Posts tagged aging

Posts tagged aging
Can Games, Puzzles Keep Aging Minds Sharp?
Older adults who enjoy mentally stimulating games may have bigger brains and sharper thinking skills than their peers, new research suggests.
The study looked at the connection between playing games such as puzzles, crosswords, cards and checkers and mental acuity for adults in their 50s and 60s.
Researchers found that people who played those games at least every other day performed better on tests of memory and other mental functions. And, based on MRI scans, they had greater tissue mass in brain areas involved in memory.
(Image: Alamy)
Older people are nearly twice as likely as their younger counterparts to have their memory and cognitive processes impaired by environmental distractions (such as irrelevant speech or written words presented along with target stimuli), according to a new study from psychologists at Rice University and Johns Hopkins University School of Medicine. Whereas other studies had found that older adults are distracted by memories of prior similar events, this was the first study to convincingly demonstrate across several tasks an impairment from environmental distractions.

“Cognitive Declines in Healthy Aging: Evidence from Multiple Aspects of Interference Resolution” appeared in a recent edition of Psychology and Aging. The study supported previous research that showed memory accuracy and the speed of cognitive processing declines with age. It also revealed that older people were at least twice as likely as younger to have irrelevant memories intrude during memory recall and also showed twice as much slowing in cognitive processing in the presence of distracting information in the environment.
The study included 102 people between the ages of 18 and 32 (average age of 21) and 60 people between the ages of 64 and 82 (average age of 71) who participated in a series of memory and cognitive tasks.
For example, when the participants were tested on remembering lists of words, individuals in the young test group remembered words on the list with an average accuracy of 81 percent; in comparison, the old test group’s accuracy was only 67 percent. When irrelevant words were introduced that were to be ignored, the young test group’s accuracy dropped to 74 percent, but the accuracy of the old test group’s performance dropped to 46 percent.
“Almost any type of memory test administered reveals a decline in memory from the age of 25 on,” said Randi Martin, the Elma W. Schneider Professor of Psychology at Rice and the study’s co-author. “However, this is the first study to convincingly demonstrate the impact of environmental interference on processing having a greater impact on older than younger adults.”
Martin hopes that the research will encourage further research of how the brain is affected by environmental distractions.
“From our perspective of studying neuroplasticity (the brain’s ability to reorganize itself after traumatic injury or neurological disorders) and testing patients with brain damage, this research is very important,” Martin said. “The tests used in this study are important tools in determining how the brain is affected by environmental interference, which is critical information in treating neurological disorders, including stroke and traumatic brain injuries.”
(Source: news.rice.edu)
Little or poor sleep may be associated with worse brain function when aging
Research published today in PLOS ONE by researchers at the University of Warwick indicates that sleep problems are associated with worse memory and executive function in older people.
Analysis of sleep and cognitive (brain function) data from 3,968 men and 4,821 women who took part in the English Longitudinal Study of Ageing (ELSA), was conducted in a study funded by the Economic and Social Research Council (ESRC). Respondents reported on the quality and quantity of sleep over the period of a month.
The study showed that there is an association between both quality and duration of sleep and brain function which changes with age.
In adults aged between 50 and 64 years of age, short sleep (<6hrs per night) and long sleep (>8hrs per night) were associated with lower brain function scores. By contrast, in older adults (65-89 years) lower brain function scores were only observed in long sleepers.
Dr Michelle A Miller says “6-8 hours of sleep per night is particularly important for optimum brain function, in younger adults”. These results are consistent with our previous research, which showed that 6-8 hours of sleep per night was optimal for physical health, including lowest risk of developing obesity, hypertension, diabetes, heart disease and stroke”.
Interestingly, in the younger pre-retirement aged adults, sleep quality did not have any significant association with brain function scores, whereas in the older adults (>65 years), there was a significant relationship between sleep quality and the observed scores.
“Sleep is important for good health and mental wellbeing” says Professor Francesco Cappuccio, “Optimising sleep at an older age may help to delay the decline in brain function seen with age, or indeed may slow or prevent the rapid decline that leads to dementia”.
Dr Miller concludes that “if poor sleep is causative of future cognitive decline, non-pharmacological improvements in sleep may provide an alternative low-cost and more accessible Public Health intervention, to delay or slow the rate of cognitive decline”.
How Aging Can Intensify Damage of Spinal Cord Injury
In the complex environment of a spinal cord injury, researchers have found that immune cells in the central nervous system of elderly mice fail to activate an important signaling pathway, dramatically lowering chances for repair after injury.
These studies were the first to show that spinal cord injuries are more severe in elderly mice than in young adults, corroborating previous anecdotal findings from clinical settings. They also revealed a previously unknown player in the repair of spinal cord injuries in young adults.
A key messenger in that pathway is a receptor on the surface of microglia, immune system cells in the central nervous system that are called into action by the trauma of the spinal cord injury.
In young adult mice, this receptor is activated by microglia to recognize and make use of an inflammation-related signaling chemical that is found in the central nervous system after a spinal cord injury. The microglia in the elderly mice, however, do not activate the receptor at all.
The study showed that the difference in receptor activation has consequences later in the recovery process. The kinds of cells recruited to the injury site in young adult mice appear to have more value in the repair process than do the cells that show up in elderly mice. A host of experiments traced those differing effects back to whether or not microglia activated the receptor.
“The microglia are regulated by several different cell types and different signals, and it appears a lot of those systems change with age,” said Jonathan Godbout, associate professor of neuroscience at The Ohio State University and senior author of the study.
“We’ve shown evidence that this more severe injury occurs in an aging animal, and that the difference in recovery is related to the ability to express the receptor. The consequence is we have a different profile of cells at the injury site, and in aging mice, that environment is less reparative.”
These differences at the cellular level were associated with vast differences in the characteristics of injury and recovery. The lesions on the injured spinal cord were 38 percent longer, on average, in elderly mice than in young adult mice. In addition, the older mice were unable to gain movement of their hind limbs by the time most younger mice had regained that mobility.
The research is published in the Journal of Neuroscience.
The receptor in question is called the IL-4 alpha receptor, and its job is to “see” the infusion of interleukin-4, or IL-4, in the central nervous system after the spinal injury. IL-4 is a cytokine, a type of protein connected to immune system function. Many cytokines promote inflammation, but IL-4 is associated with curbing inflammation.
Godbout and colleagues observed that IL-4 in the central nervous systems in both young adult and aging mice sent signals to recruit additional repair cells to the injury site – cells called macrophages and monocytes. These are types of white blood cells that originate in the bone marrow and circulate in what is known as the “periphery,” via blood and outside the central nervous system. But only in young adult mice were these types of cells contributors to wound healing and clearing of debris, necessary inflammatory functions that help rather than harm.
“This was surprising to us because aging is typically associated with increased inflammation so we’d expect to see higher levels of inflammatory cytokines in the aged mice,” said first author Ashley Fenn, who just received her Ph.D. in neuroscience from Ohio State. “But in the aged mice with a spinal cord injury, we saw reduced levels of some inflammatory signals associated with a failure to reprogram the microglia with IL-4 toward a reparative profile. That’s how we figured out the IL-4 is unique in the spinal cord injury paradigm, that it induces an inflammatory response that appears to be beneficial.”
The IL-4 in the young adult mice also led to production of arginase, a protein that serves as a biomarker of the injury repair response. Significantly less arginase was detected in the injured elderly mice, another signal that the disabled receptor interfered with IL-4’s assistance in injury repair.
The communication among systems has long been a focus of Godbout’s research. He is an investigator in Ohio State’s Institute for Behavioral Medicine Research (IBMR) and Center for Brain and Spinal Cord Repair.
“There is some level of communication going on between the central nervous system microglia and the peripheral immune system’s macrophages. In our model, differences in that communication affected the ability to bring in cells to the site of the injury. Maybe the aging microenvironment brings in cells that are less beneficial,” he said.
About 200,000 people are currently living with a spinal cord injury in the United States, and an estimated 12,000 to 20,000 new injuries occur each year, according to the Centers for Disease Control and Prevention.
Though any therapy based on this research would take many years to develop, Godbout and Fenn said that finding a drug that could stimulate expression of the IL-4 alpha receptor in elderly spinal cord injury patients might have potential to improve their outcomes.
Stress hormone linked to short-term memory loss as we age
A new study at the University of Iowa reports a potential link between stress hormones and short-term memory loss in older adults.
The study, published in the Journal of Neuroscience, reveals that having high levels of cortisol—a natural hormone in our body whose levels surge when we are stressed—can lead to memory lapses as we age.
Short-term increases in cortisol are critical for survival. They promote coping and help us respond to life’s challenges by making us more alert and able to think on our feet. But abnormally high or prolonged spikes in cortisol—like what happens when we are dealing with long-term stress—can lead to negative consequences that numerous bodies of research have shown to include digestion problems, anxiety, weight gain, and high blood pressure.
In this study, the UI researchers linked elevated amounts of cortisol to the gradual loss of synapses in the prefrontal cortex, the region of the brain that houses short-term memory. Synapses are the connections that help us process, store, and recall information. And when we get older, repeated and long-term exposure to cortisol can cause them to shrink and disappear.
“Stress hormones are one mechanism that we believe leads to weathering of the brain,” says Jason Radley, assistant professor in psychology at the UI and corresponding author on the paper. Like a rock on the shoreline, after years and years it will eventually break down and disappear.
While previous studies have shown cortisol to produce similar effects in other regions of the aging brain, this was the first study to examine its impact on the prefrontal cortex.
And although preliminary, the findings raise the possibility that short-memory decline in aging adults may be slowed or prevented by treatments that decrease levels of cortisol in susceptible individuals, says Radley. That could mean treating people who have naturally high levels of cortisol—such as those who are depressed—or those who experience repeated, long-term stress due to traumatic life events like the death of a loved one.
According to Radley and Rachel Anderson, the paper’s lead author and a second year-graduate student in psychology at the UI, short-term memory lapses related to cortisol start around age 65. That’s about the equivalent of 21 month-old rats, which the pair studied to make their discovery.
The UI scientists compared the elderly rats to four-month old rats, which are roughly the same age as a 20 year-old person. The young and elderly groups were then separated further according to whether the rats had naturally high or naturally low levels of corticosterone—the hormone comparable to cortisol in humans.
The researchers subsequently placed the rats in a T-shaped maze that required them to use their short-term memory. In order to receive a treat, they needed to recall which direction they had turned at the top of the T just 30, 60, or 120 seconds ago and then turn the opposite way each time they ran the maze.
Though memory declined across all groups as the time rats waited before running the maze again increased, older rats with high corticosterone levels consistently performed the worst. They chose the correct direction only 58 percent of the time, compared to their older peers with low corticosterone levels who chose it 80 percent of the time.
When researchers took tissue samples from the rats’ prefrontal cortexes and examined them under a microscope, they found the poor performers had smaller and 20 percent fewer synapses than all other groups, indicating memory loss.
In contrast, older rats with low corticosterone levels showed little memory loss and ran the maze nearly as well as the younger rats, who were not affected by any level of corticosterone—low or high.
Still, researchers say it’s important to remember that stress hormones are only one of a host of factors when it comes to mental decline and memory loss as we age.
New research reveals that bilingualism has a positive effect on cognition later in life. Findings published in Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society, show that individuals who speak two or more languages, even those who acquired the second language in adulthood, may slow down cognitive decline from aging.

Bilingualism is thought to improve cognition and delay dementia in older adults. While prior research has investigated the impact of learning more than one language, ruling out “reverse causality” has proven difficult. The crucial question is whether people improve their cognitive functions through learning new languages or whether those with better baseline cognitive functions are more likely to become bilingual.
"Our study is the first to examine whether learning a second language impacts cognitive performance later in life while controlling for childhood intelligence," says lead author Dr. Thomas Bak from the Centre for Cognitive Aging and Cognitive Epidemiology at the University of Edinburgh.
For the current study, researchers relied on data from the Lothian Birth Cohort 1936, comprised of 835 native speakers of English who were born and living in the area of Edinburgh, Scotland. The participants were given an intelligence test in 1947 at age 11 years and retested in their early 70s, between 2008 and 2010. Two hundred and sixty two participants reported to be able to communicate in at least one language other than English. Of those, 195 learned the second language before age 18, 65 thereafter.
Findings indicate that those who spoke two or more languages had significantly better cognitive abilities compared to what would be expected from their baseline. The strongest effects were seen in general intelligence and reading. The effects were present in those who acquired their second language early as well as late.
The Lothian Birth Cohort 1936 forms the Disconnected Mind project at the University of Edinburgh, funded by Age UK. The work was undertaken by The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross council Lifelong Health and Wellbeing Initiative (MR/K026992/1) and has been made possible thanks to funding from the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC).
"The Lothian Birth Cohort offers a unique opportunity to study the interaction between bilingualism and cognitive aging, taking into account the cognitive abilities predating the acquisition of a second language" concludes Dr. Bak. "These findings are of considerable practical relevance. Millions of people around the world acquire their second language later in life. Our study shows that bilingualism, even when acquired in adulthood, may benefit the aging brain."
After reviewing the study, Dr. Alvaro Pascual-Leone, an Associate Editor for Annals of Neurology and Professor of Medicine at Harvard Medical School in Boston, Mass. said, “The epidemiological study by Dr. Bak and colleagues provides an important first step in understanding the impact of learning a second language and the aging brain. This research paves the way for future causal studies of bilingualism and cognitive decline prevention.”
(Source: eurekalert.org)
Cynical? You May Be Hurting Your Brain Health
People with high levels of cynical distrust may be more likely to develop dementia, according to a study published in the May 28, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology.
Cynical distrust, which is defined as the belief that others are mainly motivated by selfish concerns, has been associated with other health problems, such as heart disease. This is the first study to look at the relationship between cynicism and dementia.
“These results add to the evidence that people’s view on life and personality may have an impact on their health,” said study author Anna-Maija Tolppanen, PhD, of the University of Eastern Finland in Kuopio. “Understanding how a personality trait like cynicism affects risk for dementia might provide us with important insights on how to reduce risks for dementia.”
For the study, 1,449 people with an average age of 71 were given tests for dementia and a questionnaire to measure their level of cynicism. The questionnaire has been shown to be reliable, and people’s scores tend to remain stable over periods of several years. People are asked how much they agree with statements such as “I think most people would lie to get ahead,” “It is safer to trust nobody” and “Most people will use somewhat unfair reasons to gain profit or an advantage rather than lose it.” Based on their scores, participants were grouped in low, moderate and high levels of cynical distrust.
A total of 622 people completed two tests for dementia, with the last one an average of eight years after the study started. During that time, 46 people were diagnosed with dementia. Once researchers adjusted for other factors that could affect dementia risk, such as high blood pressure, high cholesterol and smoking, people with high levels of cynical distrust were three times more likely to develop dementia than people with low levels of cynicism. Of the 164 people with high levels of cynicism, 14 people developed dementia, compared to nine of the 212 people with low levels of cynicism.
The study also looked at whether people with high levels of cynicism were more likely to die sooner than people with low levels of cynicism. A total of 1,146 people were included in this part of the analysis, and 361 people died during the average of 10 years of follow-up. High cynicism was initially associated with earlier death, but after researchers accounted for factors such as socioeconomic status, behaviors such as smoking and health status, there was no longer any link between cynicism and earlier death.
(Image: Shutterstock)
Cognitive test can differentiate between Alzheimer’s and normal aging
Researchers have developed a new cognitive test that can better determine whether memory impairments are due to very mild Alzheimer’s disease or the normal aging process.
Their study appears in the journal Neuropsychologia.
The Alzheimer’s Association estimates that the number of Americans living with Alzheimer’s disease will increase from 5 million in 2014 to as many as 16 million by 2050. Memory impairments and other early symptoms of Alzheimer’s are often difficult to differentiate from the effects of normal aging, making it hard for doctors to recommend treatment for those affected until the disease has progressed substantially.
Previous studies have shown that a part of the brain called the hippocampus is important to relational memory – the “ability to bind together various items of an event,” said Jim Monti, a University of Illinois postdoctoral research associate who led the work with psychology professor Neal Cohen, who is affiliated with the Beckman Institute at Illinois. Being able to connect a person’s name with his or her face is one example of relational memory. These two pieces of information are stored in different parts of the brain, but the hippocampus “binds” them so that the next time you see that person, you remember his or her name, Monti said.
Previous research has shown that people with Alzheimer’s disease often have impairments in hippocampal function. So the team designed a task that tested participants’ relational memory abilities.
Participants were shown a circle divided into three parts, each having a unique design. Similar to the process of name-and-face binding, the hippocampus works to bind these three pieces of the circle together. After the participants studied a circle, they would pick its exact match from a series of 10 circles, presented one at a time.
People with very mild Alzheimer’s disease did worse overall on the task than those in the healthy aging group, who, in turn, did worse than a group of young adults. The task also revealed an additional memory impairment unique to those with very mild Alzheimer’s disease, indicating the changes in cognition that result from Alzheimer’s are qualitatively different than healthy aging. This unique impairment allows researchers to statistically differentiate between those who did and those who did not have Alzheimer’s more accurately than some of the classical tests used for Alzheimer’s diagnosis, Monti said.
“That was illuminating and will serve to inform future work aimed at understanding and detecting the earliest cognitive manifestations of Alzheimer’s disease,” Monti said.
Although this new tool could eventually be used in clinical practice, more studies need to be done to refine the test, he said.
“We’d like to eventually study populations with fewer impairments and bring in neuroimaging techniques to better understand the initial changes in brain and cognition that are due to Alzheimer’s disease,” Monti said.
Perhaps one of the keys to good health isn’t just what you eat but how you taste it.

Taste buds – yes, the same ones you may blame for that sweet tooth or French fry craving – may in fact have a powerful role in a long and healthy life – at least for fruit flies, say two new studies that appear in the Proceedings of the National Academy of Sciences of the United States of America.
Researchers from the University of Michigan, Wayne State University and Friedrich Miescher Institute for Biomedical Research in Switzerland found that suppressing the animal’s ability to taste its food –regardless of how much it actually eats – can significantly increase or decrease its length of life and potentially promote healthy aging.
Bitter tastes could have negative effects on lifespan, sweet tastes had positive effects, and the ability to taste water had the most significant impact – flies that could not taste water lived up to 43% longer than other flies. The findings suggest that in fruit flies, the loss of taste may cause physiological changes to help the body adapt to the perception that it’s not getting adequate nutrients.
In the case of flies whose loss of water taste led to a longer life, authors say the animals may attempt to compensate for a perceived water shortage by storing greater amounts of fat and subsequently using these fat stores to produce water internally. Further studies are planned to better explore how and why bitter and sweet tastes affect aging.
“This brings us further understanding about how sensory perception affects health. It turns out that taste buds are doing more than we think,” says senior author of the University of Michigan-led study Scott Pletcher, Ph.D., associate professor in the Department of Molecular and Integrative Physiology and research associate professor at the Institute of Gerontology.
“We know they’re able to help us avoid or be attracted to certain foods but in fruit flies, it appears that taste may also have a very profound effect on the physiological state and healthy aging.”
Pletcher conducted the study with lead author Michael Waterson, a Ph.D graduate student in U-M’s Cellular and Molecular Biology Program.
“Our world is shaped by our sensory abilities that help us navigate our surroundings and by dissecting how this affects aging, we can lay the groundwork for new ideas to improve our health,” says senior author of the other study, Joy Alcedo, Ph.D, assistant professor in the Department of Biological Sciences at Wayne State University, formerly of the Friedrich Miescher Institute for Biomedical Research in Switzerland. Alcedo conducted the research with lead author Ivan Ostojic, Ph.D., of the Friedrich Miescher Institute for Biomedical Research in Switzerland.
Recent studies suggest that sensory perception may influence health-related characteristics such as athletic performance, type II diabetes, and aging. The two new studies, however, provide the first detailed look into the role of taste perception.
“These findings help us better understand the influence of sensory signals, which we now know not only tune an organism into its environment but also cause substantial changes in physiology that affect overall health and longevity,” Waterson says. “We need further studies to help us apply this knowledge to health in humans potentially through tailored diets favoring certain tastes or even pharmaceutical compounds that target taste inputs without diet alterations.”
(Source: uofmhealth.org)
New research suggests that certain types of brain cells may be “picky eaters,” seeming to prefer one specific energy source over others. The finding has implications for understanding the cognitive decline seen in aging and degenerative diseases such as Alzheimer’s and multiple sclerosis.

(Image caption: Neural stem cells differentiate into three different cell types: neurons (purple), oligodendrocytes (red), which produce axon insulation, and astrocytes (green), which also support neurons. Cell nuclei are shown in blue. Credit: Liana Roberts Stein)
Studying mice, investigators from Washington University School of Medicine in St. Louis showed that a specific energy source called NAD is important in cells responsible for maintaining the overall structure of the brain and for performing complex cognitive functions. NAD (nicotinamide adenine dinucleotide) is a molecule that harvests energy from nutrients in food and converts it into a form cells can use.
The work appears in two journal articles — in the May 8 issue of The EMBO Journal, a publication of the European Molecular Biology Organization, and in a recent issue of The Journal of Neuroscience.
“We are interested in understanding how cells make NAD and what implications that has for cellular function, especially in the context of aging and longevity,” said Shin-ichiro Imai, MD, PhD, professor of developmental biology and of medicine and senior author of both papers. “We know, for example, NAD levels decrease with age in tissues such as muscle and fat. We wanted to find out if the same is true in the brain.”
The investigators looked at two types of brain cells: adult neural stem cells, responsible for maintaining supplies of neurons and their supporting cells, and forebrain neurons, vital for performing complex cognitive tasks.
In The EMBO Journal, they reported that NAD levels decreased with age in the mouse hippocampus, a vital region of the brain for cognition. The researchers then used genetic techniques to find out what would happen when NAD manufacturing is turned off in the adult neural stem cells of the mouse brain.
“Neural stem cells are very metabolically expensive, so you might expect them to be particularly vulnerable to loss of an energy source,” said first author Liana Roberts Stein, PhD, postdoctoral researcher in Imai’s lab. “There are other energy sources for brain cells, such as glucose, but no one had ever looked at where NAD is coming from in these cells.”
According to the researchers, there are four pathways of NAD synthesis, and the scientists focused on just one. They wanted to find out whether this particular pathway — a longtime focus of Imai’s lab — is important for these cells or if the other routes could compensate.
The pathway begins with the B vitamin nicotinamide. Cells take dietary nicotinamide and, with a helper protein called Nampt, manufacture a molecule called NMN, which then is processed further to make NAD. When Stein eliminated Nampt from neural stem cells, several significant changes took place.
Levels of NAD dropped, and the neural stem cells stopped dividing; they stopped renewing themselves; and they stopped being able to create important cells that insulate axons, the “wires” that carry electrical signals throughout the brain. With less insulation, these signals slow down, impairing brain function.
Imai and Stein pointed out possible therapeutic implications of this finding, especially in light of what is known about cognitive decline in aging and certain diseases.
“Scientists have shown that with age there actually isn’t a large decrease in the total neuron population,” Stein said. “But there is quite a substantial decrease in white matter, which is primarily composed of cells that function in axon insulation. This pathway also could be relevant in conditions involving loss of cells that make this insulation, like multiple sclerosis.”
Imai and Stein also found they could prevent the loss of the neural stem cells missing Nampt by giving the mice NMN, the next molecule in the chain of events leading to NAD.
“We gave the mice NMN in their drinking water for 12 months,” Stein said. “And at the higher dose, we saw a rescue of the neural stem cell pool in aged mice.”
Imai called this finding exciting because it supports the possibility of a future NMN supplement.
“We think that NMN could convey a similar effect in people,” Imai said. “A future clinical trial for NMN will tell us if it has any efficacy in humans.”
In addition to maintaining stem cell populations and keeping the brain supplied with all its cell types, the investigators showed that NAD also is vital for the process of cognition itself.
Reporting in The Journal of Neuroscience, they showed that neurons of the mouse forebrain depend heavily on NAD in normal cognitive function. Instead of deleting Nampt in stem cells, this time Stein deleted it only in neurons of the forebrain. All other cells were normal, including those that make axon insulation.
Without Nampt and its eventual product, NAD, in forebrain neurons, the behavior of the mice changed dramatically, according to the investigators.
“The mice were really hyperactive, with a twofold increase in activity levels,” Stein said. “They also showed a loss of anxiety-like behaviors. These mice didn’t seem to sense or fear potentially threatening situations and showed fairly drastic memory defects.”
Stein pointed out that these neurons are in a region of the brain known to be particularly vulnerable to neurodegenerative conditions from Alzheimer’s disease to stroke.
“It’s possible that these neurons’ dependence on Nampt is responsible for their extreme susceptibility to these conditions,” she said. “It would be interesting to model some of these diseases in mice and see if supplementing NMN provides any benefit to their behavior or memory.”
“We haven’t done that study yet,” Imai added. “But this is the direction the entire field is going.”
(Source: news.wustl.edu)