Slow, steady waves keep brain humming
Such rhythmic waves linked to state of consciousness
March 29, 2018
Science Daily/Washington University School of Medicine
Very slow brain waves, long considered an artifact of brain scanning techniques, may be more important than anyone had realized. Researchers have found that very slow waves are directly linked to state of consciousness and may be involved in coordinating activity across distant brain regions.
If you keep a close eye on an MRI scan of the brain, you'll see a wave pass through the entire brain like a heartbeat once every few seconds. This ultra-slow rhythm was recognized decades ago, but no one quite knew what to make of it. MRI data are inherently noisy, so most researchers simply ignored the ultra-slow waves.
But by studying electrical activity in mouse brains, researchers at Washington University School of Medicine in St. Louis have found that the ultra-slow waves are anything but noise. They are more like waves in the sea, with everything the brain does taking place in boats upon that sea. Research to date has been focused on the goings-on inside the boats, without much thought for the sea itself. But the new information suggests that the waves play a central role in how the complex brain coordinates itself and that the waves are directly linked to consciousness.
"Your brain has 100 billion neurons or so, and they have to be coordinated," said senior author Marcus Raichle, MD, the Alan A. and Edith L. Wolff Distinguished Professor of Medicine and a professor of radiology at Mallinckrodt Institute of Radiology at the School of Medicine. "These slowly varying signals in the brain are a way to get a very large-scale coordination of the activities in all the diverse areas of the brain. When the wave goes up, areas become more excitable; when it goes down, they become less so."
The study is published March 29 in the journal Neuron.
In the early 2000s, Raichle and others discovered patterns of brain activity in people as they lay quietly in MRI machines, letting their minds wander. These so-called resting-state networks challenged the assumption that the brain quiets itself when it's not actively engaged in a task. Now we know that even when you feel like you're doing nothing, your brain is still humming along, burning almost as much energy daydreaming as solving a tough math problem.
Using resting-state networks, other researchers started searching for -- and finding -- brain areas that behaved differently in healthy people than in people with brain diseases such as schizophrenia and Alzheimer's. But even as resting-state MRI data provided new insights into neuropsychiatric disorders, they also consistently showed waves of activity spreading with a slow regularity throughout the brain, independently of the disease under study. Similar waves were seen on brain scans of monkeys and rodents.
Some researchers thought that these ultra-slow waves were no more than an artifact of the MRI technique itself. MRI gauges brain activity indirectly by measuring the flow of oxygen-rich blood over a period of seconds, a very long timescale for an organ that sends messages at one-tenth to one-hundredth of a second. Rather than a genuinely slow process, the reasoning went, the waves could be the sum of many rapid electrical signals over a relatively long time.
First author Anish Mitra, PhD, and Andrew Kraft, PhD -- both MD/PhD students at Washington University -- and colleagues decided to approach the mystery of the ultra-slow waves using two techniques that directly measure electrical activity in mice brains. In one, they measured such activity on the cellular level. In the other, they measured electrical activity layer by layer along the outer surface of the brain.
They found that the waves were no artifact: Ultra-slow waves were seen regardless of the technique, and they were not the sum of all the faster electrical activity in the brain.
Instead, the researchers found that the ultra-slow waves spontaneously started in a deep layer of mice's brains and spread in a predictable trajectory. As the waves passed through each area of the brain, they enhanced the electrical activity there. Neurons fired more enthusiastically when a wave was in the vicinity.
Moreover, the ultra-slow waves persisted when the mice were put under general anesthesia, but with the direction of the waves reversed.
"There is a very slow process that moves through the brain to create temporary windows of opportunity for long-distance signaling," Mitra said. "The way these ultra-slow waves move through the cortex is correlated with enormous changes in behavior, such as the difference between conscious and unconscious states."
The fact that the waves' trajectory changed so dramatically with state of consciousness suggests that ultra-slow waves could be fundamental to how the brain functions. If brain areas are thought of as boats bobbing about on a slow-wave sea, the choppiness and direction of the sea surely influences how easily a message can be passed from one boat to another, and how hard it is for two boats to coordinate their activity.
The researchers now are studying whether abnormalities in the trajectory of such ultra-slow waves could explain some of the differences seen on MRI scans between healthy people and people with neuropsychiatric conditions such as dementia and depression.
"If you look at the brain of someone with schizophrenia, you don't see a big lesion, but something is not right in how the whole beautiful machinery of the brain is organized," said Raichle, who is also a professor of biomedical engineering, of neurology, of neuroscience and of psychological and brain sciences. "What we've found here could help us figure out what is going wrong. These very slow waves are unique, often overlooked and utterly central to how the brain is organized. That's the bottom line."
https://www.sciencedaily.com/releases/2018/03/180329141012.htm
Neuroscientists say daily ibuprofen can prevent Alzheimer's disease
March 26, 2018
Science Daily/IOS Press
Neuroscientists have successfully carried out studies suggesting that, if started early enough, a daily regimen of the non-prescription NSAID (nonsteroidal anti-inflammatory drug) ibuprofen can prevent the onset of Alzheimer's disease.
A Vancouver-based research team led by Canada's most cited neuroscientist, Dr. Patrick McGeer, has successfully carried out studies suggesting that, if started early enough, a daily regimen of the non-prescription NSAID (nonsteroidal anti-inflammatory drug) ibuprofen can prevent the onset of Alzheimer's disease. This means that by taking an over-the-counter medication, people can ward off a disease that, according to Alzheimer's Disease International's World Alzheimer Report 2016, affects an estimated 47 million people worldwide, costs health care systems worldwide more than US$818 billion per year and is the fifth leading cause of death in those aged 65 or older.
The Alzheimer's Association estimates that there are more than 5 million cases in the United States alone, with a new case being identified every 66 seconds. The annual cost to the country in 2017 is estimated have been $259 billion, with that figure predicted to potentially rise to $1.1 trillion by 2050.
Dr. McGeer, who is President and CEO of Vancouver-based Aurin Biotech, and his wife, Dr. Edith McGeer, are among the most cited neuroscientists in the world. Their laboratory is world-renowned for their 30 years of work in neuroinflammation and neurodegenerative diseases, particularly Alzheimer's disease. A paper detailing Dr. McGeer's most recent discoveries were published Friday in the Journal of Alzheimer's Disease.
In 2016, Dr. McGeer and his team announced that they had developed a simple saliva test that can diagnose Alzheimer's disease, as well as predict its future onset. The test is based on measuring the concentration of the peptide amyloid beta protein 42 (Abeta42) secreted in saliva. In most individuals, the rate of Abeta 42 production is almost exactly the same regardless of sex or age. However, if that rate of production is two to three times higher, those individuals are destined to develop Alzheimer's disease. That is because Abeta42 is a relatively insoluble material, and although it is made everywhere in the body, deposits of it occur only in the brain, causing neuroinflammation, which destroys neurons in the brains of people with Alzheimer's disease.
Contrary to the widely held belief that Abeta 42 is made only in the brain, Dr. McGeer's team demonstrated that the peptide is made in all organs of the body and is secreted in saliva from the submandibular gland. As a result, with as little as one teaspoon of saliva, it is possible to predict whether an individual is destined to develop Alzheimer's disease. This gives them an opportunity to begin taking early preventive measures such as consuming non-prescription non-steroidal drugs (NSAIDs) such as ibuprofen.
"What we've learned through our research is that people who are at risk of developing Alzheimer's exhibit the same elevated Abeta 42 levels as people who already have it; moreover, they exhibit those elevated levels throughout their lifetime so, theoretically, they could get tested anytime," says Dr. McGeer. "Knowing that the prevalence of clinical Alzheimer's Disease commences at age 65, we recommend that people get tested ten years before, at age 55, when the onset of Alzheimer's would typically begin. If they exhibit elevated Abeta 42 levels then, that is the time to begin taking daily ibuprofen to ward off the disease.
"Unfortunately, most clinical trials to date have focused on patients whose cognitive deficits are already mild to severe, and when the therapeutic opportunities in this late stage of the disease are minimal. Consequently, every therapeutic trial has failed to arrest the disease's progression. Our discovery is a game changer. We now have a simple test that can indicate if a person is fated to develop Alzheimer's disease long before it begins to develop. Individuals can prevent that from happening through a simple solution that requires no prescription or visit to a doctor. This is a true breakthrough since it points in a direction where AD can eventually be eliminated."
https://www.sciencedaily.com/releases/2018/03/180326140239.htm
Older adults who have slower walking speeds may have increased risk for dementia
March 23, 2018
Science Daily/American Geriatrics Society
Because there's currently no cure for dementia, it's important to know about risk factors that may lead to developing it. For example, researchers have learned that older adults with slower walking speeds seem to have a greater risk than those with faster walking speeds. Recently, researchers have learned more about changes in walking speed, changes in the ability to think and make decisions, and dementia.
The researchers examined information collected from the English Longitudinal Study of Aging. The study included adults aged 60 and older who lived in England. In their study, the researchers used information collected from 2002 to 2015. They assessed participants' walking speed on two occasions in 2002-2003 and in 2004-2005, and whether or not the participants developed dementia after the tests from 2006-2015. Then, they compared the people who had developed dementia with those who had not.
Researchers discovered that of the nearly 4,000 older adults they studied, those with a slower walking speed had a greater risk of developing dementia. And people who experienced a faster decline in walking speed over a two-year period were also at higher risk for dementia. People who had a poorer ability to think and make decisions when they entered the study -- and those whose cognitive (thinking) abilities declined more quickly during the study -- were also more likely to be diagnosed with dementia.
The researchers concluded that older adults with slower walking speeds, and those who experienced a greater decline in their walking speed over time, were at increased risk for dementia. But, the researchers noted, changes in walking speed and changes in an older adult's ability to think and make decisions do not necessarily work together to affect the risk of developing dementia.
https://www.sciencedaily.com/releases/2018/03/180323121747.htm
Vegetable compound could have a key role in 'beeting' Alzheimer's disease
March 20, 2018
Science Daily/American Chemical Society
A compound in beets that gives the vegetable its distinctive red color could help slow the accumulation of misfolded proteins in the brain, a process associated with Alzheimer's disease. Scientists say this could lead to the development of drugs that could alleviate some of the long-term effects of the disease, the world's leading cause of dementia.
The researchers are presenting their work today at the 255th National Meeting & Exposition of the American Chemical Society (ACS).
"Our data suggest that betanin, a compound in beet extract, shows some promise as an inhibitor of certain chemical reactions in the brain that are involved in the progression of Alzheimer's disease," says Li-June Ming, Ph.D. "This is just a first step, but we hope that our findings will encourage other scientists to look for structures similar to betanin that could be used to synthesize drugs that could make life a bit easier for those who suffer from this disease."
More than 5 million Americans have Alzheimer's disease, according to the National Institute on Aging. Its incidence rises with age, affecting one in 10 Americans 65 and older, and one in three by age 85. Scientists are still trying to figure out what causes this progressive and irreversible brain disorder. But one prime suspect is beta-amyloid, a sticky protein fragment, or peptide, that accumulates in the brain, disrupting communication between brain cells called neurons. Much of this damage occurs, Ming says, when beta-amyloid attaches itself to metals such as iron or copper. These metals can cause beta-amyloid peptides to misfold and bind together in clumps that can promote inflammation and oxidation -- a process similar to rusting -- in nearby neurons, eventually killing them.
Previous research conducted by other scientists suggests that beetroot juice can improve oxygen flow to the aging brain and possibly improve cognitive performance. Building on this work, Ming, Darrell Cole Cerrato and colleagues at the University of South Florida wanted to find out if betanin, a beet compound used in commercial dyes that readily binds to metals, could block the effects of copper on beta-amyloid and, in turn, prevent the misfolding of these peptides and the oxidation of neurons.
In laboratory studies, the researchers conducted a series of experiments involving 3,5 di-tert-butylcatechol, or DTBC, a compound that is used as a model substance for tracking the chemistry of oxidation. Using visible spectrophotometry, the scientists measured the oxidative reaction of DTBC when exposed to beta-amyloid only, beta-amyloid bound to copper, and copper-bound beta-amyloid in a mixture containing betanin.
On its own, beta-amyloid caused little or no oxidation of DTBC. However, as expected, beta-amyloid bound to copper induced substantial DTBC oxidation. But when betanin was added to the copper-bound beta-amyloid mixture, the researchers found oxidation dropped by as much as 90 percent, suggesting that misfolding of the peptides was potentially suppressed.
"We can't say that betanin stops the misfolding completely, but we can say that it reduces oxidation," Cerrato says. "Less oxidation could prevent misfolding to a certain degree, perhaps even to the point that it slows the aggregation of beta-amyloid peptides, which is believed to be the ultimate cause of Alzheimer's."
https://www.sciencedaily.com/releases/2018/03/180320084414.htm
The brain puts the memories warehouse in order while we sleep
March 15, 2018
Science Daily/FECYT - Spanish Foundation for Science and Technology
During the hours of sleep the memory performs a cleaning shift. A study reveals that when we sleep, the neural connections that collect important information are strengthened and those created from irrelevant data are weakened until they get lost.
Throughout the day, people retain a lot of information. The brain creates or modifies the neural connections from these data, elaborating memories. But most of the information we receive is irrelevant and it does not make sense to keep it. In such a case, the brain would be overloaded.
So far there have been two hypotheses about how the sleeping brain modifies the neural connections created throughout the day: while one of them argues that all of them are reinforced during sleep hours, the other maintains that their number is reduced.
A group of scientists from the Ole Paulsen Laboratory, at the University of Cambridge (United Kingdom), has analyzed the mechanisms underlying the maintenance of memory during the phase of slow wave sleep -- the third phase of sleep without rapid eye movements in the brain during which there is more relaxation and a deeper rest.
"Depending on the experiences of a person and depending on their relevance, the size of their corresponding neuronal connections changes. Those that save important information are smaller and those that store the dispensable are larger," explains Ana González Rueda, main author of the study and researcher at the MRC Laboratory of Molecular Biology (LMB) in Cambridge.
According to the expert, in the event that all these links were reinforced equally during sleep, the brain would be saturated by an extreme overexcitement of the nervous system.
In the study, published in the Neuron journal, the researchers stimulated the neuronal connections of mice subjected to a type of anesthesia that achieves a brain state similar to the slow wave sleep phase in humans.
In the words of González Rueda, the stimulation was carried out 'blindly' because the information contained in each of the links was not known. "We developed a system to follow the evolution of a specific neuronal synapse and thus study what type of activity influences that these are maintained, grow or decrease."
What isthe maintenance of neural connections dependent on?
The results show that during slow wave sleep, the largest connections are maintained while the smaller ones are lost. This brain mechanism improves the signal-to-noise ratio -- important information remains and the dispensable is discarded -- and allows the storage of various types of information from one day to the next without losing the previous data. That is, those that have already been considered relevant are kept in that state without having to reinforce them. According to González Rueda, the brain "puts order" during the hours of sleep, discarding the weakest connections to ensure stronger and consolidated memories.
"Although the brain has an extraordinary storage capacity, maintaining connections and neuronal activities requires a lot of energy. It is much more efficient to keep only what is necessary," says the expert. "Even without maintaining all the information we receive, the brain spends 20% of the calories we consume."
This research is a first indication of the electro-physiological mechanism of sleep and opens new horizons thanks to the development of a new way of studying live synaptic plasticity.
The next objective of the experts is to research the consequences of this type of brain activity for the maintenance of certain information and to analyze new phases of sleep. "In addition to the analysis of the slow wave phase, it could be interesting to know what happens in the REM phase, during which dreams occur," concludes González Rueda.
https://www.sciencedaily.com/releases/2018/03/180315110640.htm
Cueing newly learned information in sleep improves memory, and here's how
March 8, 2018
Science Daily/Cell Press
Scientists have long known that sleep is important to the formation and retention of new memories. Memory consolidation is associated with sudden bursts of oscillatory brain activity, called sleep spindles, which can be visualized and measured on an electroencephalogram (EEG). Now researchers have found that sleep spindles also play a role in strengthening new memories when newly learned information is played back to a person during sleep.
The findings provide new insight into the process of memory consolidation during sleep. They may also suggest new ways to help people remember things better, according to the researchers.
"While it has been shown previously that targeted memory reactivation can boost memory consolidation during sleep, we now show that sleep spindles might represent the key underlying mechanism," says Bernhard Staresina of the University of Birmingham in the United Kingdom. "Thus, direct induction of sleep spindles -- for example, via transcranial electrical stimulation -- perhaps combined with targeted memory reactivation, may enable us to further improve memory performance while we sleep."
Sleep spindles are half-second to two-second bursts of brain activity, measured in the 10-16 Hertz range on an EEG. They occur during non-rapid eye movement sleep stages two and three. Earlier studies had shown that the number of spindles during the night could predict a person's memory the next day. Studies in animals also linked sleep spindles to the process by which the brain makes new connections. But many questions about the link between sleep spindles and reactivated memories during sleep remained.
Staresina along with Scott Cairney at the University of York, UK, suspected that experimental reactivation of memories might lead to a surge of sleep spindles in a sleeping person's brain. To find out, they devised an experiment in which people learned to associate particular adjectives with particular objects and scenes. Some study participants then took a 90-minute nap after their study session, whereas others stayed awake. While people napped, the researchers cued those associative memories and unfamiliar adjectives.
As expected, the researchers saw that memory cues led to an increase in sleep spindles. Interestingly, the EEG patterns during spindles enabled the researchers to discern what types of memories -- objects or scenes -- were being processed.
The findings add to evidence for an important information-processing role of sleep spindles in the service of memory consolidation, the researchers say.
"Our data suggest that spindles facilitate processing of relevant memory features during sleep and that this process boosts memory consolidation," Staresina says.
This new understanding of the way the brain normally processes and strengthens memories during sleep may help to explain how that process may go wrong in people with learning difficulties, according to the researchers. It might also lead to the development of effective interventions designed to boost memory for important information.
https://www.sciencedaily.com/releases/2018/03/180308120605.htm
Omega fish oils don’t improve school children’s reading skills or memory
March 1, 2018
Science Daily/University of Birmingham
New research has found no evidence Omega-3 fish oil supplements help aid or improve the reading ability or memory function of underperforming schoolchildren.
In the second high-quality trial of its kind, published in PLOS ONE, the researchers found an entirely different result to an earlier study carried out in 2012, where omega-3 supplements were found to have a beneficial effect on the reading ability and working memory of school children with learning needs such as ADHD.
In this second study, the researchers tested children who were in the bottom quarter of ability in reading, and found that fish oil supplements did not have any or very little effect on the children's reading ability or working memory and behaviours.
The team from the Universities of Birmingham and Oxford tested 376 children aged 7-9 years old, learning to read, but in the bottom quarter in terms of their ability.
Half of the children took a daily Omega-3 fish oil supplement and the remaining children took a placebo for 16 weeks.
Their reading and working memories were tested before and after by their parents at home and teachers in school -- with no real differences found in the outcomes.
Professor Paul Montgomery, University of Birmingham, who led the research said: "We are all keen to help kids who are struggling at school and in these times of limited resources, my view is that funds should be spent on more promising interventions. The effects here, while good for a few kids, were not substantial for the many."
Dr Thees Spreckelsen, University of Oxford, Co-Author of the report added: "Fish oil or Omega-3 fatty acids are widely regarded as beneficial. However, the evidence on benefits for children's learning and behaviour is clearly not as strong as previously thought."
https://www.sciencedaily.com/releases/2018/03/180301144543.htm
Brain stimulation helps younger, not older, adults' memory
March 1, 2018
Science Daily/University of Illinois at Chicago
A study found that while the younger adults showed memory improvement from transcranial direct current stimulation, the older adults did not.
As people grow older their memory tend to get poorer, so finding ways to improve it is an important matter of investigation given the longer contemporary lifespans that people are experiencing.
Recent research has shown that stimulating the brain with a mild electric current, known as transcranial direct current stimulation, can improve memory in both younger and older adults.
In a study published online for a forthcoming special issue on the cognitive neuroscience of aging from the Journals of Gerontology: Psychological Sciences, researchers at the University of Illinois at Chicago tested these outcomes by having younger and older sets of participants -- 48 people between the ages of 18 and 35, as well as 48 adults between the ages of 60 and 79 -- try to learn information and remember 60 face-name pairs.
Some of the study participants were given stimulation, and others received sham, or fake, stimulation. Their memories were tested both immediately after stimulation and again 24 hours later to assess effects on memory the following day.
Ultimately, the researchers found that while the younger adults showed memory improvement from stimulation, the older adults did not.
"On average the amount of improvement that younger adults showed from brain stimulation was a 50 percent improvement in memory," said Eric Leshikar, UIC clinical assistant professor of psychology and corresponding author of the study. "Importantly, we found these memory improvements both immediately after stimulation, as well as after 24 hours, suggesting that brain stimulation can effectively improve memory."
The results contradict findings from previous studies that showed that a slight electoral current through the scalp had a greater effect on cognition for older adults compared to younger adults.
Leshikar says future work will look at whether using different stimulation procedures can help propel older adults to experience memory improvement.
"It very well may be that older adults may show memory improvement from stimulation, but perhaps not under the stimulation procedures we used in this study," he said.
https://www.sciencedaily.com/releases/2018/03/180301094829.htm
Largest study of its kind finds alcohol use biggest risk factor for dementia
February 20, 2018
Science Daily/Centre for Addiction and Mental Health
Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study of over one million adults diagnosed with dementia in France.
This study looked specifically at the effect of alcohol use disorders, and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol.
Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking.
The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men (4-5 Canadian standard drinks) and 40 grams (about 3 standard drinks) per day for women.
As a result of the strong association found in this study, the authors suggest that screening, brief interventions for heavy drinking, and treatment for alcohol use disorders should be implemented to reduce the alcohol-attributable burden of dementia.
"The findings indicate that heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths," says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm. "Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths."
Dr. Rehm points out that on average, alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death for these people.
For early-onset dementia, there was a significant gender split. While the overall majority of dementia patients were women, almost two-thirds of all early-onset dementia patients (64.9%) were men.
Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia.
"As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when unfortunately alcohol treatment interventions may be too late to improve cognition," says CAMH Vice-President of Research Dr. Bruce Pollock. "Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care." The authors also noted that only the most severe cases of alcohol use disorder -- ones involving hospitalization -- were included in the study. This could mean that, because of ongoing stigma regarding the reporting of alcohol-use disorders, the association between chronic heavy drinking and dementia may be even stronger.
https://www.sciencedaily.com/releases/2018/02/180220183954.htm
Higher risk of dementia for adults with congenital heart disease
February 20, 2018
Science Daily/Cincinnati Children's Hospital Medical Center
A new study is believed to be the first to show a higher risk of dementia in adults who were born with heart disease. The study of more than 10,000 adult with congenital heart disease (CHD) in Denmark discovered a particularly increased risk for early dementia in middle-age adults.
"We've learned that CHD is a lifelong condition," says Nicolas Madsen, MD, a pediatric cardiologist at Cincinnati Children's Hospital Medical Center and senior author of the study. "Research shows that children born with heart problems are at a greater risk for one or more neurodevelopmental issues when compared to children without heart disease. We can now say that the risk for these types of problems continues well into adulthood."
The study is published online in Circulation, a journal of the American Heart Association.
Dr. Madsen and his colleagues at Aarhus University Hospital in Denmark studied 10,632 adults born between 1890 and 1982. The researchers used medical registries and a medical records review covering all Danish hospitals to identify adults with CHD diagnosed between 1963 and 2012.
The researchers found a 60 percent increased risk of dementia compared to the general population. The risk was 160 percent higher (2.6 times higher) when comparing those less than 65 years old.
Dr. Madsen says it is important to recognize that many of these adults were born during a time when medical and surgical interventions were more limited than they are today. Still, he says "we need to understand the healthcare needs and risk factors affecting the larger number of middle-age and older adults currently living with CHD."
CHD occurs in six to 10 of every 1,000 live births. Because these individuals are now living longer, the population of those with CHD is experiencing different neurodevelopmental issues than those previously described only in infants, children and young adults.
https://www.sciencedaily.com/releases/2018/02/180220143456.htm
TBI is associated with increased dementia risk for decades after injury
January 30, 2018
Science Daily/PLOS
Traumatic brain injuries increase the risk of a dementia diagnosis for more than 30 years after a trauma, though the risk of dementia decreases over time, according to a new study.
Traumatic brain injury (TBI) has been associated with dementia, but the details of that risk over time and in different TBI types have not been well studied. In the new study, the researchers tracked all diagnoses of dementia and TBI in Swedish nationwide databases from 1964 through 2012. In a retrospective cohort, 164,334 individuals with TBI were matched with control participants who did not have TBI; in a case-control cohort, 136,233 individuals diagnosed with dementia at follow-up were matched with control participants who did not develop dementia; and in a third cohort, the researchers studied 46,970 sibling pairs with one individual having a TBI.
In the first year after TBI, the risk of dementia is increased by 4- to 6-fold, the researchers found. Thereafter, the risk decreased rapidly but was still significant more than 30 years after the TBI. Overall, the risk of dementia diagnosis was increased by about 80 percent during a mean follow-up period of 15 years. The risk of dementia was higher for those with a severe TBI or multiple TBIs and was similar in men and women. Because the development of dementia can be a risk factor for accidents resulting in TBI, it's likely that in some cases, the onset of dementia preceded the TBI, so the researchers caution against making causal inferences.
"The findings of this study suggest an existence of a time- and dose-dependent risk of developing dementia more than 30 years after TBI," the authors say. "To our knowledge, no previous prospective study with similar power and follow-up time has been reported."
https://www.sciencedaily.com/releases/2018/01/180130152216.htm
Body clock disruptions occur years before memory loss in Alzheimer’s
January 29, 2018
Science Daily/Washington University in St. Louis
People with Alzheimer’s disease have disturbances in their internal body clocks that affect the sleep/wake cycle and may increase risk of developing the disorder. Researchers have found that such circadian rhythm disruptions also occur much earlier in people whose memories are intact but whose brain scans show early, preclinical evidence of Alzheimer’s.
The findings potentially could help doctors identify people at risk of Alzheimer's earlier than currently is possible. That's important because Alzheimer's damage can take root in the brain 15 to 20 years before clinical symptoms appear.
The research is published Jan. 29 in the journal JAMA Neurology.
"It wasn't that the people in the study were sleep-deprived," said first author Erik S. Musiek, MD, PhD, an assistant professor of neurology. "But their sleep tended to be fragmented. Sleeping for eight hours at night is very different from getting eight hours of sleep in one-hour increments during daytime naps."
The researchers also conducted a separate study in mice, to be published Jan. 30 in The Journal of Experimental Medicine, showing that similar circadian disruptions accelerate the development of amyloid plaques in the brain, which are linked to Alzheimer's.
Previous studies at Washington University, conducted in people and in animals, have found that levels of amyloid fluctuate in predictable ways during the day and night. Amyloid levels decrease during sleep, and several studies have shown that levels increase when sleep is disrupted or when people don't get enough deep sleep, according to research by senior author, Yo-El Ju, MD.
"In this new study, we found that people with preclinical Alzheimer's disease had more fragmentation in their circadian activity patterns, with more periods of inactivity or sleep during the day and more periods of activity at night," said Ju, an assistant professor of neurology.
The researchers tracked circadian rhythms in 189 cognitively normal, older adults with an average age of 66. Some had positron emission tomography (PET) scans to look for Alzheimer's-related amyloid plaques in their brains. Others had their cerebrospinal fluid tested for Alzheimer's-related proteins. And some had both scans and spinal fluid testing.
Of the participants, 139 had no evidence of the amyloid protein that signifies preclinical Alzheimer's. Most had normal sleep/wake cycles, although several had circadian disruptions that were linked to advanced age, sleep apnea or other causes.
But among the other 50 subjects -- who either had abnormal brain scans or abnormal cerebrospinal fluid -- all experienced significant disruptions in their internal body clocks, determined by how much rest they got at night and how active they were during the day. Disruptions in the sleep/wake cycle remained even after the researchers statistically controlled for sleep apnea, age and other factors.
The study subjects, from Washington University's Knight Alzheimer's Disease Research Center, all wore devices similar to exercise trackers for one to two weeks. Each also completed a detailed sleep diary every morning.
By tracking activity during the day and night, the researchers could tell how scattered rest and activity were throughout 24-hour periods. Subjects who experienced short spurts of activity and rest during the day and night were more likely to have evidence of amyloid buildup in their brains.
These findings in people reinforce the mouse research from Musiek's lab. In that study, working with first author Geraldine J. Kress, PhD, an assistant professor of neurology, Musiek studied circadian rhythm disruptions in a mouse model of Alzheimer's. To disrupt the animals' circadian rhythms, his team disabled genes that control the circadian clock.
"Over two months, mice with disrupted circadian rhythms developed considerably more amyloid plaques than mice with normal rhythms," Musiek said. "The mice also had changes in the normal, daily rhythms of amyloid protein in the brain. It's the first data demonstrating that the disruption of circadian rhythms could be accelerating the deposition of plaques."
Both Musiek and Ju said it's too early to answer the chicken-and-egg question of whether disrupted circadian rhythms put people at risk for Alzheimer's disease or whether Alzheimer's-related changes in the brain disrupt circadian rhythms.
"At the very least, these disruptions in circadian rhythms may serve as a biomarker for preclinical disease," said Ju. "We want to bring back these subjects in the future to learn more about whether their sleep and circadian rhythm problems lead to increased Alzheimer's risk or whether the Alzheimer's disease brain changes cause sleep/wake cycle and circadian problems."
https://www.sciencedaily.com/releases/2018/01/180129150033.htm
Aerobic exercise may mildly delay, slightly improve Alzheimer's symptoms
January 26, 2018
Science Daily/American Geriatrics Society
Geriatrics experts have suggested that exercising can improve brain health in older adults. However, not all studies of exercise and older adults have proven the benefits of exercise. A team of researchers designed a study to learn whether exercise could delay or improve AD symptoms. They reviewed 19 studies that examined the effect of an exercise training program on cognitive function in older adults who were at risk for or diagnosed with AD.
Geriatrics experts have suggested that exercising can improve brain health in older adults. The World Health Organization (WHO) has recommendations for how much older adults should exercise. They suggest that older adults perform 150 minutes a week of moderate exercise (such as brisk walking), 75 minutes a week of vigorous aerobic training, or a combination of the two types. The WHO also recommends older adults perform muscle-strengthening exercises on at least two or more days a week.
However, not all studies of exercise and older adults have proven the benefits of exercise. We don't know for sure whether exercise slows mental decline or improves older adults' ability to think and make decisions.
A team of researchers designed a study to learn whether exercise could delay or improve AD symptoms. They reviewed 19 studies that examined the effect of an exercise training program on cognitive function in older adults who were at risk for or diagnosed with AD. The studies included 1,145 older adults, most of whom were in their mid-to late 70s. Of the participants, 65 percent were at risk for AD and 35 percent had been diagnosed with AD.
The researchers published their findings in the Journal of the American Geriatrics Society.
As the researchers examined the studies, they discovered that older adults who did aerobic exercise by itself experienced a three times greater level of improvement in cognitive function than those who participated in combined aerobic training and strength training exercises. The researchers also confirmed that the amount of exercise WHO recommends for older adults was reinforced by the studies they examined.
Finally, the researchers found that older adults in the no-exercise control groups in the studies faced declines in cognitive function. Meanwhile, the older adults who exercised showed small improvements in cognitive function no matter what type of exercise they did.
The research team concluded that this study may be the first to show that for older adults who are at risk for or who have AD, aerobic exercise may be more effective than other types of exercise in preserving the ability to think and make decisions.
https://www.sciencedaily.com/releases/2018/01/180126130325.htm
Curcumin improves memory and mood
Twice-daily supplements boosted cognitive power over 18 months
January 23, 2018
Science Daily/University of California - Los Angeles
Daily consumption of a certain form of curcumin -- the substance that gives Indian curry its bright color -- improved memory and mood in people with mild, age-related memory loss.
Lovers of Indian food, give yourselves a second helping: Daily consumption of a certain form of curcumin -- the substance that gives Indian curry its bright color -- improved memory and mood in people with mild, age-related memory loss, according to the results of a study conducted by UCLA researchers.
The research, published online Jan. 19 in the American Journal of Geriatric Psychiatry, examined the effects of an easily absorbed curcumin supplement on memory performance in people without dementia, as well as curcumin's potential impact on the microscopic plaques and tangles in the brains of people with Alzheimer's disease.
Found in turmeric, curcumin has previously been shown to have anti-inflammatory and antioxidant properties in lab studies. It also has been suggested as a possible reason that senior citizens in India, where curcumin is a dietary staple, have a lower prevalence of Alzheimer's disease and better cognitive performance.
"Exactly how curcumin exerts its effects is not certain, but it may be due to its ability to reduce brain inflammation, which has been linked to both Alzheimer's disease and major depression," said Dr. Gary Small, director of geriatric psychiatry at UCLA's Longevity Center and of the geriatric psychiatry division at the Semel Institute for Neuroscience and Human Behavior at UCLA, and the study's first author.
The double-blind, placebo-controlled study involved 40 adults between the ages of 50 and 90 years who had mild memory complaints. Participants were randomly assigned to receive either a placebo or 90 milligrams of curcumin twice daily for 18 months.
All 40 subjects received standardized cognitive assessments at the start of the study and at six-month intervals, and monitoring of curcumin levels in their blood at the start of the study and after 18 months. Thirty of the volunteers underwent positron emission tomography, or PET scans, to determine the levels of amyloid and tau in their brains at the start of the study and after 18 months.
The people who took curcumin experienced significant improvements in their memory and attention abilities, while the subjects who received placebo did not, Small said. In memory tests, the people taking curcumin improved by 28 percent over the 18 months. Those taking curcumin also had mild improvements in mood, and their brain PET scans showed significantly less amyloid and tau signals in the amygdala and hypothalamus than those who took placebos.
The amygdala and hypothalamus are regions of the brain that control several memory and emotional functions.
Four people taking curcumin, and two taking placebos, experienced mild side effects such as abdominal pain and nausea.
The researchers plan to conduct a follow-up study with a larger number of people. That study will include some people with mild depression so the scientists can explore whether curcumin also has antidepressant effects. The larger sample also would allow them to analyze whether curcumin's memory-enhancing effects vary according to people's genetic risk for Alzheimer's, their age or the extent of their cognitive problems.
https://www.sciencedaily.com/releases/2018/01/180123101908.htm
Can training improve memory, thinking abilities in older adults with cognitive impairment?
January 16, 2018
Science Daily/American Geriatrics Society
A new, first-of-its-kind study was designed to assess whether cognitive training, a medication-free treatment, could improve MCI. Studies show that activities that stimulate your brain, such as cognitive training, can protect against a decline in your mental abilities. Even older adults who have MCI can still learn and use new mental skills.
Cognition is the ability to think and make decisions. Medication-free treatments that maintain cognitive health as we age are attracting the attention of medical experts. Maintaining the ability to think clearly and make decisions is crucial to older adults' well-being and vitality.
Mild cognitive impairment (MCI) is a condition that affects people who are in the early stages of dementia or Alzheimer's disease. People with MCI may have mild memory loss or other difficulties completing tasks that involve cognitive abilities. MCI may eventually develop into dementia or Alzheimer's disease. Depression and anxiety also can accompany MCI. Having these conditions can increase the risk of mental decline as people age.
A new, first-of-its-kind study was published in the Journal of the American Geriatrics Society by scientists from research centers in Montreal and Quebec City, Canada. They designed a study to learn whether cognitive training, a medication-free treatment, could improve MCI. Studies show that activities that stimulate your brain, such as cognitive training, can protect against a decline in your mental abilities. Even older adults who have MCI can still learn and use new mental skills.
For their study, researchers recruited 145 older adults around the age of 72 from Canadian memory clinics. The participants had been diagnosed with MCI, and were assigned to one of three groups. Each group included four or five participants, and met for eight weekly sessions for 120 minutes.
The three groups were:
· Cognitive training group. Members of this group participated in the MEMO program (MEMO stands for a French phrase that translates to "training method for optimal memory"). They received special training to improve their memory and attention span.
· Psycho-social group. Participants in this group were encouraged to improve their general well-being. They learned to focus on the positive aspects of their lives and find ways to increase positive situations.
· Control group. Participants had no contact with researchers and didn't follow a program.
During the time the training sessions took place, 128 of the participants completed the project. After six months, 104 completed all the sessions they were assigned.
People in the MEMO group increased their memory scores by 35 to 40 percent, said Sylvie Belleville, PhD, a senior author of the study. "Most importantly, they maintained their scores over a six-month period."
What's more, the improvement was the largest for older adults with "delayed recall." This means memory for words measured just 10 minutes after people have studied them. Because delayed memory is one of the earliest signs of Alzheimer's disease, this was a key finding.
Those who participated in the MEMO group said they used the training they learned in their daily lives. The training gave them different ways to remember things. For example, they learned to use visual images to remember names of new people, and to use associations to remember shopping lists. These lessons allowed them to continue maintaining their memory improvements after the study ended.
The people in the psycho-social group and the control group didn't experience memory benefits or improvement in their mood.
https://www.sciencedaily.com/releases/2018/01/180116144246.htm
Blueberry vinegar improves memory in mice with amnesia
December 20, 2017
Science Daily/American Chemical Society
Dementia affects millions of people worldwide, robbing them of their ability to think, remember and live as they once did. In the search for new ways to fight cognitive decline, scientists report that blueberry vinegar might offer some help. They found that the fermented product could restore cognitive function in mice.
Recent studies have shown that the brains of people with Alzheimer's disease, the most common form of dementia, have lower levels of the signaling compound acetylcholine and its receptors. Research has also demonstrated that blocking acetylcholine receptors disrupts learning and memory. Drugs to stop the breakdown of acetylcholine have been developed to fight dementia, but they often don't last long in the body and can be toxic to the liver. Natural extracts could be a safer treatment option, and some animal studies suggest that these extracts can improve cognition. Additionally, fermentation can boost the bioactivity of some natural products. So Beong-Ou Lim and colleagues wanted to test whether vinegar made from blueberries, which are packed with a wide range of active compounds, might help prevent cognitive decline.
To carry out their experiment, the researchers administered blueberry vinegar to mice with induced amnesia. Measurements of molecules in their brains showed that the vinegar reduced the breakdown of acetylcholine and boosted levels of brain-derived neurotrophic factor, a protein associated with maintaining and creating healthy neurons. To test how the treatment affected cognition, the researchers analyzed the animals' performance in mazes and an avoidance test, in which the mice would receive a low-intensity shock in one of two chambers. The treated rodents showed improved performance in both of these tests, suggesting that the fermented product improved short-term memory. Thus, although further testing is needed, the researchers say that blueberry vinegar could potentially be a promising food to help treat amnesia and cognitive decline related to aging.
https://www.sciencedaily.com/releases/2017/12/171220091735.htm
Canola oil linked to worsened memory and learning ability in Alzheimer's
December 7, 2017
Science Daily/Temple University Health System
Canola oil is one of the most widely consumed vegetable oils, yet little is known about its health effects. Now, a study links canola oil consumption in the diet with worsened memory, worsened learning ability and weight gain in mice which model Alzheimer's disease. It's the first study to suggest that canola oil is more harmful than healthful for the brain.
"Canola oil is appealing because it is less expensive than other vegetable oils, and it is advertised as being healthy," explained Domenico Praticò, MD, Professor in the Departments of Pharmacology and Microbiology and Director of the Alzheimer's Center at LKSOM, as well as senior investigator on the study. "Very few studies, however, have examined that claim, especially in terms of the brain."
Curious about how canola oil affects brain function, Dr. Praticò and Elisabetta Lauretti, a graduate student in Dr. Pratico's laboratory at LKSOM and co-author on the new study, focused their work on memory impairment and the formation of amyloid plaques and neurofibrillary tangles in an Alzheimer's disease mouse model. Amyloid plaques and phosphorylated tau, which is responsible for the formation of tau neurofibrillary tangles, contribute to neuronal dysfunction and degeneration and memory loss in Alzheimer's disease. The animal model was designed to recapitulate Alzheimer's in humans, progressing from an asymptomatic phase in early life to full-blown disease in aged animals.
Dr. Praticò and Lauretti had previously used the same mouse model in an investigation of olive oil, the results of which were published earlier in 2017. In that study, they found that Alzheimer mice fed a diet enriched with extra-virgin olive oil had reduced levels of amyloid plaques and phosphorylated tau and experienced memory improvement. For their latest work, they wanted to determine whether canola oil is similarly beneficial for the brain.
The researchers started by dividing the mice into two groups at six months of age, before the animals developed signs of Alzheimer's disease. One group was fed a normal diet, while the other was fed a diet supplemented with the equivalent of about two tablespoons of canola oil daily.
The researchers then assessed the animals at 12 months. One of the first differences observed was in body weight -- animals on the canola oil-enriched diet weighed significantly more than mice on the regular diet. Maze tests to assess working memory, short-term memory, and learning ability uncovered additional differences. Most significantly, mice that had consumed canola oil over a period of six months suffered impairments in working memory.
Examination of brain tissue from the two groups of mice revealed that canola oil-treated animals had greatly reduced levels of amyloid beta 1-40. Amyloid beta 1-40 is the more soluble form of the amyloid beta proteins. It generally is considered to serve a beneficial role in the brain and acts as a buffer for the more harmful insoluble form, amyloid beta 1-42.
As a result of decreased amyloid beta 1-40, animals on the canola oil diet further showed increased formation of amyloid plaques in the brain, with neurons engulfed in amyloid beta 1-42. The damage was accompanied by a significant decrease in the number of contacts between neurons, indicative of extensive synapse injury. Synapses, the areas where neurons come into contact with one another, play a central role in memory formation and retrieval.
"Amyloid beta 1-40 neutralizes the actions of amyloid 1-42, which means that a decrease in 1-40, like the one observed in our study, leaves 1-42 unchecked," Dr. Praticò explained. "In our model, this change in ratio resulted in considerable neuronal damage, decreased neural contacts, and memory impairment."
The findings suggest that long-term consumption of canola oil is not beneficial to brain health. "Even though canola oil is a vegetable oil, we need to be careful before we say that it is healthy," Dr. Praticò said. "Based on the evidence from this study, canola oil should not be thought of as being equivalent to oils with proven health benefits."
The next step is to carry out a study of shorter duration to determine the minimum extent of exposure necessary to produce observable changes in the ratio of amyloid beta 1-42 to 1-40 in the brain and alter synapse connections. A longer study may be warranted in order to determine whether canola oil also eventually impacts tau phosphorylation, since no effects on tau were observed over the six-month exposure period.
"We also want to know whether the negative effects of canola oil are specific for Alzheimer's disease," Dr. Praticò added. "There is a chance that the consumption of canola oil could also affect the onset and course of other neurodegenerative diseases or other forms of dementia."
https://www.sciencedaily.com/releases/2017/12/171207141624.htm
Trace elements of lithium in drinking water linked to longer life in Alzheimer's patients
December 5, 2017
Science Daily/IOS Press
Trace elements of lithium in drinking water may slow death rates from Alzheimer's disease, new research suggests. Rates of diabetes and obesity, which are important risk factors for Alzheimer's disease, also decrease if there is a particular amount of lithium in the water, says the study.
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Postdoctoral fellow Val Fajardo and Rebecca MacPherson, Assistant Professor in the Department of Health Sciences, collected statistics on various lithium levels in drinking water in 234 counties across Texas.
Lithium is a water-soluble alkali metal found in igneous rocks and mineral springs. It is commonly used to treat bipolar and other mood disorders, but at much higher doses than what occurs naturally in drinking water.
The research team, which included Associate Professor of Health Sciences Paul LeBlanc, compared lithium levels naturally found in tap water with Alzheimer's disease mortality rates, along with the incidence of obesity and diabetes, in the Texas counties.
"We found counties that had above the median level of lithium in tap water (40 micrograms per litre) experienced less increases in Alzheimer's disease mortality over time, whereas counties below that median level had even higher increases in Alzheimer's deaths over time," says Fajardo.
The frequency of obesity and Type 2 diabetes also went down when the drinking water contained similar lithium levels, the researchers found.
Fajardo says he and his team focused on Texas because data on lithium levels were "freely available."
Previous studies have demonstrated lithium's ability to protect against Alzheimer's disease, obesity and diabetes.
"However, we are one of the first groups to show that lithium's potential protective effect against Alzheimer's disease, obesity and diabetes may translate to the population setting through very low levels of lithium in tap water," says Fajardo.
The Brock research comes on the heels of an August study from the University of Copenhagen linking high lithium levels in drinking water to decreases in dementia rates.
But Fajardo warns it's too early to start advising authorities to add lithium to drinking water.
"There's so much more research we have to do before policy-makers look at the evidence and say, OK, let's start supplementing tap water with lithium just like we do in some municipalities with fluoride to prevent tooth decay," he says.
https://www.sciencedaily.com/releases/2017/12/171205144805.htm
High-intensity exercise boosts memory, new research suggests
November 22, 2017
Science Daily/McMaster University
The health advantages of high-intensity exercise are widely known but new research points to another major benefit: better memory. The findings could have implications for an aging population which is grappling with the growing problem of catastrophic diseases such as dementia and Alzheimer's.
The findings could have implications for an aging population which is grappling with the growing problem of catastrophic diseases such as dementia and Alzheimer's.
Scientists have found that six weeks of intense exercise -- short bouts of interval training over the course of 20 minutes -- showed significant improvements in what is known as high-interference memory, which, for example, allows us to distinguish our car from another of the same make and model.
The study is published in the Journal of Cognitive Neuroscience.
The findings are important because memory performance of the study participants, who were all healthy young adults, increased over a relatively short period of time, say researchers.
They also found that participants who experienced greater fitness gains also experienced greater increases in brain-derived neurotrophic factor (BDNF), a protein that supports the growth, function and survival of brain cells.
"Improvements in this type of memory from exercise might help to explain the previously established link between aerobic exercise and better academic performance," says Jennifer Heisz, an assistant professor in the Department of Kinesiology at McMaster and lead author of the study.
"At the other end of our lifespan, as we reach our senior years, we might expect to see even greater benefits in individuals with memory impairment brought on by conditions such as dementia," she says.
For the study, 95 participants completed six weeks of exercise training, combined exercise and cognitive training or no training (the control group which did neither and remained sedentary). Both the exercise and combined training groups improved performance on a high-interference memory task, while the control group did not.
Researchers measured changes in aerobic fitness, memory and neurotrophic factor, before and after the study protocol.
The results reveal a potential mechanism for how exercise and cognitive training may be changing the brain to support cognition, suggesting that the two work together through complementary pathways of the brain to improve high-interference memory.
Researchers have begun to examine older adults to determine if they will experience the same positive results with the combination of exercise and cognitive training.
"One hypothesis is that we will see greater benefits for older adults given that this type of memory declines with age," says Heisz. "However, the availability of neurotrophic factors also declines with age and this may mean that we do not get the synergistic effects."
https://www.sciencedaily.com/releases/2017/11/171122103555.htm
To forget or to remember? Memory depends on subtle brain signals
November 22, 2017
Science Daily/Scripps Research Institute
Understanding how brains actively erase memories may open new understanding of memory loss and aging, and open the possibility of new treatments for neurodegenerative disease.
The fragrance of hot pumpkin pie can bring back pleasant memories of holidays past, while the scent of an antiseptic hospital room may cause a shudder. The power of odors to activate memories both pleasing and aversive exists in many animals, from humans to the humble fruit fly.
Scientists on the Florida campus of The Scripps Research Institute (TSRI), writing in the journal Cell Reports, detailed how the intricate biochemical mechanism for storing scent-associated memories differs slightly from a less-understood mechanism for erasing unnecessary memories.
Understanding how brains actively erase memories may open new understanding of memory loss and aging, and open the possibility of new treatments for neurodegenerative disease.
In multiple ways, the processes of forgetting and remembering are alike. In fruit fly models of odor-associated learning, both the saving and erasure of memories involves dopamine activation of the brain cells. This clue in flies is important for understanding the human brain.
"The olfactory systems of flies and humans are actually quite similar in terms of neuron types and their connections," said study leader Ron Davis, Ph.D., co-chair of TSRI's Neuroscience Department.
Also, in both cases, activation of the neurons causes them to make an identical messenger molecule, cyclic AMP, leading to a cascade of activity within the cell, either building or breaking down memory storage, added Davis.
"So how do the cells know when they are getting a forgetting signal verses an acquisition signal? That was the huge, perplexing question," Davis said.
TSRI Professor Kirill Martemyanov, Ph.D., and Staff Scientist Ikuo Masuho, Ph.D., found that a type of signaling protein in neurons played a role. Masuho and Martemyanov screened a panel of these signaling proteins, called G proteins, against cells that expressed two key receptors known to be involved in memory and forgetting.
The TSRI team found one G protein, called G alpha S, that latched on to a neural dopamine receptor called dDA1, associated with memory formation. They found a different G protein, called G alpha Q, linked up with a nearby dopamine receptor called Damb, associated with the machinery of forgetting.
The next question was whether those two different G proteins could be controllers of the fly brain's memory machinery. To find out, the researchers silenced genes involved in the production of the G alpha Q protein in the flies. The flies with the protein silenced were exposed to odors in aversive situations and sent through mazes to see how well they remembered to turn away in the presence of the scent.
"If you removed G alpha Q, the flies should not forget, and indeed, they did not," Davis said. "They remembered better."
It appears in flies that some level of forgetting is a constant, healthy process, he said.
"The idea is, constantly as we learn information, there is a slow process that whittles away memories, and it continues whittling them away unless another part of the brain signals the memory is important and overrides it," Davis said.
It may be that the process of acquiring and forgetting memories ebbs and flows in a state of balance, he said. Important memories like the taste of mom's pumpkin pie might be forever retained, but trivialities like what you wore 10 years ago can fade into oblivion without consequence.
"If you have too much memory that is old and unnecessary, why keep them around? Why shouldn't you have a system for removing those for optimal function of the brain?" Davis asked. "We're getting all this information, all this learning during the day, and the brain may be saying, 'No, no, bring me back to my basal, my happy state.'"
Many questions remain to be solved, Davis noted. "We need to figure out what is downstream -- walk down the pathway to find the complete signaling system for forgetting," he said. "We are very early in this research."
https://www.sciencedaily.com/releases/2017/11/171122093120.htm