mind and body, participants can learn to respond to pain with less distress and more psychological flexibility -- which can ultimately lead to reductions in pain itself.

To measure neural pain response, study participants had their brains scanned while receiving a carefully controlled heat-based stimulus on their forearm. The researchers recorded two brain-wide signatures of pain-related activity, developed by collaborator Tor Wager, a professor of neuroscience at Dartmouth College. This innovative technique dramatically improves the ability to detect pain-related signals in the brain's complex activity. Changes in signatures can also be more easily interpreted in psychological terms.

Participants in the MBSR course showed reduction in a signature associated with the sensory intensity of pain.

"Our finding supports the idea that for new practitioners, mindfulness training directly affects how sensory signals from the body are converted into a brain response," says Wielgosz, whose work was supported by the National Institutes of Health.

The study also looked at longer-term mindfulness training. Intriguingly, practice on intensive meditation retreats was associated with changes in the neural signature for influences that shape pain indirectly -- for example, differences in attention, beliefs and expectations, factors that often increase the perceived levels of distress in non-meditators.

"Just like an experienced athlete plays a sport differently than a first-timer, experienced mindfulness practitioners seem to use their mental 'muscles' differently in response to pain than first-time meditators," Wielgosz says.

These findings help show the potential for mindfulness practice as a lifestyle behavior.

The study is also significant for the field of pain research in its use of brain-based measures of pain alongside the subjective ratings of the participants in a randomized trial. Pain researchers have long sought ways to biologically measure the effect of treatment.

"Looking at neural signatures together with patient experiences revealed insights about mindfulness that we could never have detected through either one alone," Wielgosz says.

Thus, in addition to the insights it provides about mindfulness, the researchers believe that their study can also provide a model for future research, helping to untangle the complexity of pain and ultimately reduce the burden it places on our lives.

https://www.sciencedaily.com/releases/2022/07/220728134104.htm

Vegans who lift weights may have stronger bones than other people on a plant-based diet

Vegans and omnivores who do resistance training may have similar bone structure

August 4, 2022

Science Daily/The Endocrine Society

People on a plant-based diet who do strength training as opposed to other forms of exercise such as biking or swimming may have stronger bones than other people on a vegan diet, according to new research published in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism.

About 6 percent of people in the United States are vegans. Recent research shows a plant-based diet can be associated with lower bone mineral density and increased fracture risk.

"Veganism is a global trend with strongly increasing numbers of people worldwide adhering to a purely plant-based diet," said Christian Muschitz, M.D., of St. Vincent Hospital Vienna and the Medical University of Vienna in Vienna, Austria. "Our study showed resistance training offsets diminished bone structure in vegan people when compared to omnivores."

The authors compared data from 43 men and women on a plant-based diet for at least five years and 45 men and women on an omnivore diet for at least five years. Omnivores eat meat as well as plant-based foods.

The researchers found vegan participants who did resistance training exercises such as using machines, free weights, or bodyweight resistance exercises at least once a week had stronger bones than those who did not. They also found vegans and omnivores who engaged in resistance training had similar bone structure.

"People who adhere to a vegan lifestyle should perform resistance training on a regular basis to preserve bone strength," Muschitz said.

https://www.sciencedaily.com/releases/2022/08/220804102619.htm

Researchers gain insights into the genetic and molecular machinery that predisposes individuals to Alzheimer's disease

August 5, 2022

Science Daily/The Mount Sinai Hospital / Mount Sinai School of Medicine

Mount Sinai researchers have achieved an unprecedented understanding of the genetic and molecular machinery in human microglia -- immune cells that reside in the brain -- that could provide valuable insights into how they contribute to the development and progression of Alzheimer's disease (AD). The team's findings were published in Nature Genetics.

Working with fresh human brain tissue harvested via biopsy or autopsy from 150 donors, researchers identified 21 candidate risk genes and highlighted one, SPI1, as a potential key regulator of microglia and AD risk.

"Our study is the largest human fresh-tissue microglia analysis to date of genetic risk factors that might predispose someone to Alzheimer's disease," says senior author Panos Roussos, MD, PhD, Professor of Psychiatry, and Genetic and Genomic Sciences, at the Icahn School of Medicine at Mount Sinai and Director of the Center for Disease Neurogenomics. "By better understanding the molecular and genetic mechanisms involved in microglia function, we're in a much better position to unravel the regulatory landscape that controls that function and contributes to AD. That knowledge could, in turn, pave the way for novel therapeutic interventions for a disease that currently has no effective treatments."

Microglia are primarily responsible for the immune response in the brain, and are also critical to the development and maintenance of neurons. While previous studies, including some at Mount Sinai, have identified microglia as playing a key role in the genetic risk and development of Alzheimer's disease, little is known about the epigenetic mechanics of how that occurs. Because microglia are challenging to isolate within the human brain, most previous studies have used either animal- or cell-line-based models which do not reflect the true complexity of microglia function in the brain. Another challenge has been relating AD genetic risk variation to specific molecular function because these risk factors are frequently found in the non-coding part of the genome (what used to be called "junk DNA"), which is more difficult to study.

The Mount Sinai team's solution was to access fresh brain tissue from biopsies or autopsies made possible by a collaboration between four brain bio-depositories, three at Mount Sinai and the other from Rush University Medical Center/Rush Alzheimer's Disease Center. "Using a total of 150 samples from these sources, we were able to isolate high-quality microglia, which provided unprecedented insights into genetic regulation by reflecting the entire set of regulatory components of microglia in both healthy and neurodegenerative patients," explains Dr. Roussos.

That process -- comparing epigenetic, gene expression, and genetic information from the samples of both AD and healthy aged patients -- allowed researchers to comprehensively describe how microglia functions are genetically regulated in humans. As part of their statistical analysis, they expanded the findings of prior genome-wide association studies to link identified AD-predisposing genetic variants to specific DNA regulatory sequences and genes whose dysregulation is known to directly contribute to the development of the disease. They further described the cell-wide regulatory mechanisms as a way of identifying genetic regions involved in specific aspects of the microglial activity.

From their investigation emerged new knowledge about the SPI1gene, already known to scientists, as the main microglial transcription factor regulating a network of other transcription factors and genes that are genetically linked to AD. Data the team is generating could also be important to deciphering the molecular and genetic mysteries behind other neurodegenerative diseases in which microglia play a role, including Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis.

Dr. Roussos concedes that much work remains for his team to fully understand how the identified genes contribute to the development and progression of Alzheimer's disease, and how they could be targeted with new therapeutics. He is greatly encouraged, though, by the results of single-cell analysis by his lab of microglia using highly sophisticated instruments that are uncovering the unique interactions between different types of immune cells in the brain and its periphery that are related to neurodegenerative disease. "We're seeing very exciting results through our single-cell data," Dr. Roussos reports, "and that's bringing us ever closer to understanding the genetically driven variations and cell-specific interactions of inheritable diseases like Alzheimer's."

https://www.sciencedaily.com/releases/2022/08/220805154359.htm

How microglia contribute to Alzheimer's disease

A breakdown of lipid metabolism in these brain cells promotes inflammation and interferes with neuron activity, a new study finds

August 4, 2022

Science Daily/Massachusetts Institute of Technology

One of the hallmarks of Alzheimer's disease is a reduction in the firing of some neurons in the brain, which contributes to the cognitive decline that patients experience. A new study from MIT shows how a type of cells called microglia contribute to this slowdown of neuron activity.

The study found that microglia that express the APOE4 gene, one of the strongest genetic risk factors for Alzheimer's disease, cannot metabolize lipids normally. This leads to a buildup of excess lipids that interferes with nearby neurons' ability to communicate with each other.

"APOE4 is a major genetic risk factor, and many people carry it, so the hope is that by studying APOE4, that will also provide a bigger picture of the fundamental pathophysiology of Alzheimer's disease and what fundamental cell processes have to go wrong to result in Alzheimer's disease," says Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory and the senior author of the study.

The findings suggest that if researchers could find a way to restore normal lipid metabolism in microglia, that might help to treat some of the symptoms of the disease.

MIT postdoc Matheus Victor is the lead author of the paper, which appears today in Cell Stem Cell.

Lipid overload

About 14 percent of the population has the APOE4 variant, making it the most common genetic variant that has been linked to late-onset, nonfamilial Alzheimer's disease. People who carry one copy of APOE4 have a threefold higher risk of developing Alzheimer's, and people with two copies have a tenfold higher risk.

"If you look at this another way, if you look at the entire Alzheimer's disease population, about 50 percent of them are APOE4 carriers. So, it's a very significant risk, but we still don't know why this APOE4 allele presents such a risk," Tsai says.

The APOE gene also comes in two other forms, known as APOE2, which is considered protective against Alzheimer's, and the most common form, APOE3, which is considered neutral. APOE3 and APOE4 differ by just one amino acid.

For several years, Tsai's lab has been studying the effects of APOE4 on a variety of cell types in the brain. To do this, the researchers use induced pluripotent stem cells, derived from human donors, and engineer them to express a specific version of the APOE gene. These cells can then be stimulated to differentiate into brain cells, including neurons, microglia, and astrocytes.

In a 2018 study, they showed that APOE4 causes neurons to produce large quantities of amyloid beta peptide 42, an Alzheimer's-linked molecule that causes the neurons to become hyperactive. That study found that APOE4 also affects the functions of microglia and astrocytes, leading to cholesterol accumulation, inflammation, and failure to clear amyloid beta peptides.

A 2021 follow-up showed that APOE4 astrocytes have dramatic impairments in their ability to process a variety of lipids, which leads to a buildup of molecules such as triglycerides, as well as cholesterol. In that paper, the researchers also showed that treating engineered yeast cells expressing APOE4 with choline, a dietary supplement that is a building block for phospholipids, could reverse many of the detrimental effects of APOE4.

In their new study, the researchers wanted to investigate how APOE4 affects interactions between microglia and neurons. Recent research has shown that microglia play an important role in modulating neuronal activity, including their ability to communicate within neural ensembles. Microglia also scavenge the brain looking for signs of damage or pathogens, and clear out debris.

The researchers found that APOE4 disrupts microglia's ability to metabolize lipids and prevents them from removing lipids from their environment. This leads to a buildup of fatty molecules, especially cholesterol, in the environment. These fatty molecules bind to a specific type of potassium channel embedded in neuron cell membranes, which suppresses neuron firing.

"We know that in late stages of Alzheimer's disease, there is reduced neuron excitability, so we may be mimicking that with this model," Victor says.

The buildup of lipids in microglia can also lead to inflammation, the researchers found, and this type of inflammation is believed to contribute to the progression of Alzheimer's disease.

Restoring function

The researchers also showed that they could reverse the effects of lipid overload by treating APOE4 microglia with a drug called Triacsin C, which interferes with the formation of lipid droplets. When APOE4 microglia were exposed to this drug, the researchers found that normal communication between microglia and neighboring neurons was restored.

"We can rescue the suppression of neuronal activity by APOE4 microglia, presumably through lipid homeostasis being restored, where now fatty acids are not accumulating extracellularly," Victor says.

Triacsin C can be toxic to cells, so it would likely not be suitable to use as a drug to treat Alzheimer's, but the researchers hope that other approaches to restore lipid homeostasis could help combat the disease. In Tsai's 2021 APOE4 study, she showed that choline also helps to restore normal microglia activity.

"Lipid homeostasis is actually critical for a number of cell types across the Alzheimer's disease brain, so it's not singularly a microglia problem," Victor says. "The question is, how do you restore lipid homeostasis across multiple cell types? It's not an easy task, but we're tackling that through choline, for example, which might be a really interesting angle."

The researchers are now further studying how microglia transition from a healthy state to a "lipid-burdened," inflammatory state, in hopes of discovering ways to block that transition. In previous studies in mice, they have shown that exposure to LED light flickering at a specific frequency can help to rejuvenate microglia, stimulating the cells to resume their normal functions.

https://www.sciencedaily.com/releases/2022/08/220804130645.htm

Education, job, and social life may help protect brain from cognitive decline

August 3, 2022

Science Daily/American Academy of Neurology

Why do some people with amyloid plaques in their brains associated with Alzheimer's disease show no signs of the disease, while others with the same amount of plaque have clear memory and thinking problems? Researchers looked at genetic and life course factors that may help create a "cognitive reserve" that provides a buffer against the disease in a study published in the August 3, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology.

They found that factors such as taking part in clubs, religious groups, sports or artistic activities, along with educational attainment by age 26, occupation and reading ability, may affect the brain's cognitive reserve. The study suggests that continuing to learn over a lifetime may help protect the brain, which is true even for people who have lower scores on cognitive tests in childhood. Previous studies have shown that people with low scores in childhood are more likely to have a steeper cognitive decline in old age than people with high scores.

"These results are exciting because they indicate that cognitive ability is subject to factors throughout our lifetime and taking part in an intellectually, socially and physically active lifestyle may help ward off cognitive decline and dementia," said study author Dorina Cadar, PhD, Brighton and Sussex Medical School in the United Kingdom. "It's heartening to find that building up one's cognitive reserve may offset the negative influence of low childhood cognition for people who might not have benefited from an enriching childhood and offer stronger mental resilience until later in life."

The study involved 1,184 people who were born in 1946 in the United Kingdom. They took cognitive tests when they were eight years old and again when they were 69 years old. A cognitive reserve index combined people's education level at age 26, participation in enriching leisure activities at age 43 and occupation up to age 53. Their reading ability at age 53 was also tested as a measure of overall lifelong learning separate from education and occupation.

The cognitive test participants took at age 69 has a maximum total score of 100. The average score for this group was 92, with the lowest score being 53 and the highest score being 100.

The researchers found that higher childhood cognitive skills, a higher cognitive reserve index and higher reading ability were all associated with higher scores on the cognitive test at age 69. Researchers found that for every unit increase in childhood test scores, the old-age cognitive test score increased by 0.10 points on average. For every unit increase in the cognitive reserve index, cognitive scores increased by 0.07 points on average, and for every unit increase in reading ability, cognitive scores increased by 0.22 points on average.

People with a bachelor's degree or other higher education qualifications scored 1.22 points more on average than those with no formal education. People who engaged in six or more leisure activities such as adult education classes, clubs, volunteer work, social activities and gardening scored 1.53 points more on average than people who engaged in up to four leisure activities. Those with a professional or intermediate level job scored 1.5 points more on average than those with partly skilled or unskilled occupations.

The study also found that for people with a higher cognitive reserve index and reading ability, their scores on cognitive tests did not decline as rapidly as people with lower scores, regardless of their test scores at age eight.

Michal Schnaider Beeri, PhD, of Icahn School of Medicine at Mount Sinai in New York, who wrote an editorial accompanying the study, said, "From a public health and societal perspective, there may be broad, long-term benefits in investing in high education, widening opportunities for leisure activities and providing cognitive challenging activities for people, especially those working in less skilled occupations."

A limitation of the study is that the people who remained involved in the study until age 69 may be more likely to be healthier, have better overall thinking skills and be more socially advantaged than those who did not complete the study, so the results may not reflect the general population.

https://www.sciencedaily.com/releases/2022/08/220803161028.htm

The brain already benefits from moderate physical activity

Brain regions with high oxygen demand show the largest effects

August 3, 2022

Science Daily/DZNE - German Center for Neurodegenerative Diseases

Even moderate physical activity has a positive effect on the brain. DZNE researchers led by Dr. Dr. Ahmad Aziz deduce this from examinations of 2,550 participants of the Bonn "Rhineland Study." According to their findings, certain areas of the brain are larger in physically active individuals than in those who are less active. In particular, brain regions that have a relatively high oxygen demand benefit from this effect. The research results are published in Neurology®, the medical journal of the American Academy of Neurology.

Exercise keeps body and mind healthy -- but little is known about exactly how and where physical activity affects our brains. "In previous research, the brain was usually considered as a whole," says Fabienne Fox, neuroscientist and lead author of the current study. "Our goal was to take a more detailed look at the brain and find out which regions of the brain physical activity impacts most."

Extensive Data from the Rhineland study

For their research, Fox and colleagues used data from the Rhineland Study, a large-scale population-based study conducted by DZNE in the Bonn city area. Specifically, they analyzed physical activity data from 2,550 volunteers aged 30 to 94 years, as well as brain images obtained by magnetic resonance imaging (MRI). To sample physical activity, the study participants wore an accelerometer on their upper thigh for seven days. The MRI scans provided information particularly on brain volume and thickness of the cortex.

The More Active, the Greater the Effects

"We were able to show that physical activity had a noticeable effect on almost all brain regions investigated. Generally, we can say that the higher and more intense the physical activity, the larger the brain regions were, either with regard to volume or cortical thickness," Fabienne Fox summarizes the research results. "In particular, we observed this in the hippocampus, which is considered the control center of memory. Larger brain volumes provide better protection against neurodegeneration than smaller ones." However, the dimensions of the brain regions do not increase linearly with physical activity. The research team found the largest, almost sudden volume increase when comparing inactive and only moderately physically active study participants -- this was particularly evident in older individuals over the age of 70.

"In principle, this is very good news -- especially for those who are reluctant to exercise," says Ahmad Aziz, who heads the research group "Population and Clinical Neuroepidemiology" at DZNE. "Our study results indicate that even small behavioral changes, such as walking 15 minutes a day or taking the stairs instead of the elevator, may have a substantial positive effect on the brain and potentially counteract age-related loss of brain matter and the development of neurodegenerative diseases. In particular, older adults can already profit from modest increases of low intensity physical activity."

Young and somewhat athletic subjects who usually engaged in moderate to intense physical activity also had relatively high brain volumes. However, in even more active subjects, these brain regions were slightly larger. Also here it showed: the more active, the greater the effect, although at high levels of physical activity, the beneficial effects tended to level off.

Brain Regions that Benefit the Most

To characterize the brain regions that benefited most from physical activity, the research team searched databases for genes that are particularly active in these brain areas. "Mainly, these were genes that are essential for the functioning of mitochondria, the power plants of our cells," says Fabienne Fox. This means that there are particularly large numbers of mitochondria in these brain regions. Mitochondria provide our body with energy, for which they need a lot of oxygen. "Compared to other brain regions, this requires increased blood flow. This is ensured particularly well during physical activity, which could explain why these brain regions benefit from exercise," says Ahmad Aziz.

Exercise Protects

The bioinformatic analysis further showed that there is a large overlap between genes whose expression is affected by physical activity and those that are impacted by neurodegenerative diseases such as Alzheimer's, Parkinson's, or Huntington's disease. This could offer a potential explanation for why physical activity has a neuroprotective effect, the research team concludes. "With our study, we were able to characterize brain regions that benefit from physical activity to an unprecedented level of detail," says Ahmad Aziz. "We hope our results will provide important leads for further research."

And also approaches for everyday use: "With our results, we want to provide a further impetus to become more physically active -- to promote brain health and prevent neurodegenerative diseases," says Fabienne Fox. "Even modest physical activity can help. Thus, it's just a small effort -- but with a big impact."

https://www.sciencedaily.com/releases/2022/08/220803112611.htm

Microscopic blood vessel disease in the brain's white matter associated with worse cognition in Alzheimer's

August 2, 2022

Science Daily/Medical College of Georgia at Augusta University

Disease of the microscopic blood vessels that feed the white matter of our brain is associated with worse cognitive function and memory deficits in individuals with Alzheimer's, scientists report.

"The main message of this paper is the mixed pathology as we call it -- microvascular disease and Alzheimer's -- is associated with more brain damage, more white matter damage and more inflammation," says Dr. Zsolt Bagi, vascular biologist in the Department of Physiology at the Medical College of Georgia at Augusta University.

Theirs and other recent findings suggest that some people with Alzheimer's who have brain changes widely associated with the condition, like amyloid plaques, may not develop dementia without this underlying vascular dysfunction, the researchers write in the journal GeroScience.

"We are proposing that if you prevent development of the microvascular component, you may at least add several years of more normal functioning to individuals with Alzheimer's," Bagi says.

He and by Dr. Stephen Back, pediatric neurologist, Clyde and Elda Munson Professor of Pediatric Research and an expert in white matter injury and repair in the developing and adult brain at Oregon Health & Science University, are co-corresponding authors of the new study.

The good news is that vascular disease is potentially modifiable, Bagi says, by reducing major contributors like hypertension, obesity, diabetes and inactivity.

The scientists looked at the brains of 28 individuals who participated in the Adult Changes in Thought Study, or ACT, a joint initiative of Kaiser Permanente Washington Research Institute and the University of Washington, whose scientists also were collaborators on the new study.

ACT is a longitudinal study of the cognitive health of community volunteers from the Seattle, Washington area with the goal of finding ways to delay or prevent memory decline. Participants age 65 or older with no cognitive problems upon enrollment are followed until their death, and about 25% agree to autopsy and making genomic DNA from their blood and/or brain tissue available to scientists.

The individuals that served as controls for the study had no indication of Alzheimer's or vascular disease in their brain. Other groups had Alzheimer's without vascular disease, vascular disease without indicators of Alzheimer's or both Alzheimer's and vascular disease.

Their focus in the studies was the white matter, which accounts for about 50% of the brain mass, enables different regions of the brain to communicate and is packed with long arms called axons that connect neurons to each other and to other cells across the body like muscle cells; and, the microscopic arterioles that directly feed white matter with blood, oxygen and nutrients.

They wanted to test their theory that when these hair-thin arterioles had difficulty dilating and so supporting this part of the brain, it resulted in changes to the white matter that were evident on sophisticated MRIs, especially when microvascular problems coexisted with the more classic brain changes of Alzheimer's.

They found that the arterioles of those who had been diagnosed with Alzheimer's and dysfunction of these tiny arteries did have an impaired ability to dilate in response to the powerful blood vessel dilator bradykinin, compared to those without obvious microvascular dysfunction. Problems with dilation were associated with white matter injury and changes to the white matter structure that were visible on MRI.

Expression of the precursor for the also-powerful blood vessel dilator nitric oxide also was reduced in these individuals with both conditions while the expression of superoxide generating NOX1, which damages blood vessels, was increased.

Arteriole dysfunction also was associated with more white matter injury based on what was visible on those sophisticated MRI scans and the increased number of brain cells, called astrocytes, which support neurons.

The investigators had previously reported an increase in these astrocytes in brains with the microvascular changes. This time they saw that when Alzheimer's and the microvascular changes were both present, the astrocytes became more reactive, inflammatory and damaging.

Colleagues at Oregon Health & Science University, led by Back, looked at the same brain tissue with a sophisticated MRI technique called diffusion tensor imaging, that uses water diffusion between cells to look at the microstructure of white matter and its connectivity.

They could not visualize individual arterioles because they are too small -- about 30 microns or .0011811 inches -- to see without a microscope. But they could see the white matter damage that resulted from arteriole disease, and again found the correlation between the vascular impairment and tissue damage that Bagi described from directly visualizing the tissue. This type of blood vessel disease was present in 50% of the brains they studied, and other autopsy studies have indicated a similarly high rate.

In those with less indicators of brain changes, they found the arterioles were better able to dilate, that area of the brain had better connectivity and less damage apparent on the postmortem MRI.

Impaired ability of these small vessels in the white matter to dilate is known to be associated with white matter injury, like that visible on the specialized MRI scans. And there is evidence in both laboratory studies and humans that this vascular dysfunction does not just worsen but plays a role in the development of cognitive decline and dementia in people with Alzheimer's, the investigators write.

In fact, the vascular dysfunction may be present before the damage to the brain tissue and cognitive dysfunction is apparent. In research animals bred to develop Alzheimer's, for example, there is evidence of problems with the microvasculature in areas of the brain associated with Alzheimer's, like the hippocampus, a center of learning and memory, at a very young age.

The new work confirms the growing concept that small blood vessel disease may help predict the severity of dementia and/or use of DTI MRI may help identify those patients with early enough disease that strategies to reduce or slow small blood vessel disease may help delay or reduce their cognitive loss. The technique might also help assess the potential benefit of intervention.

"These individuals might especially benefit if they would exercise, control blood sugar level and control their blood pressure," Bagi says.

Some patients with Alzheimer's disease are known to have white matter hyperintensities on MRI scan, basically damaged areas that show up particularly bright on the scan and are associated with problems like dementia. A significant proportion of individuals with Alzheimer's also have conditions like high lipid levels in their blood and hypertension that are known to impair blood vessel function, including the smallest vasculature, Bagi notes. Small blood vessel disease in the brain also is common in aging and may indicate an increased risk of problems like stroke or dementia. Sophisticated brain scans also often indicate microinfarcts, essentially microscopic strokes, which also tend to increase with age and are associated with memory impairment.

Age and a family history are major risk factor for Alzheimer's and there are two categories of genes associated with an increased risk, including risk genes, like APOE-e4, the first gene identified and the one that has the strongest impact on risk, according to the Alzheimer's Organization. Then there are those genes that can directly cause Alzheimer's, called deterministic genes, which impact production or processing of beta-amyloid, the main component of the plaque associated with Alzheimer's, but even having these rare genes are not a guarantee of disease.

"You have some genetic predisposition but people realize that not everybody develops memory decline or cognitive deficits unless something else is coming in," Bagi says. He notes that they have not yet analyzed the genes for this study.

Next steps include studying the associations they found in more human brains and more studies to better understand exactly how the small blood vessel disease happens, which could point toward new targets to intervene.

https://www.sciencedaily.com/releases/2022/08/220802105025.htm

Common viruses may be triggering the onset of Alzheimer's disease

Shingles infection may activate dormant neurological herpes viruses, causing inflammation and accumulation of Alzheimer's associated proteins in the brain

August 2, 2022

Science Daily/Tufts University

Alzheimer's disease can begin almost imperceptibly, often masquerading in the early months or years as forgetfulness that is common in older age. What causes the disease remains largely a mystery.

But researchers at Tufts University and the University of Oxford, using a three-dimensional human tissue culture model mimicking the brain, have shown that varicella zoster virus (VZV), which commonly causes chickenpox and shingles, may activate herpes simplex (HSV), another common virus, to set in motion the early stages of Alzheimer's disease.

Normally HSV-1 -- one of the main variants of the virus -- lies dormant within the neurons of the brain, but when it is activated it leads to accumulation of tau and amyloid beta proteins, and loss of neuronal function -- signature features found in patients with Alzheimer's.

"Our results suggest one pathway to Alzheimer's disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain," said Dana Cairns, GBS12, a research associate in the Biomedical Engineering Department. "While we demonstrated a link between VZV and HSV-1 activation, it's possible that other inflammatory events in the brain could also awaken HSV-1 and lead to Alzheimer's disease."

The study is published in the Journal of Alzheimer's Disease.

Viruses Lying in Wait

"We have been working off a lot of established evidence that HSV has been linked to increased risk of Alzheimer's disease in patients," said David Kaplan, Stern Family Professor of Engineering and chair of the Department of Biomedical Engineering at Tufts' School of Engineering. One of the first to hypothesize a connection between herpes virus and Alzheimer's disease is Ruth Itzhaki of the University of Oxford, who collaborated with the Kaplan lab on this study.

"We know there is a correlation between HSV-1 and Alzheimer's disease, and some suggested involvement of VZV, but what we didn't know is the sequence of events that the viruses create to set the disease in motion," he said. "We think we now have evidence of those events."

According to the World Health Organization, an estimated 3.7 billion people under the age of 50 have been infected with HSV-1 -- the virus that causes oral herpes. In most cases it is asymptomatic, lying dormant within nerve cells.

When activated, it can cause inflammation in nerves and skin, causing painful open sores and blisters. Most carriers -- and that's one in two Americans according to the CDC -- will have between very mild to no symptoms before the virus becomes dormant.

Varicella zoster virus is also extremely common, with about 95 percent of people having been infected before the age of 20. Many of those cases are expressed as chicken pox. VZV, which is a form of herpes virus, can also remain in the body, finding its way to nerve cells before then becoming dormant.

Later in life, VZV can be reactivated to cause shingles, a disease characterized by blisters and nodules in the skin that form in a band-like pattern and can be very painful, lasting for weeks or even months. One in three people will eventually develop a case of shingles in their lifetime.

The link between HSV-1 and Alzheimer's disease only occurs when HSV-1 has been reactivated to cause sores, blisters, and other painful inflammatory conditions.

How Sleeping Viruses May Wake

To better understand the cause-and-effect relationship between the viruses and Alzheimer's disease, the Tufts researchers re-created brain-like environments in small 6 millimeter-wide donut-shaped sponges made of silk protein and collagen.

They populated the sponges with neural stem cells that grow and become functional neurons capable of passing signals to each other in a network, just as they do in the brain. Some of the stem cells also form glial cells, which are typically found in the brain and help keep the neurons alive and functioning.

The researchers found that neurons grown in the brain tissue can be infected with VZV, but that alone did not lead to the formation of the signature Alzheimer's proteins tau and beta-amyloid -- the components of the tangled mess of fibers and plaques that form in Alzheimer's patients' brains -- and that the neurons continued to function normally.

However, if the neurons already harbored quiescent HSV-1, the exposure to VZV led to a reactivation of HSV, and a dramatic increase in tau and beta-amyloid proteins, and the neuronal signals begin to slow down.

"It's a one-two punch of two viruses that are very common and usually harmless, but the lab studies suggest that if a new exposure to VZV wakes up dormant HSV-1, they could cause trouble," said Cairns.

"It's still possible that other infections and other pathways of cause and effect could lead to Alzheimer's disease, and risk factors such as head trauma, obesity, or alcohol consumption suggest they may intersect at the re-emergence of HSV in the brain," she added.

The researchers observed that the VZV infected samples started to produce a higher level of cytokines -- proteins which are often involved in triggering an inflammatory response. Kaplan noted that VZV is known in many clinical cases to cause inflammation in the brain, which could possibly lead to activation of dormant HSV and increased inflammation.

Repeat cycles of HSV-1 activation can lead to more inflammation in the brain, production of plaques, and accumulation of neuronal and cognitive damage.

A vaccine for VZV -- to prevent chickenpox and shingles -- has also been shown to considerably reduce the risk of dementia. It's possible that the vaccine is helping to stop the cycle of viral reactivation, inflammation, and neuronal damage.

The researchers also noted the long-term neurological effects that some COVID patients have experienced from the SARS-CoV-2 virus, particularly among the elderly, and that both VZV and HSV-1 can be reactivated after a COVID infection. Keeping an eye on possible follow-on cognitive effects and neurodegeneration would be advisable in these cases, they said.

https://www.sciencedaily.com/releases/2022/07/220729173148.htm

COVID-19 infection in crucial brain regions may lead to accelerated brain aging

Study finds this may put vulnerable individuals at risk for irreversible neurological conditions

July 28, 2022

Science Daily/Houston Methodist

A new study by Houston Methodist researchers reviews the emerging insights and evidence that suggest COVID-19 infections may have both short- and long-term neurological effects. Major findings include that COVID-19 infections may predispose individuals to developing irreversible neurological conditions, may increase the likelihood of strokes and may increase the chance of developing persistent brain lesions that can lead to brain bleeding.

Led by corresponding authors Joy Mitra, Ph.D., Instructor, and Muralidhar L. Hegde, Ph.D., Professor of Neurosurgery, with the Division of DNA Repair within the Center for Neuroregeneration at the Houston Methodist Research Institute, the research team described their findings in an article titled "SARS-CoV-2 and the Central Nervous System: Emerging Insights into Hemorrhage-Associated Neurological Consequences and Therapeutic Considerations" online in press July 16 in the journal Ageing Research Reviews.

Still a major burden on our daily lives, a great deal of research has shown that the impacts of the disease go far beyond the actual time of infection. Since the onset of the pandemic, COVID-19 has surpassed a death toll of over 5.49 million worldwide and over 307 million confirmed positive cases, with the U.S. accounting for almost 90 million of those cases, according to the Our World in Data website.

COVID-19 is known to invade and infect the brain, among other major organs. While a lot of research has been done to help us understand the evolution, infection and pathology of the disease, there is still a great deal that remains unclear about the long-term effects, especially on the brain.

The coronavirus infection can cause long-term and irreversible neurodegenerative diseases, particularly in the elderly and other vulnerable populations. Several brain imaging studies on COVID-19 victims and survivors have confirmed the formation of microbleed lesions in deeper brain regions related to our cognitive and memory functions. In this review study, researchers have critically evaluated the possible chronic neuropathological outcomes in aging and comorbid populations if timely therapeutic intervention is not implemented.

Microbleeds are emerging neuropathological signatures frequently identified in people suffering from chronic stress, depressive disorders, diabetes and age-associated comorbidities. Based on their earlier findings, the investigators discuss how COVID-19-induced microhemorrhagic lesions may exacerbate DNA damage in affected brain cells, resulting in neuronal senescence and activation of cell death mechanisms, which ultimately impact brain microstructure-vasculature. These pathological phenomena resemble hallmarks of neurodegenerative conditions like Alzheimer's and Parkinson's diseases and are likely to aggravate advanced-stage dementia, as well as cognitive and motor deficits.

The effects of COVID-19 infection on various aspects of the central nervous system are currently being studied. For instance, 20-30% of COVID-19 patients report a lingering psychological condition known as "brain fog" where individuals suffer from symptoms such as memory loss, difficulty in concentrating, forgetting daily activities, difficulty in selecting the right words, taking longer than usual time to complete a regular task, disoriented thought processes and emotional numbness.

More severe long-term effects analyzed in the Houston Methodist review article include predispositions for Alzheimer's, Parkinson's and related neurodegenerative diseases, as well as cardiovascular disorders due to internal bleeding and blood clotting-induced lesions in the part of the brain that regulates our respiratory system, following the COVID-19 symptoms. Additionally, cellular aging is thought to be accelerated in COVID-19 patients. A plethora of cellular stresses inhibit the virus-infected cells from undergoing their normal biological functions and let them enter into "hibernation mode" or even die completely.

The study also suggests various strategies to improve some of these long-term neuropsychiatric and neurodegenerative outcomes, as well as outlines the importance of the therapeutic regimen of the "nanozyme" in combination with various FDA-approved drugs that may prove successful to fight against this catastrophic disease.

However, given the ever-evolving nature of this field, associations like the ones described in this review show the fight against COVID-19 is far from over, say the investigators, and reinforce the message that getting vaccinated and maintaining proper hygiene are key in trying to prevent such long-term and detrimental consequences.

https://www.sciencedaily.com/releases/2022/07/220728143030.htm

Rapid loss of smell predicts dementia and smaller brain areas linked to Alzheimer's

July 28, 2022

Science Daily/University of Chicago Medical Center

Though we often undervalue our ability to smell compared to our abilities to see and hear, our olfactory sense provides our brain with critical information, from detecting potential dangers like smoke to recognizing the sweet smell of baking cookies.

Researchers at the University of Chicago Medicine have discovered another reason to appreciate our sniffers. Not only can a decline in a person's sense of smell over time predict their loss of cognitive function, it can foretell structural changes in regions of the brain important in Alzheimer's disease and dementia.

The findings, based on a longitudinal study of 515 older adults published July 2 in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, could lead to the development of smell-test screening to detect cognitive impairment earlier in patients.

"This study provides another clue to how a rapid decline in the sense of smell is a really good indicator of what's going to end up structurally occurring in specific regions of the brain," said senior author Jayant M. Pinto, MD, a professor of surgery at the University of Chicago and ENT specialist who studies olfactory and sinus disease.

It's estimated more than 6 million Americans have Alzheimer's disease, which is characterized by memory loss and other symptoms, such as mood changes and trouble completing everyday tasks. There is no cure for Alzheimer's, but some medications can temporarily slow its symptoms.

Memory plays a critical role in our ability to recognize smells, and researchers have long known of a link between the sense of smell and dementia. The plaques and tangles that characterize tissue affected by Alzheimer's disease often appear in olfactory and memory- associated areas before developing in other parts of the brain. It's still unknown if this damage actually causes the decline in a person's sense of smell.

Pinto and his team wanted to see whether it was possible to identify alterations in the brain that correlated with a person's loss of smell and cognitive function over time.

"Our idea was that people with a rapidly declining sense of smell over time would be in worse shape -and more likely to have brain problems and even Alzheimer's itself -than people who were slowly declining or maintaining a normal sense of smell," said Rachel Pacyna, a rising fourth-year medical student at the University of Chicago Pritzker School of Medicine and lead author of the study.

The team tapped anonymized patient data from Rush University's Memory and Aging Project (MAP), a study group begun in 1997 to research chronic conditions of aging and neurodegenerative disease such as Alzheimer's disease. MAP participants are older adults living in retirement or senior housing communities in Northern Illinois and are tested annually for their ability to identify certain smells, for cognitive function and for signs of dementia, among other health parameters. Some participants also received an MRI scan.

The UChicago Medicine scientists found that a rapid decline in a person's sense of smell during a period of normal cognition predicted multiple features of Alzheimer's disease, including smaller gray matter volume in the areas of the brain related to smell and memory, worse cognition and higher risk of dementia in these older adults. In fact, the risk of sense of smell loss was similar to carrying the APOE-e4 gene, a known genetic risk factor for developing Alzheimer's.

The changes were most noticeable in the primary olfactory regions, including the amygdala and entorhinal cortex, which is a major input to the hippocampus, a critical site in Alzheimer's disease.

"We were able to show that the volume and shape of grey matter in olfactory and memory-associated areas of the brains of people with rapid decline in their sense of smell were smaller compared to people who had less severe olfactory decline," said Pinto.

An autopsy is the gold standard for confirming whether someone had Alzheimer's, and Pinto hopes to eventually extend these findings by examining brain tissue for markers of Alzheimer's. The team also hopes to study the effectiveness of using smell tests in clinics -- in ways similar to how vision and hearing tests are used -- as a means of screening and tracking older adults for signs of early dementia, and to develop new treatments.

Smell tests are an inexpensive, easy-to-use tool that consists of a series of sticks that are similar in appearance to felt-tip pens. Each stick is infused with a distinct scent that individuals must identify from a set of four choices.

"If we could identify people in their 40s, 50s and 60s who are at higher risk early on, we could potentially have enough information to enroll them into clinical trials and develop better medications," said Pacyna.

The study was limited in that participants received only one MRI scan, which meant the team lacked the data to pinpoint when structural changes in the brains began or how quickly brain regions shrunk.

"We have to take our study in the context of all of the risk factors that we know about Alzheimer's, including the effects of diet and exercise," said Pinto. "Sense of smell and change in the sense of smell should be one important component in the context of an array of factors that we believe affect the brain in health and ageing.

Also, because most MAP participants were white, additional research is needed to determine whether underrepresented populations are similarly affected. The team's prior work showed marked disparities by race, with African Americans facing the most severe impairment in smell function.

Pinto's previous studies have examined the sense of smell as an important marker for declining health in older adults. His 2014 paper revealed older adults with no sense of smell were three times more likely to die within five years -- a better predictor of death than a diagnosis of lung disease, heart failure or cancer.

https://www.sciencedaily.com/releases/2022/07/220728075930.htm

Chores, exercise, and social visits linked to lower risk of dementia

July 27, 2022

Science Daily/American Academy of Neurology

Physical and mental activities, such as household chores, exercise, and visiting with family and friends, may help lower the risk of dementia, according to a new study published in the July 27, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study looked at the effects of these activities, as well as mental activities and use of electronic devices in people both with and without higher genetic risk for dementia.

"Many studies have identified potential risk factors for dementia, but we wanted to know more about a wide variety of lifestyle habits and their potential role in the prevention of dementia," said study author Huan Song, MD, PhD, of Sichuan University in Chengdu, China. "Our study found that exercise, household chores, and social visits were linked to a reduced risk of various types of dementia."

The study involved 501,376 people from a UK database without dementia with an average age of 56.

Participants filled out questionnaires at the beginning of the study, including one on physical activities. They were asked how often they participated in activities such as climbing a flight of stairs, walking, and participating in strenuous sports. They were also asked about household chores, job-related activities, and what kind of transportation they used, including walking or biking to work.

Participants completed another questionnaire on mental activities. They were asked about their education level, whether they attend adult education classes, how often they visit with friends and family, visit pubs or social clubs or religious groups, and how often they use electronic devices such as playing computer games, watching TV, and talking on the phone.

Additionally, participants reported whether they had any immediate family members with dementia. This helped researchers determine if they had a genetic risk for Alzheimer's disease. Study participants were followed an average of 11 years. At the end of the study, 5,185 people had developed dementia.

After adjusting for multiple factors such as age, income, and smoking, researchers found that most physical and mental activities studied showed links to the risk of dementia. Importantly, the findings remain after considering the high correlations and interactions of these activities. People who were highly engaged in activity patterns including frequent exercises, household chores, and daily visits of family and friends had 35%, 21%, and 15% lower risk of dementia, respectively, compared to people who were the least engaged in these activity patterns.

Researchers also looked at dementia incidence rates by identified activity patterns. The rate in people who exercised frequently was 0.45 cases for every 1,000 person-years compared to 1.59 for people who rarely exercised. Person-years take into account the number of people in a study as well as the amount of time spent in the study. Those who frequently did household chores had a rate of 0.86 cases for every 1,000 person-years compared to 1.02 for people who rarely did household chores. People who visited family daily had a rate of 0.62 cases for every 1,000 person-years compared to 0.8 cases for those who only visited friends and family once every few months.

"Our study has found that by engaging more frequently in healthy physical and mental activities people may reduce their risk of dementia," Song said. "More research is needed to confirm our findings. However, our results are encouraging that making these simple lifestyle changes may be beneficial."

The researchers found that all participants benefited from the protective effect of physical and mental activities, whether or not they had a family history of dementia.

A limitation of the study was that people reported their own physical and mental activity, so they may not have remembered and reported these activities correctly.

https://www.sciencedaily.com/releases/2022/07/220727163109.htm

Eating more ultra-processed foods associated with increased risk of dementia

July 27, 2022

Science Daily/American Academy of Neurology

People who eat the highest amounts of ultra-processed foods like soft drinks, chips and cookies may have a higher risk of developing dementia than those who eat the lowest amounts, according to a new study published in the July 27, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology. Researchers also found that replacing ultra-processed foods in a person's diet with unprocessed or minimally processed foods was associated with a lower risk. The study does not prove that ultra-processed foods cause dementia. It only shows an association.

Ultra-processed foods are high in added sugar, fat and salt, and low in protein and fiber. They include soft drinks, salty and sugary snacks, ice cream, sausage, deep-fried chicken, yogurt, canned baked beans and tomatoes, ketchup, mayonnaise, packaged guacamole and hummus, packaged breads and flavored cereals.

"Ultra-processed foods are meant to be convenient and tasty, but they diminish the quality of a person's diet," said study author Huiping Li, PhD, of Tianjin Medical University in China. "These foods may also contain food additives or molecules from packaging or produced during heating, all of which have been shown in other studies to have negative effects on thinking and memory skills. Our research not only found that ultra-processed foods are associated with an increased risk of dementia, it found replacing them with healthy options may decrease dementia risk."

For the study, researchers identified 72,083 people from the UK Biobank, a large database containing the health information of half a million people living in the United Kingdom. Participants were age 55 and older and did not have dementia at the start of the study. They were followed for an average of 10 years. By the end of the study, 518 people were diagnosed with dementia.

During the study, participants filled out at least two questionnaires about what they ate and drank the previous day. Researchers determined how much ultra-processed food people ate by calculating the grams per day and comparing it to the grams per day of other foods to create a percentage of their daily diet. They then divided participants into four equal groups from lowest percentage consumption of ultra-processed foods to highest.

On average, ultra-processed foods made up 9% of the daily diet of people in the lowest group, an average of 225 grams per day, compared to 28% for people in the highest group, or an average of 814 grams per day. One serving of items like pizza or fish sticks was equivalent to 150 grams. The main food group contributing to high ultra-processed food intake was beverages, followed by sugary products and ultra-processed dairy.

In the lowest group, 105 of the 18,021 people developed dementia, compared to 150 of the 18,021 people in the highest group.

After adjusting for age, gender, family history of dementia and heart disease and other factors that could affect risk of dementia, researchers found that for every 10% increase in daily intake of ultra-processed foods, people had a 25% higher risk of dementia.

Researchers also used study data to estimate what would happen if a person substituted 10% of ultra-processed foods with unprocessed or minimally processed foods, like fresh fruit, vegetables, legumes, milk and meat. They found that such a substitution was associated with a 19% lower risk of dementia.

"Our results also show increasing unprocessed or minimally processed foods by only 50 grams a day, which is equivalent to half an apple, a serving of corn, or a bowl of bran cereal, and simultaneously decreasing ultra-processed foods by 50 grams a day, equivalent to a chocolate bar or a serving of fish sticks, is associated with 3% decreased risk of dementia," said Li. "It's encouraging to know that small and manageable changes in dietmay make a difference in a person's risk of dementia."

Li noted that further research is needed to confirm the findings.

Maura E. Walker, PhD, of Boston University in Massachusetts, who wrote an editorial accompanying the study, said, "While nutrition research has started to focus on food processing, the challenge is categorizing such foods as unprocessed, minimally processed, processed and ultra-processed. For example, foods like soup would be classified differently if canned versus homemade. Plus, the level of processing is not always aligned with diet quality. Plant-based burgers that qualify as high quality may also be ultra-processed. As we aim to understand better the complexities of dietary intake, we must also consider that more high-quality dietary assessments may be required."

A limitation of the study was that cases of dementia were determined by looking at hospital records and death registries rather than primary care data, so milder cases may have been overlooked. .

https://www.sciencedaily.com/releases/2022/07/220727163045.htm

Finding the right memory strategy to slow cognitive decline

A new study compares two popular forms of cognitive training that people often use to improve learning and memory

July 25, 2022

Science Daily/Michigan Medicine - University of Michigan

What's the best way to improve your memory as you age? Turns out, it depends, a new study suggests. But your fourth-grade math teacher may have been onto something with that phrase to help you remember how to work out a complicated problem: Please Excuse My Dear Aunt Sally.

A new study led by researchers from the University of Michigan and Penn State College of Medicine compared two approaches for people with an early form of memory loss.

The two are mnemonic strategy training, which aims to connect what someone is trying to remember to something else like a word, phrase or song (such as the Dear Aunt Sally mnemonic), and spaced retrieval training, which gradually increases the amount of time between tests of remembering something.

People with mild cognitive impairment, which can but does not always lead to a later Alzheimer's disease diagnosis, were better able to remember information when using one of these cognitive training approaches. However, the data, and brain scans that revealed which areas of the brain were more active, showed each activity works differently.

"Our research shows that we can help people with mild cognitive impairment improve the amount of information they learn and remember; however, different cognitive training approaches engage the brain in distinct ways," said lead and corresponding author Benjamin Hampstead, Ph.D. Hampstead is a professor of psychiatry at Michigan Medicine and the VA Ann Arbor Healthcare System. He directs the Research Program on Cognition and Neuromodulation Based Interventions and leads the Clinical Core and co-leads the Neuroimaging Core at the federally funded Michigan Alzheimer's Disease Research Center.

"Mnemonic strategy training increased activity in brain areas often affected by Alzheimer's disease, which likely explains why this training approach helped participants remember more information and for longer," Hampstead said "In contrast, those completing rehearsal-based training showed reduced brain activity, which suggests they were processing the information more efficiently."

Hampstead and his team worked with Krish Sathian, MBBS, Ph.D., professor and chair of Penn State's Department of Neurology and director of Penn State Neuroscience Institute. Sathian noted that cognitive training approaches are likely to become increasingly important in synergy with the new pharmacological treatments on the horizon for those with neurodegenerative disorders.

Moving forward, Hampstead said researchers and clinicians can use this type of information to help identify the best-fit non-pharmacologic treatments for their patients with memory impairment.

https://www.sciencedaily.com/releases/2022/07/220722123233.htm

Early Alzheimer's detection up to 17 years in advance

July 21, 2022

Science Daily/Ruhr-University Bochum

A sensor identifies misfolded protein biomarkers in the blood. This offers a chance to detect Alzheimer's disease before any symptoms occur. Researchers intend to bring it to market maturity.

Alzheimer's disease has a symptom-free period of 15 to 20 years before the first clinical symptoms emerge. Using an immuno-infrared sensor developed in Bochum, a research team is able to identify signs of Alzheimer's disease in the blood up to 17 years before the first clinical symptoms appear. The sensor detects the misfolding of the protein biomarker amyloid-beta. As the disease progresses, this misfolding causes characteristic deposits in the brain, so-called plaques.

"Our goal is to determine the risk of developing Alzheimer's dementia at a later stage with a simple blood test even before the toxic plaques can form in the brain, in order to ensure that a therapy can be initiated in time," says Professor Klaus Gerwert, founding director of the Centre for Protein Diagnostics (PRODI) at Ruhr-Universität Bochum. His team cooperated for the study with a group at the German Cancer Research Centre in Heidelberg (DKFZ) headed by Professor Hermann Brenner.

The team published the results obtained with the immuno-infrared sensor in the journal Alzheimer's & Dementia: The Journal of the Alzheimer's Association on 19 July 2022. This study is supported by a comparative study published in the same journal on 2 March 2022, in which the researchers used complementary single-molecule array (SIMOA) technology.

Early detection of symptom-free people with a high risk of Alzheimer's disease

The researchers analysed blood plasma from participants in the ESTHER study conducted in Saarland for potential Alzheimer's biomarkers. The blood samples had been taken between 2000 and 2002 and then frozen. At that time, the test participants were between 50 and 75 years old and hadn't yet been diagnosed with Alzheimer's disease. For the current study, 68 participants were selected who had been diagnosed with Alzheimer's disease during the 17-year follow-up and compared with 240 control subjects without such a diagnosis. The team headed by Klaus Gerwert and Hermann Brenner aimed to find out whether signs of Alzheimer's disease could already be found in the blood samples at the beginning of the study.

The immuno-infrared sensor was able to identify the 68 test subjects who later developed Alzheimer's disease with a high degree of test accuracy. For comparison, the researchers examined other biomarkers with the complementary, highly sensitive SIMOA technology -- specifically the P-tau181 biomarker, which is currently being proposed as a promising biomarker candidate in various studies. "Unlike in the clinical phase, however, this marker is not suitable for the early symptom-free phase of Alzheimer's disease," as Klaus Gerwert summarises the results of the comparative study. "Surprisingly, we found that the concentration of glial fibre protein (GFAP) can indicate the disease up to 17 years before the clinical phase, even though it does so much less precisely than the immuno-infrared sensor." Still, by combining amyloid-beta misfolding and GFAP concentration, the researchers were able to further increase the accuracy of the test in the symptom-free stage.

Start-up aims to bring immuno-infrared sensor to market maturity

The Bochum researchers hope that an early diagnosis based on the amyloid-beta misfolding could help to apply Alzheimer's drugs at such an early stage that they have a significantly better effect -- for example, the drug Aduhelm, which was recently approved in the USA. "We plan to use the misfolding test to establish a screening method for older people and determine their risk of developing Alzheimer's dementia," says Klaus Gerwert. "The vision of our newly founded start-up betaSENSE is that the disease can be stopped in a symptom-free stage before irreversible damage occurs." Even though the sensor is still in the development phase, the invention has already been patented worldwide. BetaSENSE aims to bring the immuno-infrared sensor to market and have it approved as a diagnostic device so that it can be used in clinical labs.

Clinical trials with Alzheimer's drugs often fail

Approved by the FDA in the USA in spring 2021, the drug Aduhelm has been shown to clear amyloid-beta plaques from the brain. However, previous studies showed it had only a minor effect on clinical symptoms such as memory loss and disorientation. Consequently, the European Medicines Agency decided in winter 2021 not to approve the drug in Europe. "Up to now, clinical trials for Alzheimer's drugs have been failing by the dozen, apparently because the established plaque tests used in the trials don't flag up the disease in time," says Gerwert. "It seems that once plaques are deposited, they induce irreversible damage in the brain." In the tests used to date, the plaques are either detected directly in the brain with the complex and expensive PET scan technology or indirectly determined in a less complex way using protein biomarker concentrations in invasively obtained cerebrospinal fluid with ELISA or mass spectrometry technology. In contrast to established plaque diagnostics, the immuno-infrared sensor indicates the earlier misfolding of amyloid-beta, which causes the later plaque deposition. "However, it is still controversially discussed whether this misfolding is the cause of Alzheimer's disease or if it's just an accompanying factor," points out Gerwert. "For the therapeutic approach, this question is crucial, but it is irrelevant for the diagnosis. The misfolding indicates the onset of Alzheimer's disease."

"The exact timing of therapeutic intervention will become even more important in the future," predicts Léon Beyer, first author and PhD student in Klaus Gerwert's team. "The success of future drug trials will depend on the study participants being correctly characterised and not yet showing irreversible damage at study entry."

Biomarkers for Parkinson's and ALS

Misfolded proteins play a central role in many neurodegenerative diseases, such as Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis (ALS). As the researchers have showed, the immuno-infrared sensor can in principle also be used to detect other misfolded proteins, such as TDP-43, which is characteristic of ALS. They don't measure the concentration of a specific protein, but detect its misfolding using disease-specific antibodies. "Most importantly, this platform technology enables us to make a differential, precise biomarker-based diagnosis in the early stages of neurodegenerative diseases, in which the currently applied symptom-based diagnosis is very difficult and prone to errors," stresses Gerwert.

https://www.sciencedaily.com/releases/2022/07/220721132038.htm

Do benefits of physical, mental activity on thinking differ for men and women?

July 20, 2022

Science Daily/American Academy of Neurology

Studies have shown that physical and mental activity help preserve thinking skills and delay dementia. A new study suggests that these benefits may vary for men and women. The study is published in the July 20, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology.

The study looked at the effects of physical and mental activities, such as reading, going to classes, or playing cards or games, on cognitive reserve in the areas of thinking speed and memory. Cognitive reserve is the buffer that occurs when people have strong thinking skills even when their brains show signs of the underlying changes associated with cognitive impairment and dementia.

"We found that greater physical activity was associated with greater thinking speed reserve in women, but not in men," said study author Judy Pa, PhD, of the University of California, San Diego. "Taking part in more mental activities was associated with greater thinking speed reserve for both men and women."

Greater physical activity was not associated with memory reserve in men or women.

The study involved 758 people with an average age of 76. Some had no thinking or memory problems, some had mild cognitive impairment, and some had dementia. The participants had brain scans and took thinking speed and memory tests. To calculate cognitive reserve, people's thinking tests scores were compared against the changes in the brain associated with dementia, such as the total volume of the hippocampus, a key brain region impacted by Alzheimer's disease.

People were also asked about their usual weekly physical activity. For mental activity, they were asked whether they participated in three types of activities in the past 13 months: reading magazines, newspapers or books; going to classes; and playing cards, games or bingo. They were given one point for each type of activity, for a maximum of three points.

For mental activity, participants averaged 1.4 points. For physical activity, participants took part in an average of at least 15 minutes per week of activities that elevate heart rates such as brisk walking and biking.

Pa said that each additional mental activity people participated in corresponded to 13 fewer years of aging in their processing speed in their thinking skills -- 17 years among men and 10 years among women.

"As we have arguably few-to-no effective treatments for Alzheimer's disease, prevention is crucial. An ounce of prevention is worth a pound of treatment," Pa said. "To know that people could potentially improve their cognitive reserve by taking simple steps such as going to classes at the community center, playing bingo with their friends or spending more time walking or gardening is very exciting."

Pa said that based on the effect sizes seen in the study, a doubling of the amount of physical activity would be equivalent to an estimated 2.75 fewer years of aging when it comes to women's processing speed in their thinking skills.

Researchers also looked at whether the relationship between physical and mental activities and cognitive reserve was affected by the gene that carries the strongest risk for Alzheimer's, called APOE e4. They found that for women, having the gene lessens the effects of the beneficial relationship between physical and mental activities and cognitive reserve.

The study does not prove that physical and mental activities help improve cognitive reserve. It only shows an association.

A limitation of the study was that people reported their own physical and mental activity, so they may not have remembered correctly. Also, structural and societal factors that affect cognitive reserve, such as education, were not measured in the study.

The study was supported by the National Institute on Aging and the National Center for Advancing Translational Sciences.

https://www.sciencedaily.com/releases/2022/07/220720193720.htm

Tracking daily movement patterns may one day help predict dementia

Study explores possibility that changes in daily activity patterns may predict Alzheimer's and other cognitive decline in older adults

July 19, 2022

Science Daily/Johns Hopkins University Bloomberg School of Public Health

Researchers found significant differences in movement patterns between participants with normal cognition and those with mild cognitive impairment or Alzheimer's disease.

Wearable movement-tracking devices may someday be useful in providing early warnings of cognitive decline among older adults, suggest new findings from researchers at the Johns Hopkins Bloomberg School of Public Health.

The researchers analyzed data from ActiGraph activity monitors, which use an activity-tracking sensor similar to those found in Fitbits and Apple watches, worn by nearly 600 participants in a long-running community-based health study of older adults. They found significant differences in movement patterns between participants with normal cognition and those with mild cognitive impairment or Alzheimer's disease. These differences included less activity during waking hours and more fragmented activity during afternoons among the mild cognitive impairment/Alzheimer's participants.

The results were published July 19 in the Journal of Alzheimer's Disease.

"We tend to think of physical activity as a potential therapy to slow cognitive decline, but this study reminds us that cognitive decline may in turn slow physical activity -- and we might someday be able to monitor and detect such changes for earlier and more efficient testing to delay and maybe prevent cognitive impairment that leads to Alzheimer's," says study lead author Amal Wanigatunga, PhD, MPH, assistant scientist in the Department of Epidemiology at the Bloomberg School.

The recent introduction of wearable activity-tracking devices, which are now used by tens of millions of people around the world, has presented an important opportunity for health researchers to measure and track changes in physical movement. The devices can provide automatic, objective measures of daytime physical activity, sleep patterns, heart rate, and blood oxygen levels -- and they are typically Internet-connected, allowing their manufacturers to build datasets covering millions of users. Researchers previously did not have such an easy way to access such health-relevant data at such a large scale.

The aim of the new study was to determine if activity-tracker patterns recorded from a cohort of older adults differ meaningfully between the cognitively normal and the cognitively impaired. Alzheimer's disease, the most common form of dementia, is known to be a decades-long process, and researchers generally expect that future disease-modifying interventions will be more effective when started earlier in the disease course. If scientists could identify a distinctive change in activity that predicts the slide into mild cognitive impairment and, eventually, Alzheimer's and other forms of dementia, then in principle older individuals who show this change in activity could be given further cognitive testing -- and, when available, earlier treatment.

The study made use of data from a larger, ongoing health research project known as the Baltimore Longitudinal Study of Aging (BLSA), in which the National Institute on Aging has been studying thousands of people in the Baltimore area since 1958. The analysis was based on 585 BLSA participants for whom sufficient activity-tracker data and cognitive assessments were available during the period July 2015-December 2019. These included 36 participants with either mild cognitive impairment or Alzheimer's diagnoses.

Adjusting for differences based on age, sex, and race, the researchers found that overall differences in all-day activity measures were not strongly different between the mild cognitive impairment/Alzheimer's and normal cognition groups. However, when the researchers focused on activity patterns during certain times of the day, some differences were revealed.

In the mornings (6 a.m. to noon) and even more so in the afternoons (noon to 6 p.m.), the mild cognitive impairment/Alzheimer's group had significantly lower measures of activity compared to the normal group. The most striking finding was that activity "fragmentation" -- a breaking-up of activity into smaller time periods -- was 3.4 percent higher for the mild cognitive impairment/Alzheimer's participants during the afternoon period.

"Seeing this difference in the afternoons was interesting -- one of the main symptoms of Alzheimer's dementia is the 'sundowning' phenomenon involving increased confusion and mood changes that start in the afternoon, and it might be that these activity markers are capturing some movement related to these symptoms," Wanigatunga says.

The findings, he notes, are preliminary because of the cross-sectional, "snapshot" nature of the study design, though they do support the idea that cognitive decline into mild cognitive impairment and dementia is accompanied by changes in activity patterns.

He and his colleagues plan additional studies that will follow participants over time, to see if measurable yet slight changes in everyday activity patterns help capture early symptomology of mild cognitive impairment and subsequent Alzheimer's disease dementia. 

https://www.sciencedaily.com/releases/2022/07/220719162105.htm

Brain stimulation improves motor skill learning at older age

July 27, 2022

Science Daily/Ecole Polytechnique Fédérale de Lausanne

Even though we don't think about it, every movement we make in our daily life essentially consists of a sequence of smaller actions in a specific order. The only time we realize this is when we have to learn a new motor skill, like a sport, a musical instrument, a new dance routine or even a new electronic device such as a smart phone or videogame controller.

Perhaps unsurprisingly, there is a lot of research invested in figuring out how humans acquire sequential motor skills, with a majority of studies in healthy young adults. Studies involving older individuals (and common experience) show that the older we get, the harder it is and the longer it takes to learn new motor skills, suggesting an age-related decrease in learning ability.

"As learning is crucial for continuously adapting and staying integrated in daily life, improving these impaired functions will help to maintain the quality of life as we age, especially in view of the constant increase in life expectancy seen worldwide," says Professor Friedhelm Hummel who holds the Defitech Chair of Clinical Neuroengineering at EPFL's School of Life Sciences.

In a new study, Hummel and his PhD student Pablo Maceira-Elvira have found that transcranial brain stimulation can improve the age-related impairment in learning new motor skills.

The study used a common way of evaluating how well a person learns new motor skills called the "finger-tapping task." It involves typing a sequence of numbers as fast and as accurately as possible. The task is popular in studies because it simulates activities that require high dexterity -- such as playing the piano or typing on a keyboard -- while providing an objective measure of "improvement," defined as a person increasing their speed without losing accuracy.

Scientists refer to this as a "shift in the speed-accuracy tradeoff," and it constitutes a key feature of learning. One of the ways the brain achieves this shift is by grouping individual motor actions into so called "motor chunks": spontaneously emerging brain structures that reduce a person's mental load, while optimizing the mechanical execution of the motor sequence. "Motor chunks emerge reliably when young adults train on the finger-tapping task, but previous studies show either lacking or deficient motor chunks in older adults," says Pablo Maceira-Elvira.

The early bird gets the motor skill

The study first trained and tested groups of younger and older adults on learning a new sequence of finger-tapping task, and revealed fundamental differences between the two. Young adults learned the finger-tapping task most efficiently by prioritizing the improvement of the accuracy during their first training session and by focusing on improving their speed thereafter. This led to a shift in the speed-accuracy tradeoff, which allowed efficient motor chunks to emerge early on.

"Older adults showed decreased fast online learning and absent offline learning," says Maceira-Elvira. "In other words, while young adults show sharp performance increases early in training and improve overnight, older adults improve at a more moderate pace and even worsen overnight." In contrast, older adults improved their accuracy gradually over the course of training, generating efficient motor chunks only after more extensive practice.

Brain stimulation improvements 

Extensive research has been carried out on novel neurotechnologies that may restore learning impairment in older people. "Recent studies have shown we can enhance motor skill acquisition by applying non-invasive brain stimulation to the motor cortex, with anodal transcranial direct current stimulation (atDCS) attracting both academic and commercial interest in recent years due to its unobtrusiveness, portability and affordability," says Hummel.

In the current study, the researchers applied atDCS to the participants and found that it helped older adults to improve their accuracy sharply earlier on in training and in a pattern similar to that seen in young adults. "Stimulation accelerated the shift in the speed-accuracy tradeoff and enabled an earlier emergence of efficient motor chunks, with 50% of older adults generating these structures during the first training session," says Maceira-Elvira.

He adds: "The study suggests that atDCS can at least partially restore motor skill acquisition in individuals with diminished learning mechanisms, by facilitating the storage of task-relevant information, quickly reducing mental load and allowing the optimization of the mechanical execution of the sequence."

"These studies add to the better understanding of age-related deficits in motor skill acquisition and offer a novel strategy to non-invasively restore these deficits," says Hummel. "These findings open novel opportunities of interventional strategies adjusted to the specific learning phase to restore deficits due to healthy aging or neurological disorder such as stroke."

https://www.sciencedaily.com/releases/2022/07/220720150625.htm

Harm from blue light exposure increases with age, research in flies suggests

July 27, 2022

Science Daily/Oregon State University

The damaging effects of daily, lifelong exposure to the blue light emanating from phones, computers and household fixtures worsen as a person ages, new research by Oregon State University suggests.

The study, published today in Nature Partner Journals Aging, involved Drosophila melanogaster, the common fruit fly, an important model organism because of the cellular and developmental mechanisms it shares with other animals and humans.

Jaga Giebultowicz, a researcher in the OSU College of Science who studies biological clocks, led a collaboration that examined the survival rate of flies kept in darkness and then moved at progressively older ages to an environment of constant blue light from light-emitting diodes, or LEDs.

The darkness-to-light transitions occurred at the ages of two, 20, 40 and 60 days, and the study involved blue light's effect on the mitochondria of the flies' cells.

Mitochondria act as a cell's power plant, generating adenosine triphosphate, or ATP, a source of chemical energy.

In earlier research, Giebultowicz showed that prolonged exposure to blue light affected flies' longevity, regardless of whether it shined in their eyes.

"The novel aspect of this new study is showing that chronic exposure to blue light can impair energy-producing pathways even in cells that are not specialized in sensing light," Giebultowicz said. "We determined that specific reactions in mitochondria were dramatically reduced by blue light, while other reactions were decreased by age independent of blue light. You can think of it as blue light exposure adding insult to injury in aging flies."

Collaborating with Giebultowicz on the work, partially funded by the National Institutes of Health, were Yujuan Song, Jun Yang and David Hendrix of the OSU College of Science, Matthew Robinson of the College of Public Health and Human Sciences, and Alexander Law and Doris Kretzschmar of Oregon Health & Science University.

The scientists note that natural light is crucial for a person's circadian rhythm -- the 24-hour cycle of physiological processes such as brain wave activity, hormone production and cell regeneration that are important factors in eating and sleeping patterns.

But there is evidence suggesting that increased exposure to artificial light is a risk factor for sleep and circadian disorders, Giebultowicz said. And with the prevalent use of LED lighting and device displays, humans are subjected to increasing amounts of light in the blue spectrum since commonly used LEDs emit a high fraction of blue light.

"This technology, LED lighting, even in most developed countries, has not been used long enough to know its effects across the human lifespan," she said. "There are increasing concerns that extended exposure to artificial light, especially blue-enriched LED light, may be detrimental to human health. While the full effects of blue light exposure across the lifespan are not yet known in humans, accelerated aging observed in short-lived model organism should alert us to the potential of cellular damage by this stressor."

In the meantime, there are a few things people can do to help themselves that don't involve sitting for hours in darkness, the researchers say. Eyeglasses with amber lenses will filter out the blue light and protect your retinas. And phones, laptops and other devices can be set to block blue emissions.

"Our previous work demonstrated that daily lifelong exposure to blue light, but not other visible wavelengths, has damaging effects on the brain, motor abilities and lifespan of the model organism," Giebultowicz said. "Now we're reporting that the damaging effects of blue light on the flies are strongly age dependent -- the same length of exposure to the same intensity of light decreases lifespan and increases neurodegeneration more significantly in old flies than in young ones."

In the earlier research, flies subjected to daily cycles of 12 hours in light and 12 hours in darkness had shorter lives compared to flies kept in total darkness or those kept in light with the blue wavelengths filtered out.

The flies exposed to blue light showed damage to their retinal cells and brain neurons and had impaired locomotion -- the flies' ability to climb the walls of their enclosures, a common behavior, was diminished.

Some of the flies in the experiment were mutants that didn't develop eyes, and even those eyeless flies displayed impairment, suggesting flies didn't have to see the light to be harmed by it.

https://www.sciencedaily.com/releases/2022/07/220727132656.htm