Posts tagged aging
Articles and news from the latest research reports.
Heavy Drinking in Middle Age May Speed Memory Loss by up to Six Years in Men
Middle-aged men who drink more than 36 grams of alcohol, or two and a half US drinks per day, may speed their memory loss by up to six years later on, according to a study published in the January 15, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. On the other hand, the study found no differences in memory and executive function in men who do not drink, former drinkers and light or moderate drinkers. Executive function deals with attention and reasoning skills in achieving a goal.
“Much of the research evidence about drinking and a relationship to memory and executive function is based on older populations,” said study author Séverine Sabia, PhD, of the University College London in the United Kingdom. “Our study focused on middle-aged participants and suggests that heavy drinking is associated with faster decline in all areas of cognitive function in men.”
The study involved 5,054 men and 2,099 women whose drinking habits were assessed three times over 10 years. A drink was considered wine, beer or liquor. Then, when the participants were an average age of 56, they took their first memory and executive function test. The tests were repeated twice over the next 10 years.
The study found that there were no differences in memory and executive function decline between men who did not drink and those who were light or moderate drinkers—those who drank less than 20 grams, or less than two US drinks per day. Heavy drinkers showed memory and executive function declines between one-and-a-half to six years faster than those who had fewer drinks per day.
Racism May Accelerate Aging in African American Men
A new University of Maryland-led study reveals that racism may impact aging at the cellular level. Researchers found signs of accelerated aging in African American men who reported high levels of racial discrimination and who had internalized anti-Black attitudes. Findings from the study, which is the first to link racism-related factors and biological aging, are published in the American Journal of Preventive Medicine.
Racial disparities in health are well-documented, with African Americans having shorter life expectancy, and a greater likelihood of suffering from aging-related illnesses at younger ages compared to whites. Accelerated aging at the biological level may be one mechanism linking racism and disease risk.
“We examined a biomarker of systemic aging, known as leukocyte telomere length,” explained Dr. David H. Chae, assistant professor of epidemiology at UMD’s School of Public Health and the study’s lead investigator. Shorter telomere length is associated with increased risk of premature death and chronic disease such as diabetes, dementia, stroke and heart disease. “We found that the African American men who experienced greater racial discrimination and who displayed a stronger bias against their own racial group had the shortest telomeres of those studied,” Chae explained.
Telomeres are repetitive sequences of DNA capping the ends of chromosomes, which shorten progressively over time – at a rate of approximately 50-100 base pairs annually. Telomere length is variable, shortening more rapidly under conditions of high psychosocial and physiological stress. “Telomere length may be a better indicator of biological age, which can give us insight into variations in the cumulative ‘wear and tear’ of the organism net of chronological age,” said Chae. Among African American men with stronger anti-black attitudes, investigators found that average telomere length was 140 base pairs shorter in those reporting high vs. low levels of racial discrimination; this difference may equate to 1.4 to 2.8 years chronologically.
Participants in the study were 92 African American men between 30-50 years of age. Investigators asked them about their experiences of discrimination in different domains, including work and housing, as well as in getting service at stores or restaurants, from the police, and in other public settings. They also measured racial bias using the Black-White Implicit Association Test. This test gauges unconscious attitudes and beliefs about race groups that people may be unaware of or unwilling to report.
Even after adjusting for participants’ chronological age, socioeconomic factors, and health-related characteristics, investigators found that the combination of high racial discrimination and anti-black bias was associated with shorter telomeres. On the other hand, the data revealed that racial discrimination had little relationship with telomere length among those holding pro-black attitudes. “African American men who have more positive views of their racial group may be buffered from the negative impact of racial discrimination,” explained Chae. “In contrast, those who have internalized an anti-black bias may be less able to cope with racist experiences, which may result in greater stress and shorter telomeres.”
The findings from this study are timely in light of regular media reports of racism facing African American men. “Stop-and-frisk policies, and other forms of criminal profiling such as ‘driving or shopping while black’ are inherently stressful and have a real impact on the health of African Americans,” said Chae. Researchers found that racial discrimination by police was most commonly reported by participants in the study, followed by discrimination in employment. In addition, African American men are more routinely treated with less courtesy or respect, and experience other daily hassles related to racism.
Chae indicated the need for additional research to replicate findings, including larger studies that follow participants over time. “Despite the limitations of our study, we contribute to a growing body of research showing that social toxins disproportionately impacting African American men are harmful to health,” Chae explained. “Our findings suggest that racism literally makes people old.”
(Image: Shutterstock)
Study Shows Where Alzheimer’s Starts and How It Spreads
Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer’s disease and in mouse models of the disease, Columbia University Medical Center (CUMC) researchers have clarified three fundamental issues about Alzheimer’s: where it starts, why it starts there, and how it spreads. In addition to advancing understanding of Alzheimer’s, the findings could improve early detection of the disease, when drugs may be most effective. The study was published today in the online edition of the journal Nature Neuroscience.
“It has been known for years that Alzheimer’s starts in a brain region known as the entorhinal cortex,” said co-senior author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, professor of radiology, and director of the Alzheimer’s Disease Research Center. “But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected.”
The study also shows that, over time, Alzheimer’s spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation. The researchers suspect that Alzheimer’s spreads “functionally,” that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.
A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist. “The LEC is especially vulnerable to Alzheimer’s because it normally accumulates tau, which sensitizes the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer’s,” said co-senior author Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.
In the study, the researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults enrolled in the Washington Heights-Inwood Columbia Aging Project (WHICAP). All of the adults were free of dementia at the time of enrollment.
“Dr. Richard Mayeux’s WHICAP study enables us to follow a large group of healthy elderly individuals, some of whom have gone on to develop Alzheimer’s disease,” said Dr. Small. “This study has given us a unique opportunity to image and characterize patients with Alzheimer’s in its earliest, preclinical stage.”
The 96 adults were followed for an average of 3.5 years, at which time 12 individuals were found to have progressed to mild Alzheimer’s disease. An analysis of the baseline fMRI images of those 12 individuals found significant decreases in cerebral blood volume (CBV) — a measure of metabolic activity — in the LEC compared with that of the 84 adults who were free of dementia.
A second part of the study addressed the role of tau and APP in LEC dysfunction. While previous studies have suggested that entorhinal cortex dysfunction is associated with both tau and APP abnormalities, it was not known how these proteins interact to drive this dysfunction, particularly in preclinical Alzheimer’s.
To answer this question, explained first author Usman Khan, an MD-PhD student based in Dr. Small’s lab, the team created three mouse models, one with elevated levels of tau in the LEC, one with elevated levels of APP, and one with elevated levels of both proteins. The researchers found that the LEC dysfunction occurred only in the mice with both tau and APP.
The study has implications for both research and treatment. “Now that we’ve pinpointed where Alzheimer’s starts, and shown that those changes are observable using fMRI, we may be able to detect Alzheimer’s at its earliest preclinical stage, when the disease might be more treatable and before it spreads to other brain regions,” said Dr. Small. In addition, say the researchers, the new imaging method could be used to assess the efficacy of promising Alzheimer’s drugs during the disease’s early stages.
A New—and Reversible—Cause of Aging
Researchers have discovered a cause of aging in mammals that may be reversible.
The essence of this finding is a series of molecular events that enable communication inside cells between the nucleus and mitochondria. As communication breaks down, aging accelerates. By administering a molecule naturally produced by the human body, scientists restored the communication network in older mice. Subsequent tissue samples showed key biological hallmarks that were comparable to those of much younger animals.
“The aging process we discovered is like a married couple—when they are young, they communicate well, but over time, living in close quarters for many years, communication breaks down,” said Harvard Medical School Professor of Genetics David Sinclair, senior author on the study. “And just like with a couple, restoring communication solved the problem.”
This study was a joint project between Harvard Medical School, the National Institute on Aging, and the University of New South Wales, Sydney, Australia, where Sinclair also holds a position.
The findings are published Dec. 19 in Cell.
Communication breakdown
Mitochondria are often referred to as the cell’s “powerhouse,” generating chemical energy to carry out essential biological functions. These self-contained organelles, which live inside our cells and house their own small genomes, have long been identified as key biological players in aging. As they become increasingly dysfunctional overtime, many age-related conditions such as Alzheimer’s disease and diabetes gradually set in.
Researchers have generally been skeptical of the idea that aging can be reversed, due mainly to the prevailing theory that age-related ills are the result of mutations in mitochondrial DNA—and mutations cannot be reversed.
Sinclair and his group have been studying the fundamental science of aging—which is broadly defined as the gradual decline in function with time—for many years, primarily focusing on a group of genes called sirtuins. Previous studies from his lab showed that one of these genes, SIRT1, was activated by the compound resveratrol, which is found in grapes, red wine and certain nuts.
Ana Gomes, a postdoctoral scientist in the Sinclair lab, had been studying mice in which this SIRT1 gene had been removed. While they accurately predicted that these mice would show signs of aging, including mitochondrial dysfunction, the researchers were surprised to find that most mitochondrial proteins coming from the cell’s nucleus were at normal levels; only those encoded by the mitochondrial genome were reduced.
“This was at odds with what the literature suggested,” said Gomes.
As Gomes and her colleagues investigated potential causes for this, they discovered an intricate cascade of events that begins with a chemical called NAD and concludes with a key molecule that shuttles information and coordinates activities between the cell’s nuclear genome and the mitochondrial genome. Cells stay healthy as long as coordination between the genomes remains fluid. SIRT1’s role is intermediary, akin to a security guard; it assures that a meddlesome molecule called HIF-1 does not interfere with communication.
For reasons still unclear, as we age, levels of the initial chemical NAD decline. Without sufficient NAD, SIRT1 loses its ability to keep tabs on HIF-1. Levels of HIF-1 escalate and begin wreaking havoc on the otherwise smooth cross-genome communication. Over time, the research team found, this loss of communication reduces the cell’s ability to make energy, and signs of aging and disease become apparent.
“This particular component of the aging process had never before been described,” said Gomes.
While the breakdown of this process causes a rapid decline in mitochondrial function, other signs of aging take longer to occur. Gomes found that by administering an endogenous compound that cells transform into NAD, she could repair the broken network and rapidly restore communication and mitochondrial function. If the compound was given early enough—prior to excessive mutation accumulation—within days, some aspects of the aging process could be reversed.
Cancer connection
Examining muscle from two-year-old mice that had been given the NAD-producing compound for just one week, the researchers looked for indicators of insulin resistance, inflammation and muscle wasting. In all three instances, tissue from the mice resembled that of six-month-old mice. In human years, this would be like a 60-year-old converting to a 20-year-old in these specific areas.
One particularly important aspect of this finding involvesHIF-1. More than just an intrusive molecule that foils communication, HIF-1 normally switches on when the body is deprived of oxygen. Otherwise, it remains silent. Cancer, however, is known to activate and hijack HIF-1. Researchers have been investigating the precise role HIF-1 plays in cancer growth.
“It’s certainly significant to find that a molecule that switches on in many cancers also switches on during aging,” said Gomes. “We’re starting to see now that the physiology of cancer is in certain ways similar to the physiology of aging. Perhaps this can explain why the greatest risk of cancer is age.”
“There’s clearly much more work to be done here, but if these results stand, then certain aspects of aging may be reversible if caught early,” said Sinclair.
The researchers are now looking at the longer-term outcomes of the NAD-producing compound in mice and how it affects the mouse as a whole. They are also exploring whether the compound can be used to safely treat rare mitochondrial diseases or more common diseases such as Type 1 and Type 2 diabetes. Longer term, Sinclair plans to test if the compound will give mice a healthier, longer life.
(Source: hms.harvard.edu)
Sleep-Deprived Mice Show Connections Among Lack of Shut-eye, Diabetes, Age
Sleep, or the lack of it, seems to affect just about every aspect of human physiology. Yet, the molecular pathways through which sleep deprivation wreaks its detrimental effects on the body remain poorly understood. Although numerous studies have looked at the consequences of sleep deprivation on the brain, comparatively few have directly tested its effects on peripheral organs.
During sleep deprivation cells upregulate the UPR – the unfolded protein response – a process where misfolded proteins get refolded or degraded.
Five years ago, researchers at the Perelman School of Medicine, University of Pennsylvania, showed that the UPR is an adaptive response to stress induced by sleep deprivation and is impaired in the brains of old mice. Those findings suggested that inadequate sleep in the elderly, who normally experience sleep disturbances, could exacerbate an already-impaired protective response to protein misfolding that happens in aging cells. Protein misfolding and clumping is associated with many diseases such as Alzheimer’s and Parkinson’s, noted Nirinjini Naidoo, Ph.D., research associate professor in the Division of Sleep Medicine in that study.
Naidoo is also senior author of a follow-up study in Aging Cell this month that shows, for the first time, an effect of sleep deprivation on the UPR in peripheral tissue, in this case, the pancreas. They showed that stress in pancreatic cells due to sleep deprivation may contribute to the loss or dysfunction of these cells important to maintaining proper blood sugar levels, and that these functions may be exacerbated by normal aging.
“The combined effect of aging and sleep deprivation resulted in a loss of control of blood sugar reminiscent of pre-diabetes in mice,” says Naidoo. “We hypothesize that older humans might be especially susceptible to the effects of sleep deprivation on the disruption of glucose homeostasis via cell stress.”
Working with Penn colleague Joe Baur, Ph.D., assistant professor of Physiology, Naidoo started a collaboration to look at the relationship of sleep deprivation, the UPR, and metabolic response with age. Other researchers had suggested that the death of beta cells associated with type 2 diabetes may be due to stress in a cell compartment called the endoplasmic reticulum (ER). The UPR is one part of the quality control system in the ER, where some proteins are made.
Knowing this, Naidoo and Baur asked if sleep deprivation (SD) causes ER stress in the pancreas, via an increase in protein misfolding, and in turn, how this relates to aging.
The team examined tissues in mice for cellular stress following acute SD, and they also looked for cellular stress in aging mice. Their results show that both age and SD combine to induce cellular stress in the pancreas.
Older mice fared markedly worse when subjected to sleep deprivation. Pancreas tissue from older mice or from young animals subjected to sleep deprivation exhibited signs of protein misfolding, yet both were able to maintain insulin secretion and control blood sugar levels. Pancreas tissue from acutely sleep-deprived aged animals exhibited a marked increase in CHOP, a protein associated with cell death, suggesting a maladaptive response to cellular stress with age that was amplified by sleep deprivation.
Acute sleep deprivation caused increased plasma glucose levels in both young and old animals. However, this change was not overtly related to stress in beta cells, since plasma insulin levels were not lower following acute lack of sleep.
Accordingly, young animals subjected to acute sleep deprivation remained tolerant to a glucose challenge. In a chronic sleep deprivation experiment, young mice were sensitized to insulin and had improved control of their blood sugar, whereas aged animals became hyperglycemic and failed to maintain appropriate plasma insulin concentrations.
While changes in insulin secretion are unlikely to play a major role in the acute effects of SD, cellular stress in pancreatic tissue suggests that chronic SD may contribute to the loss or dysfunction of endocrine cells, and that these effects may be exacerbated by normal aging, say the researchers.
Estrogen: Not just produced by the ovaries
A UW-Madison research team reports today that the brain can produce and release estrogen — a discovery that may lead to a better understanding of hormonal changes observed from before birth throughout the entire aging process.
The new research shows that the hypothalamus can directly control reproductive function in rhesus monkeys and very likely performs the same action in women.
Scientists have known for about 80 years that the hypothalamus, a region in the brain, is involved in regulating the menstrual cycle and reproduction. Within the past 40 years, they predicted the presence of neural estrogens, but they did not know whether the brain could actually make and release estrogen.
Most estrogens, such as estradiol, a primary hormone that controls the menstrual cycle, are produced in the ovaries. Estradiol circulates throughout the body, including the brain and pituitary gland, and influences reproduction, body weight, and learning and memory. As a result, many normal functions are compromised when the ovaries are removed or lose their function after menopause.
"Discovering that the hypothalamus can rapidly produce large amounts of estradiol and participate in control of gonadotropin-releasing hormone neurons surprised us," says Ei Terasawa, professor of pediatrics at the UW School of Medicine and Public Health and senior scientist at the Wisconsin National Primate Research Center. "These findings not only shift the concept of how reproductive function and behavior is regulated but have real implications for understanding and treating a number of diseases and disorders."
For diseases that may be linked to estrogen imbalances, such as Alzheimer’s disease, stroke, depression, experimental autoimmune encephalomyelitis and other autoimmune disorders, the hypothalamus may become a novel area for drug targeting, Terasawa says. “Results such as these can point us in new research directions and find new diagnostic tools and treatments for neuroendocrine diseases.”
The study, published today in the Journal of Neuroscience, “opens up entirely new avenues of research into human reproduction and development, as well as the role of estrogen action as our bodies age,” reports the first author of the paper, Brian Kenealy, who earned his Ph.D. this summer in the Endocrinology and Reproductive Physiology Program at UW-Madison. Kenealy performed three studies. In the first experiment, a brief infusion of estradiol benzoate administered into the hypothalamus of rhesus monkeys that had surgery to remove their ovaries rapidly stimulated GnRH release. The brain took over and began rapidly releasing this estrogen in large pulsing surges.
In the second experiment, mild electrical stimulation of the hypothalamus caused the release of both estrogen and GnRH (thus mimicking how estrogen could induce a neurotransmitter-like action). Third, the research team infused letrazole, an aromatase inhibitor that blocks the synthesis of estrogen, resulting in a lack of estrogen as well as GnRH release from the brain. Together, these methods demonstrated how local synthesis of estrogen in the brain is important in regulating reproductive function.
The reproductive, neurological and immune systems of rhesus macaques have proven to be excellent biomedical models for humans over several decades, says Terasawa, who focuses on the neural and endocrine mechanisms that control the initiation of puberty. “This work is further proof that these animals can teach us about so many basic functions we don’t fully understand in humans.”
Leading up to this discovery, Terasawa said, recent evidence had shown that estrogen acting as a neurotransmitter in the brain rapidly induced sexual behavior in quails and rats. Kenealy’s work is the first evidence of this local hypothalamic action in primates, and in those that don’t even have ovaries.
"The discovery that the primate brain can make estrogen is key to a better understanding of hormonal changes observed during every phase of development, from prenatal to puberty, and throughout adulthood, including aging," Kenealy says.
(Source: news.wisc.edu)
New compound for slowing the aging process can lead to novel treatments for brain diseases
A successful joint collaboration between researchers at the Hebrew university of Jerusalem and the startup company TyrNovo may lead to a potential treatment of brain diseases. The researchers found that TyrNovo’s novel and unique compound, named NT219, selectively inhibits the process of aging in order to protect the brain from neurodegenerative diseases, without affecting lifespan. This is a first and important step towards the development of future drugs for the treatment of various neurodegenerative maladies.
Human neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases share two key features: they stem from toxic protein aggregation and emerge late in life. The common temporal emergence pattern exhibited by these maladies proposes that the aging process negatively regulates protective mechanisms that prevent their manifestation early in life, exposing the elderly to disease. This idea has been the major focus of the work in the laboratory of Dr. Ehud Cohen of the Department of Biochemistry and Molecular Biology, at the Institute for Medical Research Israel-Canada in the Hebrew University of Jerusalem’s Faculty of Medicine.
Cohen’s first breakthrough in this area occurred when he discovered, working with worms, that reducing the activity of the signaling mechanism conveyed through insulin and the growth hormone IGF1, a major aging regulating pathway, constituted a defense against the aggregation of the Aβ protein which is mechanistically-linked with Alzheimer’s disease. Later, he found that the inhibition of this signaling route also protected Alzheimer’s-model mice from behavioral impairments and pathological phenomena typical to the disease. In these studies, the path was reduced through genetic manipulation, a method not applicable in humans.
Dr. Hadas Reuveni, the CEO of TyrNovo, a startup company formed for the clinical development of NT219, and Prof. Alexander Levitzki from the Department of Biological Chemistry at the Hebrew University, with their research teams, discovered a new set of compounds that inhibit the activity of the IGF1 signaling cascade in a unique and efficient mechanism, primarily for cancer treatment, and defined NT219 as the leading compound for further development.
Now, in a fruitful collaboration Dr. Cohen and Dr. Reuveni, together with Dr. Cohen’s associates Tayir El-Ami and Lorna Moll, have demonstrated that NT219 efficiently inhibits IGF1 signaling, in both worms and human cells. The inhibition of this signaling pathway by NT219 protected worms from toxic protein aggregation that in humans is associated with the development of Alzheimer’s or Huntington’s disease.
The discoveries achieved during this project, which was funded by the Rosetrees Trust of Britain, were published this week in the journal Aging Cell (“A novel inhibitor of the insulin/IGF signaling pathway protects from age-onset, neurodegeneration-linked proteotoxicity”). The findings strengthen the notion that the inhibition of the IGF1 signaling pathway has a therapeutic potential as a treatment for neurodegenerative disorders. They also point at NT219 as the first compound that provides protection from neurodegeneration-associated toxic protein aggregation through a selective manipulation of aging.
Cohen, Reuveni and Levitzki have filed a patent application that protects the use of NT219 as a treatment for neurodegenerative maladies through Yissum, the technology transfer company of the Hebrew University. Dr. Gil Pogozelich, chairman of Goldman Hirsh Partners Ltd., which holds the controlling interest in TyrNovo, says that he sees great importance in the cooperation on this project with the Hebrew University, and that TyrNovo represents a good example of how scientific and research initiatives can further health care together with economic benefits.
Recently, Dr. Cohen’s laboratory obtained an ethical approval to test the therapeutic efficiency of NT219 as a treatment in Alzheimer’s-model mice, hoping to develop a future treatment for hitherto incurable neurodegenerative disorders.
Brain aging is conclusively linked to genes; a crucial first step in finding biological mechanisms of normal aging
For the first time in a large study sample, the decline in brain function in normal aging is conclusively shown to be influenced by genes, say researchers from the Texas Biomedical Research Institute and Yale University.
“Identification of genes associated with brain aging should improve our understanding of the biological processes that govern normal age-related decline,” said John Blangero, Ph.D., a Texas Biomed geneticist and the senior author of the paper. The study, funded by the National Institutes of Health (NIH), is published in the November 4, 2013 issue of the Proceedings of the National Academy of Sciences. David Glahn, Ph.D., an associate professor of psychiatry at the Yale University School of Medicine, is the first author on the paper.
In large pedigrees including 1,129 people aged 18 to 83, the scientists documented profound aging effects from young adulthood to old age, on neurocognitive ability and brain white matter measures. White matter actively affects how the brain learns and functions. Genetic material shared amongst biological relatives appears to predict the observed changes in brain function with age.
Participants were enrolled in the Genetics of Brain Structure and Function Study and drawn from large Mexican Americans families in San Antonio. Brain imaging studies were conducted at the University of Texas Health Science Center at San Antonio Research Imaging Institute directed by Peter Fox, M.D.
“The use of large human pedigrees provides a powerful resource for measuring how genetic factors change with age,” Blangero said.
By applying a sophisticated analysis, the scientists demonstrated a heritable basis for neurocognitive deterioration with age that could be attributed to genetic factors. Similarly, decreasing white matter integrity with age was influenced by genes., The investigators further demonstrated that different sets of genes are responsible for these two biological aging processes.
“A key advantage of this study is that we specifically focused on large extended families and so we were able to disentangle genetic from non-genetic influences on the aging process,” said Glahn.
(Source: txbiomed.org)
Learning New Skills Keeps an Aging Mind Sharp
Older adults are often encouraged to stay active and engaged to keep their minds sharp, that they have to “use it or lose it.” But new research indicates that only certain activities — learning a mentally demanding skill like photography, for instance — are likely to improve cognitive functioning.
These findings, forthcoming in Psychological Science, a journal of the Association for Psychological Science, reveal that less demanding activities, such as listening to classical music or completing word puzzles, probably won’t bring noticeable benefits to an aging mind.
“It seems it is not enough just to get out and do something—it is important to get out and do something that is unfamiliar and mentally challenging, and that provides broad stimulation mentally and socially,” says psychological scientist and lead researcher Denise Park of the University of Texas at Dallas. “When you are inside your comfort zone you may be outside of the enhancement zone.”
The new findings provide much-needed insight into the components of everyday activities that contribute to cognitive vitality as we age.
“We need, as a society, to learn how to maintain a healthy mind, just like we know how to maintain vascular health with diet and exercise,” says Park. “We know so little right now.”
For their study, Park and colleagues randomly assigned 221 adults, ages 60 to 90, to engage in a particular type of activity for 15 hours a week over the course of three months.
Some participants were assigned to learn a new skill — digital photography, quilting, or both — which required active engagement and tapped working memory, long-term memory and other high-level cognitive processes.
Other participants were instructed to engage in more familiar activities at home, such as listening to classical music and completing word puzzles. And, to account for the possible influence of social contact, some participants were assigned to a social group that included social interactions, field trips, and entertainment.
At the end of three months, Park and colleagues found that the adults who were productively engaged in learning new skills showed improvements in memory compared to those who engaged in social activities or non-demanding mental activities at home.
“The findings suggest that engagement alone is not enough,” says Park. “The three learning groups were pushed very hard to keep learning more and mastering more tasks and skills. Only the groups that were confronted with continuous and prolonged mental challenge improved.”
The study is particularly noteworthy given that the researchers were able to systematically intervene in people’s lives, putting them in new environments and providing them with skills and relationships:
“Our participants essentially agreed to be assigned randomly to different lifestyles for three months so that we could compare how different social and learning environments affected the mind,” says Park. “People built relationships and learned new skills — we hope these are gifts that keep on giving, and continue to be a source of engagement and stimulation even after they finished the study.”
Park and colleagues are planning on following up with the participants one year and five years down the road to see if the effects remain over the long term. They believe that the research has the potential to be profoundly important and relevant, especially as the number of seniors continues to rise:
“This is speculation, but what if challenging mental activity slows the rate at which the brain ages?” asks Park. “Every year that you save could be an added year of high quality life and independence.”
Musicians have sharper minds are able to pick up mistakes and fix them quicker than the rest of us, according to new research.
The study, by researchers at the University of St Andrews, suggests that musical activity could protect against decline in mental abilities through age or illness.
The work, published in the journal Neuropsychologia, extends previous findings that mental abilities are positively related to musical skills. The researchers say that the latest findings demonstrate the potential for ‘far reaching benefits’ of musical activity on mental and physical well-being.
The study was led by St Andrews psychologist Dr Ines Jentzsch, who compared the cognitive ability of amateur musicians versus non-musicians in performing simple mental tasks.
The most striking difference she found lay in the musicians’ ability to recognise and correct mistakes. Not only that, but they responded faster than those with little or no musical training, with no loss in accuracy. This is perhaps not surprising since musicians learn to be constantly aware of their performance, but to not be overly affected by mistakes.
Dr Jentzsch, a Reader in the University’s School of Psychology and Neuroscience, commented, “Our study shows that even moderate levels of musical activity can benefit brain functioning.
“Our findings could have important implications as the processes involved are amongst the first to be affected by aging, as well as a number of mental illnesses such as depression. The research suggests that musical activity could be used as an effective intervention to slow, stop or even reverse age- or illness-related decline in mental functioning.”
The study compared groups of amateur musicians with varying levels of time they had spent in practicing their instrument to a non-musician control group. They then measured each group’s behavioural and brain responses to simple mental tests.
The results showed that playing a musical instrument, even at moderate levels, improves the ability to monitor our behavior for errors and adjust subsequent responses more effectively when needed.
Dr Jentzsch, herself a keen pianist, continued, “Musical activity cannot only immensely enrich our lives but the associated benefits for our physical and mental functioning could be even more far-reaching than proposed in our and previous research.
“Music plays an important role in virtually all societies. Nevertheless, in times of economic hardship, funds for music education are often amongst the first to be cut.
“We strongly encourage political decision makers to reconsider funding cuts for arts education and to increase public spending for music tuition.
“In addition, adults who have never played an instrument or felt too old to learn should be encouraged to take up music - it’s never too late.”