Calcium Supplements Linked to Dementia Risk in Women with Certain Health Conditions

(American Academy of Neurology) According to a new study, calcium supplements may be associated with an increased risk of dementia in older women who have had a stroke or other signs of cerebrovascular disease. The research is published in the August 17, 2016, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Cerebrovascular disease is a group of disorders that affect blood flow in the brain. These diseases, including stroke, are the fifth leading cause of death in the United States and increase the risk of developing dementia.

“Osteoporosis is a common problem in the elderly. Because calcium deficiency contributes to osteoporosis, daily calcium intake of 1000 to 1200 mg is recommended. Getting this recommended amount through diet alone can be difficult, so calcium supplements are widely used,”

said study author Silke Kern, MD, PhD with the University of Gothenburg in Sweden.

“Recently, however, the use of supplements and their effect on health has been questioned.”

The study involved 700 dementia-free women between the ages of 70 and 92 who were followed for five years. Participants took a variety of tests at the beginning and end of the study, including tests of memory and thinking skills. A CT brain scan was performed in 447 participants at the start of the study.

Scientists also looked at the use of calcium supplements in the participants and whether they were diagnosed with dementia over the course of the study. A total of 98 women were taking calcium supplements at the start of the study and 54 women had already experienced a stroke. During the study, 54 more women had strokes, and 59 women developed dementia. Among the women who had CT scans, 71 percent had lesions on their brains’ white matter, which is a marker for cerebrovascular disease.

The study found that the women who were treated with calcium supplements were twice as likely to develop dementia than women who did not take supplements. But when the researchers further analyzed the data, they found that the increased risk was only among women with cerebrovascular disease.

Women with a history of stroke who took supplements had a nearly seven times increased risk of developing dementia than women with a history of stroke who did not take calcium supplements.

Women with white matter lesions who took supplements were three times as likely to develop dementia as women who had white matter lesions and did not take supplements.

Women without a history of stroke or women without white matter lesions had no increased risk when taking calcium supplements.

Overall, 14 out of 98 women who took supplements developed dementia, or 14 percent, compared to 45 out of 602 women who did not take supplements, or 8 percent. A total of six out of 15 women with a history of stroke who took supplements developed dementia, compared to 12 out of 93 women with a history of stroke who did not take supplements. Among the women with no history of stroke, 18 out of 83 who took supplements developed dementia, compared to 33 out of the 509 who did not take supplements.

“It is important to note that our study is observational, so we cannot assume that calcium supplements cause dementia,”

said Kern.

The author also noted that the study was small and results cannot be generalized to the overall population, and additional studies are needed to confirm the findings.

Kern noted that calcium from food affects the body differently than calcium from supplements and appears to be safe or even protective against vascular problems.

The study was supported by grants from the American Alzheimer’s Association, Swedish Research Council, Swedish Research Council for Health, Working Life and Welfare. To learn more about dementia and stroke, please visit

The American Academy of Neurology, an association of 30,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, concussion, Parkinson’s disease and epilepsy.

For more information about the American Academy of Neurology, visit or find us on Facebook, Twitter, Google+ and YouTube.


©2016 American Academy of Neurology – All Rights Reserved.


Diet and Exercise Can Reduce Protein Build-Ups Linked to Alzheimer’s

(UCLA) A study by researchers at UCLA’s Semel Institute for Neuroscience and Human Behavior has found that a healthy diet, regular physical activity and a normal body mass index  can reduce the incidence of protein build-ups that are associated with the onset of Alzheimer’s disease.

In the study, 44 adults ranging in age from 40 to 85 (mean age: 62.6) with mild memory changes but no dementia underwent an experimental type of PET scan to measure the level of plaque and tangles in the brain. Researchers also collected information on participants’ body mass index, levels of physical activity, diet and other lifestyle factors. Plaque, deposits of a toxic protein called beta-amyloid in the spaces between nerve cells in the brain; and tangles, knotted threads of the tau protein found within brain cells, are considered the key indicators of Alzheimer’s.

The study found that each one of several lifestyle factors — a healthy body mass index, physical activity and a Mediterranean diet — were linked to lower levels of plaques and tangles on the brain scans. (The Mediterranean diet is rich in fruits, vegetables, legumes, cereals and fish and low in meat and dairy, and characterized by a high ratio of monounsaturated to saturated fats, and mild to moderate alcohol consumption.)

“The fact that we could detect this influence of lifestyle at a molecular level before the beginning of serious memory problems surprised us,” said Dr. David Merrill, the lead author of the study, which appears in the September issue of the American Journal of Geriatric Psychiatry.

Earlier studies have linked a healthy lifestyle to delays in the onset of Alzheimer’s. However, the new study is the first to demonstrate how lifestyle factors directly influence abnormal proteins in people with subtle memory loss who have not yet been diagnosed with dementia, Merrill said. Healthy lifestyle factors also have been shown to be related to reduced shrinking of the brain and lower rates of atrophy in people with Alzheimer’s.

Older age is the No. 1 non-modifiable risk factor for Alzheimer’s disease, which affects an estimated 5.2 million people in the United States and results in more than $200 billion in health care costs annually.

“The study reinforces the importance of living a healthy life to prevent Alzheimer’s, even before the development of clinically significant dementia,” Merrill said.

“This work lends key insight not only into the ability of patients to prevent Alzheimer’s disease, but also physicians’ ability to detect and image these changes.”

The next step in the research will be to combine imaging with intervention studies of diet, exercise and other modifiable lifestyle factors, such as stress and cognitive health, Merrill said.

Merrill sees patients with cognitive problems, particularly memory loss, at the UCLA Psychiatry Cognitive Health Clinic and Research Program.


The research was funded by National Institutes of Health (MH077650, AT003480, P01-AG024831, AG13308, P50 AG 16570, MH/AG58156, AG10123 and M01-RR00865), the Department of Energy (DE-FC03-87-ER60615), the Larry L. Hillblom Foundation, the Fran and Ray Stark Foundation Fund for Alzheimer’s Disease Research, the Ahmanson Foundation, the Lovelace Foundation, the National Science Foundation, UCLA’s Claude D. Pepper Older Americans Independence Center funded by the National Institute on Aging (5P30AG028748), the American Federation of Aging Research, the John A. Hartford Foundation and the Centers of Excellence National Program, and the NIH/National Center for Advancing Translational Sciences UCLA CTSI (UL1TR000124).

By Kathy Sviti

© 2016 UCLA All Rights Reserved.


“Knockout” Head Injuries Linked to Parkinson’s, but Not Alzheimer’s

(Scientific America) Massive new study turns up surprises on the long-term fallout of unconsciousness-causing brain injuries that occur early in life.

There has long been debate about a link between serious blows to the head and the development of neurodegenerative diseases later in life. Research has made cases for and against a relationship between traumatic brain injuries and neurological ailments such as Alzheimer’s, Parkinson’s and general dementia. Now the question is drawing ever more scrutiny as the alarming extent of these injuries becomes better known—and new research is finally casting some light on this murky and often quietly terrifying topic.

A large-scale analysis of three separate studies published this week in JAMA Neurology found no association between unconsciousness-causing traumatic brain injuries (TBI) and Alzheimer’s disease or general dementia—but it did find a strong association between TBI and Parkinson’s disease.

“I can’t decide if the positive or negative findings are more surprising,” says one of the study’s investigators, physician and Alzheimer’s researcher Paul Crane at the University of Washington.

The positive association his team found between Parkinson’s and TBI was not entirely novel, but Crane says the magnitude of the link was unexpected. The researchers found the risk of Parkinson’s rose threefold for people whose head injuries had caused them to go unconscious for more than an hour.

The more contentious finding is the lack of an association between TBI and Alzheimer’s. Prior research has been divided on whether there is a link, but many of the previous studies have been smaller in scale and conducted less-comprehensive analyses.

“Although early studies suggested a clear link between TBI and an increased risk for Alzheimer’s disease, this has not been replicated,” explains Frances Corrigan at the University of Adelaide, who studies how TBI influences neurodegeneration.

The intrinsically challenging nature of such research—and the large number of subjects needed to establish a significant result—add to the difficulty of confirming a link, says Corrigan, who was not involved in Crane’s study.

The fact that this study only looked at late-onset Alzheimer’s, which is far more common than early-onset, may have contributed to the lack of an association with TBI, Crane says. Prior studies, which did not exclude people with early-onset Alzheimer’s, may have found a link only with that form of the disease, and the sheer size of the new analysis may lend that link more credence.

“If there were a signal there across the three studies we really should have seen it,” Crane says, “and we didn’t.”

In addition to its scale, this study has another unusual advantage: It used autopsy data. Most of the prior research on the link between TBI and Alzheimer’s used clinical criteria to confirm that subjects had suffered from Alzheimer’s. But the observable signs and symptoms in still-living patients are usually not specific enough to rule out similar problems such as general dementia. Autopsy evidence is clearer because researchers can physically look for brain changes that are known to result from Alzheimer’s and not from other neurodegenerative disorders.

Autopsy data is obviously a lot harder to come by, however. Most people do not get brain autopsies when they die, so a researcher has to enroll subjects in a study while they are alive—so that on their death their brains will be donated. Crane says this difficult approach enabled him and colleagues to gather a great deal of valuable information.

The analysis looked at 7,130 people across three separate studies beginning in 1994 and followed them over the ensuing decades to look for cognitive changes and development of neurodegenerative diseases. Not all participants gave consent for their brains to be donated for autopsies but where that data was available the study authors combed the clinical information for the pathological signs of neurodegeneration. More than 1,500 people in the study did donate their brains and had undergone autopsies at the time the research was analyzed, and the scientists are continuing to collect data as the participants age.

The study did not examine multiple brain injuries like the ones many athletes and soldiers experience, so it does not claim to have concrete findings related to chronic traumatic encephalopathy (CTE), a neurodegenerative disorder that people exposed to repeated head injuries can develop. The new findings only speak to what Crane calls the “garden variety” pattern of head injury—referring to the more common situation of having just one TBI incident—which may have very different implications.

Not looking at CTE raises questions about biased findings. CTE has only been recognized as a distinct disease in the last decade, so it has been fairly easy to attribute CTE-related cognitive problems as a more general form of age-related dementia, explains neuropathologist William Stewart at the University of Glasgow, who was not involved in Crane’s research. Unless you specifically look for and recognize the physical changes during autopsy, he says, you could be missing the signs.

“This is why it took so long to identify CTE in TBI survivors other than boxers,” he says. “And here we are now in 2016 realizing that CTE is associated with exposure to TBI, no matter whether boxers or footballers, a single moderate or severe injury, or a repetitive mild one.”

This is perhaps the largest study to-date that uses autopsy data to analyze the long-term outcomes of TBI, and Crane says the findings have shown him that prevention is becoming more important than ever—it is the only surefire way to prevent the neurodegenerative effects.

“We found most of our exposure for long durations was under age 25,” he says. With a 40-year lag time between the exposure and the onset of these diseases, he says we have to practice prevention now.

“My hashtag is ‘all brains matter’.”


By Sara Chodosh

© 2016 Scientific American, a Division of Nature America, Inc.


New Research Hints at Pattern of Alzheimer’s Spread in the Brain

(The Guardian) Protein variations could provide explanation as to why some brain tissues are vulnerable and help predict an individual’s risk of developing the disease.

Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain.

Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not.

Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease.

brain vulnerabilities

The ‘vulnerability map”’, produced by looking at the levels of certain proteins in the brains of healthy individuals, is consistent with the map of how Alzheimer’s progresses.
Illustration: Freer et al. Sci. Adv. 2016

The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins – variations that are present decades before the onset of the disease.

“Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study.

The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease.

Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study.

“It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult.

But others are less convinced by the results.

“This might be part of the explanation as to why Alzheimer’s disease kills some cells and not others, but it is undoubtedly a complex problem and this is only part of the answer to that problem,” said John Hardy, professor of neuroscience at University College London.

“This paper has only looked at a few brain regions and really only at a few cell [types],” he added.

“So it points towards the idea that there is an intrinsic reason for selectivity but it does not really prove it.”

Published in the journal Science Advances by scientists from the University of Cambridge, the research involved the analysis of data relating to more than 500 brain tissues from six healthy individuals, aged between 24 and 57 years of age.

The team looked at the levels of a family of molecules known as mRNA, that are encoded by genes and which are required to produce proteins. From this analysis, the researchers found that they were able to predict the levels of proteins across the brain, allowing them to map the levels of proteins associated with Alzheimer’s disease.

The scientists found that regions of the brain with higher levels of proteins prone to clumping in plaques and tangles corresponded to regions that generally show early evidence of Alzheimer’s disease.

The team also found a link between the susceptibility of regions to Alzheimer’s disease and levels of a group of proteins that are known to affect the clumping of those that form plaques and tangles.

The scientists found that the “vulnerability map”, produced by looking at the levels of these proteins in the brains of healthy individuals, is consistent with the map of how Alzheimer’s progresses.

That, the researchers say, suggests that the vulnerability of particular tissues to Alzheimer’s disease could, in part, be down to a combination of higher levels of plaque and tangle-forming proteins and problematic levels of proteins that affect their clumping.

The scientists say the findings could lead to new ways to predict an individual’s risk of developing Alzheimer’s disease.

“Although we all have these patterns, in some people the patterns are more extreme, and in some others are less. Those in which the imbalance is greater, are more at risk,” said Michele Vendruscolo, co-author of the research, although he stresses that research to back up the suggestion has yet to be carried out.

Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK, said:

“These findings suggest that our susceptibility to Alzheimer’s may not only be dictated by abnormal changes in the brain, but by how our brains are hardwired to react to those changes.”

“Understanding the molecular mechanisms that underpin susceptibility to diseases like Alzheimer’s has the potential to open the door to new treatment and prevention approaches,” he added.

“Building a complete picture of the biology driving a complex disease like Alzheimer’s gives scientists the best chance of developing effective treatments against it.”



© 2016 Guardian News and Media Limited or its affiliated companies. All rights reserved.


Eat Mediterranean: Your Brain Will Reap the Benefit

(Frontiers) Eating a Mediterranean diet can slow down cognitive decline.

The Mediterranean diet can improve your mind, as well your heart, shows a study published in the open-access journal Frontiers in Nutrition.

Following a Mediterranean diet was shown to be associated with slower rates of cognitive decline, reduced conversion to Alzheimer’s, and improvements in cognitive function.

The main foods in the Mediterranean diet (MedDiet) include plant foods, such as leafy greens, fresh fruit and vegetables, cereals, beans, seeds, nuts, and legumes. The MedDiet is also low in dairy, has minimal red meat, and uses olive oil as its major source of fat.

Leading author Roy Hardman from the Centre for Human Psychopharmacology Swinburne University of Technology Melbourne Australia and his colleagues evaluated all the available papers between 2000-2015 that investigated if and how a MedDiet may impact cognitive processes over time. In total, 18 out of the 135 articles met their strict inclusion criteria.

“The most surprising result was that the positive effects were found in countries around the whole world. So regardless of being located outside of what is considered the Mediterranean region, the positive cognitive effects of a higher adherence to a MedDiet were similar in all evaluated papers;” he said.

Attention, memory, and language improved. Memory, in particular, was positively affected by the MedDiet including improvements in: delayed recognition, long-term, and working memory, executive function, and visual constructs.

“Why is a higher adherence to the MedDiet related to slowing down the rate of cognitive decline? The MedDiet offers the opportunity to change some of the modifiable risk factors,” he explained.

“These include reducing inflammatory responses, increasing micronutrients, improving vitamin and mineral imbalances, changing lipid profiles by using olive oils as the main source of dietary fats, maintaining weight and potentially reducing obesity, improving polyphenols in the blood, improving cellular energy metabolism and maybe changing the gut micro-biota, although this has not been examined to a larger extent yet.”

Moreover, the benefits to cognition afforded by the MedDiet were not exclusive to older individuals. Two of the included studies focused on younger adults and they both found improvements in cognition using computerized assessments.

The researchers stress that research in this area is important due to the expected extensive population aging over the next 20-30 years. They envision that the utilization of a dietary pattern, such as the MedDiet, will be an essential tool to maintain quality of life and reduce the potential social and economic burdens of manifested cognitive declines like dementia.

“I would therefore recommend people to try to adhere or switch to a MedDiet, even at an older age,” Hardman added.

Like many researchers, Hardman takes his research home:

“I follow the diet patterns and do not eat any red meats, chicken or pork. I have fish two-three times per week and adhere to a Mediterranean style of eating.”


Copyright © 2016 by the American Association for the Advancement of Science (AAAS)


Anti-Inflammatory Drug Shows Promise for Alzheimer’s Disease Treatment

(United Press International) The NSAID mefenamic acid, used to help control menstrual pain, may also have an effect on reversing memory problems linked to Alzheimer’s disease, researchers report in a recent study.

A common anti-inflammatory drug reversed memory problems similar to Alzheimer’s disease in mice, suggesting inflammation makes the disease worse and that treating inflammation may lessen its effects.

The non-steroidal anti-inflammatory drug mefenamic acid, marketed as Ponstel, helped fix memory problems in mice, according to researchers at the University of Manchester, though researchers say trials in humans are necessary.

Previous studies have shown brain inflammation contributes to the intensification of Alzheimer’s disease, which researchers say makes it an obvious target for treatment.

Ponstel is a prescription NSAID used to control mild-to-severe pain, specifically pain and blood loss during menstruation. The drug targets an inflammatory pathway called NLRP3 inflammasome, which can damage brain cells — which is why the researchers tested it in mice with Alzheimer’s-like symptoms.

“Until now, no drug has been available to target this pathway, so we are very excited by this result,” Dr. David Brough, a researchers at the University of Manchester, said in a press release.

“However, much more work needs to be done until we can say with certainty that it will tackle the disease in humans as mouse models don’t always faithfully replicate the human disease.”

For the study, published in the journal Nature Communications, researchers treated two groups of 10 mice with Alzheimer’s disease symptoms, giving one mefenamic acid through a miniature pump implanted under their skin for one month and the other a placebo delivered the same way.

Memory loss in mice treated with the drug had Alzheimer’s symptoms reverse, seeing memory return to levels seen in mice without the disease.

While the drug showed potential, and already is used for treatment in humans, the researchers say further research will be needed to identify potential side effects in patients taking it for Alzheimer’s, as well as establish whether it is effective.

“Because this drug is already available and the toxicity and pharmacokinetics of the drug is known, the time for it to reach patients should, in theory, be shorter than if we were developing completely new drugs,” Brough said.

“We are now preparing applications to perform early phase II trials to determine a proof-of-concept that the molecules have an effect on neuroinflammation in humans.”


By Stephen Feller

Copyright © 2016 United Press International, Inc. All Rights Reserved.


App Helps Dementia Patients Find Memories

(Cornell University) People suffering from Alzheimer’s and other forms of age-related dementia sometimes have trouble recognizing friends and family or knowing what to talk about when they visit. A new app created by a group of Cornell students offers to help patients stay connected to their memories — and thus to their friends and family — and perhaps will even help them keep a conversation going.

Remember Me! is a smartphone app developed by engineering master’s degree graduates Karthik Venkataramaiah, Vishal Kumkar, Shivananda Pujeri and Mihir Shah. They demonstrated their work at the 123rd Annual Conference of the American Society for Engineering Education St. Lawrence Conference held at Cornell April 8-9.

“We found that each one of us at some point of time had interacted with people who suffer memory loss,” Venkataramaiah said. “We thought we should build something that would help bring back memories.”

The app is installed on the phones of the patient and friends, family and caregivers. Using GPS tracking and a connection to the cloud, the app can flash an alert to the patient when one of the group members is nearby. The phone tells the patient who is approaching and his or her relationship to that person, and it displays a slideshow of previously uploaded pictures. If the patient receives a text or phone call from someone registered in the app, a screen pops up with similar information.

“In anyone with a memory loss the first thing you do is to show them pictures and see if they are able to get back the memories,” Venkataramaiah explained.

Once a conversation begins, the app can assist with reminders based on stored facts and previous conversations, perhaps suggesting questions to ask based on information it has about life events.

The app was developed, Venkataramaiah said, after about a month of consultation with people who have friends or relatives with dementia. Some of those people tried out early versions and came back with suggestions for additional features.

The developers plan to apply natural-language processing techniques on the patient’s speech patterns to predict what the patient might say next.

Also planned is a feature that would remind the patient of important life events with a “Call this person” suggestion.

Caregivers can send reminders to take medicine, make phone calls or complete particular tasks, and they can use the GPS feature to locate the patient.

Remember Me! is currently an Android app, with an iOS version in development. The team is planning to spin their work off as a startup and is exploring funding options. A commercial launch is being considered for August.

Venkataramaiah is now a software development engineer at Microsoft. Kumkar and Pujeri work at Oracle; Shivananda and Shah are at Amazon.


By Bill Steel

©2016 Cornell Chronical


Lower BMI, Weight Loss in Later Life Linked with Alzheimer’s

(Massachusetts General Hospital) BWH/MGH study associates lower body mass index with greater deposits of Alzheimer’s-associated amyloid plaques in the brains of older individuals

Researchers at Brigham and Women’s Hospital (BWH) and Massachusetts General Hospital (MGH) have found an association between lower weight and more extensive deposits of the Alzheimer’s-associated protein beta-amyloid in the brains of cognitively normal older individuals. The association — reported in the Journal of Alzheimer’s Disease — was seen in particular among individuals carrying the APOE4 gene variant, which is known to increase the risk of Alzheimer’s.

“Elevated cortical amyloid is believed to be the first stage of the preclinical form of Alzheimer’s disease, so our findings suggest that individuals who are underweight late in life may be at greater risk for this disease,” says Gad Marshall, MD, of the MGH and BWH Departments of Neurology, senior author of the report.

“Finding this association with a strong marker of Alzheimer’s disease risk reinforces the idea that being underweight as you get older may not be a good thing when it comes to your brain health.”

While the concept of a preclinical version of Alzheimer’s disease is theoretical and not yet being used to guide clinical diagnosis or treatment, the current hypothesis involves three stages. Individuals at stage 1 are cognitively normal but have elevated amyloid deposits; stage 2 adds evidence of neurodegeneration, such as elevated tau deposits or characteristic loss of certain brain tissues, with no cognitive symptoms; and stage 3 adds cognitive changes that, while still in a normal range, indicate a decline for that individual. The current study is part of the MGH-based Harvard Aging Brain Study (HABS), designed to identify markers that predict who is likely to develop Alzheimer’s disease and how soon symptoms are likely to develop.

This investigation explored the relationship between body mass index (BMI) and beta amyloid levels in the brains of the first 280 participants to enroll in HABS, who were ages 62 to 90, cognitively normal and in good general health. Participants’ initial enrollment data included medical histories; physical exams; testing for the presence of APOE4, the major genetic risk factor for late-onset Alzheimer’s; and PET imaging with Pittsburgh compound B (PiB), which can visualize amyloid plaques in the brain.

After adjusting for factors including age, sex, education and APOE4 status, researchers found that having a lower BMI was associated with greater retention of PiB, indicating more extensive amyloid deposits in the brain. The association was most pronounced in normal-weight participants, who were the group with the lowest BMI in the study. Analysis focused on APOE status revealed that the association between lower BMI and greater PiB retention was particularly significant for individuals with the APOE4 gene variant, which is associated with increased Alzheimer’s disease risk.

Researchers hope that future studies will explain the mechanism behind the association between lower BMI and increased amyloid levels.

“A likely explanation for the association is that low BMI is an indicator for frailty – a syndrome involving reduced weight, slower movement and loss of strength that is known to be associated with Alzheimer’s risk,” says Marshall, who is an assistant professor of Neurology at Harvard Medical School.

“One way to get closer to determining any cause and effect relationship will be following these individuals over time to see whether their baseline BMI does predict the development of symptoms, which we are doing in HABS, and eventually investigating whether maintaining or even increasing BMI in late life has an effect on outcomes. Right now, we’re also studying whether BMI is associated with any other clinical and imaging markers of Alzheimer’s disease.”


David C. Hsu, MD, formerly with the MGH Department of Psychiatry and the BWH Department of Neurology and now at Mercy Medical Group in Sacramento, Calif., is lead author of the Journal of Alzheimer’s Disease paper. This study was supported by the Harvard Aging Brain Study (NIH/NIA P01 AG036694, R01 AG037497, and R01 AG046396), K23 AG033634, K24 AG035007, and the Massachusetts Alzheimer’s Disease Research Center (P50AG005134).


Copyright © 2016 by the American Association for the Advancement of Science (AAAS)