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.
Share:
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