The study also found that this rewiring involves fibers that supply input to the cerebral cortex, the part of the brain that is responsible for sensory perception, motor control, and cognition.

“This study overturns decades-old beliefs that most of the brain is hard-wired before a critical period that ends when one is a young adult,” said Marcel Oberlaender, Ph.D., a neuroscientist at the Max Planck Florida Institute (MPFI) and first author on the paper. “By changing the nature of sensory experience, we were able to demonstrate that the brain can rewire, even at an advanced age. This may suggest that if one stops learning and experiencing new things as one ages, a substantial amount of connections within the brain may be lost.”

The researchers examined the brains of older rats, focusing on an area of the brain known as the thalamus, which processes and delivers information obtained from sensory organs to the cerebral cortex. Connections between the thalamus and the cortex have been thought to stop changing by early adulthood, but this was not found to be the case in this study, according to Oberlaender.

As nocturnal animals, rats rely on their whiskers as sensory organs to explore and navigate their environment. This makes the whisker system an ideal model for studying whether the brain can be remodeled by changing sensory experiences, the researchers note. By trimming the whiskers, and preventing the rats from receiving sensory input, the scientists sought to determine whether extensive rewiring of the connections between the thalamus and cortex would occur.

They found that the animals with trimmed whiskers had altered axons, fibers along which information is conveyed from one nerve cell to many others, while those whose whiskers were not trimmed had no changes.

The researchers said their findings were particularly striking as the rats were considered relatively old. This implies that rewiring can still take place at an age not previously thought possible, according to the researchers. Also notable was that the rewiring happened rapidly — in as little as a few days, the researchers add.

“We’ve shown that the structure of the rodent brain is in constant flux, and that this rewiring is shaped by sensory experience and interaction with the environment,” said Oberlaender.

“These changes seem to be life-long and may pertain to other sensory systems and species, including people. Our findings open the possibility of new avenues of research on development of the aging brain using quantitative anatomical studies combined with noninvasive imaging technologies suitable for humans, such as functional MRI (fMRI).”

The study was possible due to advances in high-resolution imaging and reconstruction techniques, developed in part by Oberlaender at MPFI. These techniques enable researchers to trace the fine and complex branching patterns of individual axons, with typical diameters less than a thousandth of a millimeter, throughout the entire brain.

The study was published in the May 24 issue of Neuron.

Source: Max Planck Florida Institute

The UK study suggests older people with robust brain “wiring” – connections of nerve fibers from different and distinct areas of the brain – are able to process information quickly and that this makes them generally smarter. Accordingly, the research suggests joining distant parts of the brain together with better wiring improves mental performance, signifying that intelligence is not found in a single part of the brain.

Moreover, a degraded condition of this wiring or “white matter” – the billions of nerve fibers that transmit signals around the brain – can negatively affect our intelligence by altering networks and slowing down processing speed.

University of Edinburgh researchers say this demonstrates that the deterioration of white matter with age is likely to be a significant cause of age-related cognitive decline.

In the study, the research team used three different brain imaging techniques in compiling the results, including two that have never been used before in the study of intelligence. These techniques measure the amount of water in brain tissue, indicate structural loss in the brain, and show how well the nerve fibers are insulated.

The researchers examined scans and results of thinking and reaction time tests from 420 people in the Lothian Birth Cohort of 1936, a group of nearly 1,100 people whose intelligence and general health have been tracked since they were 11years of age.

Study author and psychologist Dr. Lars Penke said, “Our results suggest a first plausible way how brain structure differences lead to higher intelligence. The results are exciting for our understanding of human intelligence differences at all ages.

“They also suggest a clear target for seeking treatment for mental difficulties, be they pathological or age-related. That the brain’s nerve connections tend to stay the same throughout the brain means we can now look at factors that affect the overall condition of the brain, like its blood supply.”

As our society ages, uncovering the secrets of good thinking skills in old age is a high priority.

“The research team is now looking at what keeps the brain’s connections healthy,” Penke said. ”We value our thinking skills, and research should address how we might retain them or slow their decline with age.”

Co-author Mark Bastin, M.D., said, “These findings are exciting as they show how quantitative brain imaging can provide novel insights into the links between brain structure and cognitive ability. This is a key research area given the importance of identifying strategies for retaining good mental ability into older age.”

Such findings could have a real impact on tackling mental decline in later life, including dementia.

Source: University of Edinburgh

According to researchers at the Georgia Health Sciences University, amyloid is excreted by all neurons, but rates dramatically increase in Alzheimer’s. In response to the excessive amyloid, astrocytes, which deliver blood, oxygen and nutrients to neurons in addition to hauling off some of the garbage, get activated and inflamed.

In a new study, the researchers have shown astrocytes also respond by packaging the lipid ceramide with the protein PAR-4, which can do damage on their own, but together are a more “deadly duo,” said Dr. Erhard Bieberich, a biochemist at the Medical College of Georgia at the university.

“If the neuron makes something toxic and dumps it at your door, what would you do?” said Bieberich, corresponding author of the study published in the Journal of Biological Chemistry. “You would probably do something to defend yourself.”

The researchers hypothesize that this lipid-coated package ultimately kills them both, which could help explain the brain-cell death and shrinkage that occurs in Alzheimer’s.

“If the astrocytes die, the neurons die,” Bieberich explained.

An avenue for future pursuit is whether a ceramide antibody could be a viable treatment for Alzheimer’s, he added.

Source: Georgia Health Sciences University 

Red and yellow cells photo by shutterstock.

The study also found that monounsaturated fat was associated with better overall cognitive function and memory.

The research team analyzed data from the Women’s Health Study, which included nearly 40,000 women who were 45 years and older. The researchers focused on data from 6,000 women, all over the age of 65. The women participated in three cognitive function tests, which were spaced out every two years for an average testing span of four years. The women also filled out very detailed food frequency surveys at the start of the Women’s Health Study, before the cognitive testing began.

“When looking at changes in cognitive function, what we found is that the total amount of fat intake did not really matter, but the type of fat did,” said Olivia Okereke, M.D., M.S., BWH Department of Psychiatry.

Women who consumed the highest amounts of saturated fat, which can come from animal fats such as red meat and butter, had worse overall cognition and memory over the four years of testing. Women who ate the most of the monounsaturated fats, which can be found in olive oil, had better patterns of cognitive scores over time.

Okereke notes that strategies to prevent cognitive decline in older people are particularly important. Even subtle declines in cognitive functioning can lead to higher risk of developing more serious problems, such as dementia and Alzheimer’s disease, she noted.

This study is published online by Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society.

Source: Brigham and Women’s Hospital

This is the first study to follow individuals with dementia until death regardless of whether they died from dementia or another condition.  In fact, most people with dementia, even advanced dementia, die from a physical condition such as cancer, heart disease or pneumonia.

The study tracked individuals with dementia to determine where they received care and in what order. Instead of finding these patients moving directly from home to hospital to nursing home as presumed, the researchers discovered that many individuals with dementia go back and forth. Transitions in care are numerous and follow no set path.

“This is a study on what it is like to live with dementia over a five- to 10-year period,” said Regenstrief Institute investigator Christopher Callahan, M.D., Cornelius and Yvonne Pettinga Professor in Aging Research at Indiana University School of Medicine and director of the Indiana University Center for Aging Research.

“You probably won’t proceed on a straight line from home to hospital to nursing home. You will experience multiple transitions as you progress from mild to moderate to advanced dementia.”

Although 74 percent of the time dementia patients go to a nursing home after being hospitalized, they typically don’t stay there. Only about a quarter will return to the hospital in less than a month. Many of the remainder will go back home.

The researchers found that a majority of care for those with dementia, even severe dementia, is provided by families.

“These results challenge previous assumptions,” said Callahan, who founded the IU Center for Aging Research in 1997.

“Our findings will provide important information for all those concerned with managing the care of older adults — families, physicians, social workers, policy-makers, Medicare and Medicaid, insurance companies, hospital and nursing home administrators, as well as aging individuals. Caring for people living with dementia requires the attention of our entire health care system.”

The research appears in the Journal of the American Geriatrics Society.

Source:  Indiana University

Scientists from the United States and Israel think they’ve found a clue to the secret of the East African rodent’s long life: Throughout their lives, naked mole rats are blessed with large amounts of a protein essential for normal brain function.

“Naked mole rats have the highest level of a growth factor called NRG-1 in the cerebellum,” said Yael Edrey, doctoral student at The University of Texas Health Science Center San Antonio’s Barshop Institute for Longevity and Aging Studies, who notes that the growth factor’s “levels are sustained throughout their life, from development through adulthood.”

Edrey is the lead author of research that compared lifelong NRG-1 levels across seven species of rodents, from mice and guinea pigs to blind mole rats and Damaraland mole rats.

The researchers monitored NRG-1 levels in naked mole rats at different ages ranging from 1 day to 26 years. The other six rodent species have maximum life spans of 3 to 19 years.

The research team hypothesized that long-lived species would maintain higher levels of NRG-1 in the cerebellum, which coordinates movements and maintains bodily equilibrium.

Among each of the species, the longest-lived members exhibited the highest lifelong levels of NRG-1. The naked mole rat had the most robust and enduring supply, according to Edrey, who noted that, “in both mice and in humans, NRG-1 levels go down with age.”

“The strong correlation between this protective brain factor and maximum life span highlights a new focus for aging research, further supporting earlier findings that it is not the amount of oxidative damage an organism encounters that determines species life span but rather that the protective mechanisms may be more important,” said senior author Rochelle Buffenstein, Ph.D.

The research is described in a recent issue of Aging Cell.

Source: The University of Texas Health Science Center at San Antonio

The focus of the study was “excess brain activity” commonly associated with conditions that cause mild cognitive decline and memory loss, and are linked to an increased risk of Alzheimer’s, according to lead author Michela Gallagher, Ph.D., a professor of psychological and brain sciences in the Johns Hopkins University’s Krieger School of Arts and Sciences.

Previously, it had been thought that this hyperactivity in the hippocampus was the brain’s attempt to compensate for a weakness in forming new memories, she said. Instead, the researchers found that this excess activity contributes to conditions such as amnestic mild cognitive impairment (aMCI), in which patients’ memories are worse than would be expected in healthy people the same age.

“In the case of aMCI, it has been suggested that the increased hippocampal activation may serve a beneficial function by recruiting additional neural ‘resources’ to compensate for those that are lost,” she said. “However, animal studies have raised the alternative view that this excess activation may be contributing to memory impairment.”

To test how a reduction in that hippocampal activity would affect patients with aMCI, Gallagher’s team administered a low dose of a drug used to treat epilepsy. The goal was to reduce the test subjects’ activity to levels that were similar to those of healthy subjects in a control group.

The researchers used functional magnetic resonance imaging to determine the levels of excess activity, and how much the drug reduced that activity.

The research team found that the subjects who had been treated with an effective dose of the drug did better on a memory task.

According to Gallagher, the increased hippocampal activity observed in conditions that precede Alzheimer’s may be one of the underlying mechanisms contributing to neurodegeneration and memory loss.

Studies have found that if patients with aMCI are followed for a number of years, those with the greatest excess activation have the greatest decline in memory, and are more likely to receive a diagnosis of Alzheimer’s over the next four to six years, she said.

“Apart from a direct role in memory impairment, there is concern that elevated activity in vulnerable neural networks could be causing additional damage and possibly promoting the widespread disease-related degeneration that underlies cognitive decline and the conversion to Alzheimer’s Disease,” Gallagher said.

“Therefore, reducing the elevated activity in the hippocampus may help to restore memory and protect the brain. It will require a carefully monitored, lengthier clinical trial to determine if that is the case.”

The research was published in the May 10 issue of the journal Neuron.

Source: Johns Hopkins University

More than five million people in the United States suffer from Alzheimer’s disease (AD), at a health care cost (in 2010 dollars) of approximately $172 billion.

“Prevalence and costs of AD and other dementias are projected to rise dramatically during the next 40 years unless a prevention or a cure can be found. Therefore, it is critical to gain a greater understanding of the key risk factors and etiologic underpinnings of dementia from a population-based perspective,” the authors write.

Deborah E. Barnes, Ph.D., M.P.H., of the University of California, San Francisco and colleagues evaluated data from 13,535 long-term Kaiser Permanente members.

The team examined depressive symptoms assessed in midlife and in late life and risks of developing dementia, Alzheimer disease and vascular dementia. Vascular dementia, or VaD, results from brain damage caused by impaired blood flow to the brain.

Depressive symptoms were present in 14.1 percent of study participants in midlife only, 9.2 percent in late life only and 4.2 percent in both.

During six years of followup, 22.5 percent of patients were diagnosed with dementia; 5.5 percent with Alzheimer disease and 2.3 percent with VaD.

When examining AD and VaD separately, patients with late-life depressive symptoms had a two-fold increase in AD risk, and patients with midlife and late-life symptoms had more than a three-fold increase in VaD risk.

“Our findings suggest that chronic depression during the life course may be etiologically associated with an increased risk of dementia, particularly VaD, whereas depression that occurs for the first time in late life is likely to reflect a prodromal stage of dementia, in particular AD,” the authors conclude.

Source: Arch Gen Psychiatry 2012;69[5]:493-498.

The new research looked at the levels of beta-amyloid in the blood as a proxy for beta-amyloid deposits in the brain.

“While it’s not easy to measure the level of beta-amyloid deposits in the brain in this type of study, it is relatively easy to measure the levels of beta-amyloid in the blood, which, to a certain degree, relates to the level in the brain,” said study author Nikolaos Scarmeas, M.D., M.S., with Columbia University Medical Center in New York.

Investigators reviewed the diet for 1,219 people older than age 65 and free of dementia. On average, researchers looked back at dietary records for 1.2 years.

Participant’s blood was tested for the beta-amyloid with specific attention directed at 10 nutrients, including saturated fatty acids, omega-3 and omega-6 polyunsaturated fatty acids, mono-unsaturated fatty acid, vitamin E, vitamin C, beta-carotene, vitamin B12, folate and vitamin D.

Researchers discovered the more omega-3 fatty acids a person consumed, the lower their blood beta-amyloid levels.

Ingesting one gram of omega-3 per day (equal to approximately half a fillet of salmon per week), is associated with 20 to 30 percent lower blood beta-amyloid levels.

Other nutrients were not associated with plasma beta-amyloid levels. The results stayed the same after adjusting for age, education, gender, ethnicity, amount of calories consumed and whether a participant had the APOE gene, a risk factor for Alzheimer’s disease.

Although the findings confirm the benefit of an omega-3 diet for improving blood beta-amyloid levels, the trust test is whether the diet reduces beta-amyloid deposits in the brain.

“Determining through further research whether omega-3 fatty acids or other nutrients relate to spinal fluid or brain beta-amyloid levels or levels of other Alzheimer’s disease related proteins can strengthen our confidence on beneficial effects of parts of our diet in preventing dementia,” said Scarmeas.

The study is published online in the journal Neurology.

Source: American Academy of Neurology

Researchers say that while previous studies have shown that exercising your body and your mind will help your memory, this study is the first to report a synergistic interaction between computer activities and moderate exercise in protecting the brain function in people better than 70 years old.

In the study, researchers followed 926 people in Olmsted County, Minn., ages 70 to 93, who completed self-reported questionnaires on physical exercise, and computer use for the past year.

In the survey, investigators defined moderate physical exercise as brisk walking, hiking, aerobics, strength training, golfing without a golf cart, swimming, doubles tennis, yoga, martial arts, using exercise machines and weightlifting.

Mentally stimulating activities included reading, crafts, computer use, playing games, playing music, group and social and artistic activities and watching less television.

Of those activities the study singled out computer use because of its popularity, said study author Yonas E. Geda, M.D., M.Sc., a physician scientist with Mayo Clinic in Arizona.

“The aging of baby boomers is projected to lead to dramatic increases in the prevalence of dementia,” Geda said. “As frequent computer use has becoming increasingly common among all age groups, it is important to examine how it relates to aging and dementia. Our study further adds to this discussion.”

The study examined exercise, computer use and the relationship to neurological risks such as mild cognitive impairment.

Mild cognitive impairment is memory loss beyond the norm based on age and education, yet not significant enough to influence activities of daily living.

Of the study participants who did not exercise and did not use a computer, 20.1 percent were cognitively normal and 37.6 percent showed signs of mild cognitive impairment.

Of the participants who both exercise and use a computer, 36 percent were cognitively normal and 18.3 percent showed signs of MCI.

Source: Mayo Clinic

Scientists at the University of Cambridge scanned the brains of 120 people who were about the same age and had similar IQs. Half were dependent on cocaine, while the other 60 had no history of substance abuse.

The researchers found that cocaine users lost about 3.08 ml brain volume per year, almost twice the rate of healthy volunteers, who only lost about 1.69 ml per year. The accelerated age-related decline was most prominent in the prefrontal and temporal cortex, important regions of the brain associated with attention, decision-making, and self-regulation, as well as memory.

“As we age, we all lose grey matter,” said Dr. Karen Ersche of the Behavioral and Clinical Neuroscience Institute (BCNI) at the University of Cambridge.

“However, what we have seen is that chronic cocaine users lose grey matter at a significantly faster rate, which could be a sign of premature aging. Our findings provide new insight into why the cognitive deficits typically seen in old age have frequently been observed in middle-aged chronic users of cocaine.”

The findings highlight the need for preventative strategies, she noted.

“Young people taking cocaine today need to be educated about the long-term risk of aging prematurely,” she said.

Source: University of Cambridge

A new report explains that what you do in old age may mean more for maintaining a youthful brain than what you did earlier in life.

Researchers have published their findings in the journal Cell Press.

“Although some memory functions do tend to decline as we get older, several elderly show well preserved functioning and this is related to a well-preserved, youth-like brain,” said Lars Nyberg of Umeå University in Sweden.

Maintaining mental acumen is not associated with the degree of education one has obtained. Experts say that Ph.Ds are as likely as high-school dropouts to experience memory loss with old age. Occupation also has limited relevance as the benefits from a complex or demanding career diminish quickly after retirement.

Researchers say engagement is the secret to success. Individuals who are socially, mentally and physically stimulated show better cognitive performance, with a brain that appears younger than its years.

“There is quite solid evidence that staying physically and mentally active is a way towards brain maintenance,” Nyberg said.

Researchers say a preventive strategy is an important shift in focus for the field. Prior studies have focused on understanding ways in which the brain copes with or compensates for cognitive decline in aging.

The new focus argues for the importance of avoiding those age-related brain changes in the first place. Genes play some role, but life choices and other environmental factors, especially in old age, are critical.

Elderly people generally do have more trouble remembering meetings or names, Nyberg said. But those memory losses often happen later than many often think, after the age of 60. Older people also continue to accumulate knowledge and to use what they know effectively, often to very old ages.

“Taken together, a wide range of findings provides converging evidence for marked heterogeneity in brain aging,” the scientists write.

“Critically, some older adults show little or no brain changes relative to younger adults, along with intact cognitive performance, which supports the notion of brain maintenance. In other words, maintaining a youthful brain, rather than responding to and compensating for changes, may be the key to successful memory aging.”

Source: Cell Press

Dr. Alois Alzheimer’s discovery of the physical changes in the brain in the early 1900s has caused researchers to focus on the plaque deposits he found in autopsied brains of diseased patients.  If the plaque causes the disease, discovering the plaque before a patient’s symptoms worsen could mean closing in on a cure.

Amyvid travels in the bloodstream to the brain, where it binds to amyloid plaques, and enables the plaques to be seen in a PET scan (Positron Emission Tomography). Having the ability to diagnose the disease without waiting for a postmortem would be a significant leap in the treatment and prevention of Alzheimer’s disease.

Diagnosis of Alzheimer’s is made through tests designed to measure cognitive functions. Other than observation of a patient’s behavior, there is no medical method or test available to prove the existence of Alzheimer’s disease. The autopsy of a patient’s brain will confirm the diagnosis, but gives little comfort to the patient’s family.

Making an early diagnosis of a disease which has unknown causes and no treatment is not necessarily cause for celebration.  A patient may show signs of dementia due to a brain tumor, stroke, or other neurovascular disease. Using Amyvid to expose the presence of plaque deposits in the brain can potentially rule out these other diseases and put the blame on Alzheimer’s.

But if plaque deposits are found, it may or may not be due to Alzheimer’s since autopsies of some healthy brains have shown plaque deposits too. When a patient is experiencing memory loss, confusion, impairment of reasoning ability, along with plaque deposits in the brain, the diagnosis is Alzheimer’s.

Treatment Options and Clinical Trials

Patients diagnosed with Alzheimer’s will not benefit from the knowledge that they have a progressive, chronic disease that will eat away at their brain until all memory including their own identity is lost. It is little comfort to provide an early diagnosis without an accompanying treatment plan.

Temporarily managing the symptoms with drugs like Pfizer’s Aricept may be an option, but curing the disease is the ultimate goal. Pharmaceutical companies have been trying to develop a treatment for Alzheimer ’s disease for many years. Experimental drugs have gone into clinical trials, some have failed, and some are still in process.

Pfizer and Eli Lilly currently have drugs in clinical trials that are designed to break up the beta amyloid protein, which is the substance that forms plaque.  Bapineuzumab (Pfizer) and Solanezumab (Lilly) are drugs that bind with the beta amyloid protein, and cause it to break apart with eventual removal by the blood stream. If these drugs survive the clinical trials and gain approval by the FDA, the world will breathe a huge collective sigh of relief in the hope that a cure for Alzheimer’s is real.

Offering solutions for a disease when the cause is not known may seem like a backward approach.  Defining a disease and describing the symptoms is normally followed by the development of tests for accurate diagnosis, and finally a course of treatment or cure. In the case of Alzheimer’s, cures have been developed without knowing the cause and diagnosis has not been possible until after death. Since healthy brains can also contain plaque deposits, the ability to see plaque deposits on a brain via a PET scan is not absolute proof of Alzheimer’s disease.

Perhaps not seeing plaque deposits is a more encouraging result of Amyvid.

Research has been done on the Apolipoprotein E (ApoE) gene found on chromosome 19 to determine the cause of the plaque deposits. This gene causes the production of a lipoprotein that aids in cholesterol transport in the bloodstream. Healthy brains are able to remove the resulting plaque deposits. Of the different types, or alleles of ApoE, ApoE4 has been found to be present in approximately 40 percent of Alzheimer’s patients. Whether this is a coincidence or not remains to be discovered. Further studies on the genetic connection are ongoing.

The fear of developing Alzheimer’s is very real in people who have relatives with the disease, or are nearing age 65 when incidence of Alzheimer’s disease rises. The FDA’s approval of Amyvid for clinical use is encouraging, but without a cure, diagnosis can only bring despair. Confirmation of what has already been experienced in symptoms of memory loss and confusion gives no comfort. Perhaps the most valuable use of Amyvid is in the confirmation of the absence of plaque on PET scans. At least this would confirm the absence of Alzheimer ’s disease.

Source: Drugsdb.com – The Internet Drug Information & Side Effects Database.

In the new study, Joaquin Lugo, Ph.D., discovered that missing potassium channels in the brain caused mice to be unable to navigate using spatial cues. These mice also showed showed diminished learning ability in an experiment dealing with fear conditioning.

The findings may have implications for humans with damage to the hippocampus, a brain structure critical to memory and learning, said Lugo.

“By targeting chemical pathways that alter those potassium channels, we may eventually be able to apply the findings to humans and reverse some of the cognitive deficits in people with epilepsy and other neurological disorders,” Lugo said.

The findings are published online in the journal Learning & Memory.

The channel, called Kv4.2, delivers potassium, which aids neuron function in the brain’s hippocampus. The hippocampus forms memory for long-term storage in the brain. Potassium also helps to regulate excitability of neurons.

Individuals who have epilepsy sometimes exhibit altered or missing Kv.4.2 channels or similar types of channels.

In the study, researchers investigated navigational capabilities using “knockout” mice — those without the channel. These mice were tested in a water maze four feet in diameter and 12 inches deep, with eight trials daily — each lasting about a minute — over four days. Their performance was compared with that of normal mice.

Both groups responded to visual cues — colored symbols — in learning their way around the maze, but the knockout mice did not respond as well as the normal mice in terms of spatial cues — hidden platforms in the water.

“When the mice don’t have this channel, it hurts their ability to learn,” Lugo said.

Source: Baylor University

Flavonoids are compounds found in plants that typically have powerful antioxidant and anti-inflammatory properties. Researchers believe the consumption of flavonoids can reduce the cellular stress and inflammation that causes cognitive decline.

Previous studies of the positive effects of flavonoids, particularly anthocyanidins, have been limited to animal models or very small trials in older persons. Nevertheless, these trials have shown that greater consumption of foods with these compounds improve cognitive function.

The current study is published in the Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society.

Dementia or cognitive decline is expected to be a serious public health issue as the population of Americans 65 years of age and older expands. This population has grown faster than the total U.S. population for the decade 2000-2010 — before the leading edge of the baby boomers generation reached 65 in 2011.

“As the U.S. population ages, understanding the health issues facing this group becomes increasingly important,” said Dr. Elizabeth Devore with Brigham and Women’s Hospital and Harvard Medical School in Boston, Mass. “Our study examined whether greater intake of berries could slow rates of cognitive decline.”

Researchers used data from the Nurses’ Health Study — a group of 121,700 female, registered nurses between the ages of 30 and 55 who completed health and lifestyle questionnaires beginning in 1976.

Since 1980 participants were surveyed every four years regarding their frequency of food consumption. Between 1995 and 2001, cognitive function was measured in 16,010 subjects over the age of 70 years, at 2-year intervals. Women included in the present study had a mean age of 74 and mean body mass index of 26.

Researchers discovered that increased consumption of blueberries and strawberries appear to slow cognitive decline in older women. A greater intake of anthocyanidins and total flavonoids was also associated with reduce cognitive degeneration.

Investigators do provide the caveat that although they controlled for other health factors in the modeling, they cannot rule out the possibility that the preserved cognition in those who eat more berries may be also influenced by other lifestyle choices, such as exercising more.

“We provide the first epidemiologic evidence that berries may slow progression of cognitive decline in elderly women,” noted Devore. “Our findings have significant public health implications as increasing berry intake is a fairly simple dietary modification to test cognition protection in older adults.”

Source: Wiley-Blackwell

Strawberries and blueberries photo by shutterstock.