Unwanted Side Effects May Plague Potential Alzheimer’s Disease Drugs Under Development

June 25, 2013

Researchers in Berlin and Munich, Germany and Oxford, United Kingdom, have revealed that a protein well known for its role in Alzheimer’s disease controls spindle development in muscle and leads to impaired movement in mice when the protein is absent or treated with inhibitors. The results, which are published in The EMBO Journal, suggest that drugs under development to target the beta-secretase-1 protein, which may be potential treatments for Alzheimer’s disease, might produce unwanted side effects related to defective movement.

Alzheimer’s disease is the most common form of dementia found in older adults. The World Health Organization estimates that approximately 18 million people worldwide have Alzheimer’s disease. The number of people affected by the disease may increase to 34 million by 2025. Scientists know that the protein beta-secretase-1 or Bace1, a protease enzyme that breaks down proteins into smaller molecules, is involved in Alzheimer’s disease. Bace1 cleaves the amyloid precursor protein and generates the damaging Abeta peptides that accumulate as plaques in the brain leading to disease. Now scientists have revealed in more detail how Bace1 works.

“Our results show that mice that lack Bace1 proteins or are treated with inhibitors of the enzyme have difficulties in coordination and walking and also show reduced muscle strength,” remarked Carmen Birchmeier, one of the authors of the paper, Professor at the Max-Delbrück-Center for Molecular Medicine in Berlin, Germany, and an EMBO Member. “In addition, we were able to show that the combined activities of Bace1 and another protein, neuregulin-1 or Nrg1, are needed to sustain the muscle spindles in mice and to maintain motor coordination.”

Muscle spindles are sensory organs that are found throughout the muscles of vertebrates. They are able to detect how muscles stretch and convey the perception of body position to the brain. The researchers used genetic analyses, biochemical studies and interference with pharmacological inhibitors to investigate how Bace1 works in mice. “If the signal strength of a specific form of neuregulin-1 known as IgNrg1 is gradually reduced, increasingly severe defects in the formation and maturation of muscle spindles are observed in mice. Furthermore, it appears that Bace1 is required for full IgNrg1 activity. The graded loss of IgNrg1 activity results in the animals having increasing difficulties with movement and coordination,” says Cyril Cheret, the first author of the work.

Drug developers are interested in stopping the Bace1 protein in its tracks because it represents a promising route to treat Alzheimer’s disease. If the protein were inhibited, it would interfere with the generation of the smaller damaging proteins that accumulate in the brain as amyloid plaques and would therefore provide some level of protection from the effects of the disease.

“Our data indicate that one unwanted side effect of the long-term inhibition of Bace1 might be the disruption of muscle spindle formation and impairment of movement. This finding is relevant to scientists looking for ways to develop drugs that target the Bace1 protein and should be considered,” says Birchmeier.

Several Bace1 inhibitors are currently being tested in phase II and phase III clinical trials for the treatment of Alzheimer’s disease.

Bace1 and neuregulin-1 (Nrg1) cooperate to control formation and maintenance of muscle spindles

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Protein That Contributes to Cognitive Decline in Alzheimer’s Identified

June 25, 2013

Researchers at Columbia University Medical Center (CUMC) have demonstrated that a protein called caspase-2 is a key regulator of a signaling pathway that leads to cognitive decline in Alzheimer’s disease. The findings, made in a mouse model of Alzheimer’s, suggest that inhibiting this protein could prevent the neuronal damage and subsequent cognitive decline associated with the disease. The study was published this month in the online journal Nature Communications.

One of the earliest events in Alzheimer’s is disruption of the brain’s synapses (the small gaps across which nerve impulses are passed), which can lead to neuronal death. Although what drives this process has not been clear, studies have indicated that caspace-2 might be involved, according to senior author Michael Shelanski, MD, PhD, the Delafield Professor of Pathology & Cell Biology, chair of the Department of Pathology & Cell Biology, and co-director of the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at CUMC.

Several years ago, in tissue culture studies of mouse neurons, Dr. Shelanski found that caspace-2 plays a critical role in the death of neurons in the presence of amyloid beta, the protein that accumulates in the neurons of people with Alzheimer’s. Other researchers have shown that caspase-2 also contributes to the maintenance of normal synaptic functions.

Dr. Shelanski and his team hypothesized that aberrant activation of caspase-2 may cause synaptic changes in Alzheimer’s disease. To test this hypothesis, the researchers crossed J20 transgenic mice (a common mouse model of Alzheimer’s) with caspase-2 null mice (mice that lack caspase-2). They compared the animals’ ability to negotiate a radial-arm water maze, a standard test of cognitive ability, with that of regular J20 mice and of normal mice at 4, 9, and 14 months of age.

The results for the three groups of mice were similar at the first two intervals. At 14 months, however, the J20/caspase-2 null mice did significantly better in the water maze test than the J20 mice and similarly to the normal mice. “We showed that removing caspase-2 from J20 mice prevented memory impairment — without significant changes in the level of soluble amyloid beta,” said co-lead author Roger Lefort, PhD, associate research scientist at CUMC.

Analysis of the neurons showed that the J20/caspase-2 null mice had a higher density of dendritic spines than the J20 mice. The more spines a neuron has, the more impulses it can transmit.

“The J20/caspase-2 null mice showed the same dendritic spine density and morphology as the normal mice — as opposed to the deficits in the J20 mice,” said co-lead author Julio Pozueta, PhD. “This strongly suggests that caspase-2 is a critical regulator in the memory decline associated with beta-amyloid in Alzheimer’s disease.”

The researchers further validated the results in studies of rat neurons in tissue culture.

Finally, the researchers found that caspase-2 interacts with RhoA, a critical regulator of the morphology (form and structure) of dendritic spines. “It appears that in normal neurons, caspase-2 and RhoA form an inactive complex outside the dendritic spines,” said Dr. Lefort. “When the complex is exposed to amyloid beta, it breaks apart, activating the two components.” Once activated, caspase-2 and RhoA enter the dendritic spines and contribute to their demise, possibly by interacting with a third molecule, the enzyme ROCK-II.

“This raises the possibility that if you can inhibit one or all of these molecules, especially early in the course of Alzheimer’s, you might be able to protect neurons and slow down the cognitive effects of the disease,” said Dr. Lefort.

The paper is titled, “Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice.” The other contributors are Julio Pozueta, PhD (co-lead author), Elena M. Ribe, Carol M. Troy, and Ottavio Arancio, all based at CUMC at the time of the study.

Dr. Pozueta was an associate research scientist at CUMC at the time of this research and is currently a senior analyst at Prescient Life Sciences. The remaining authors declare no financial or other conflicts of interests.

The study was supported by grants from the National Institutes of Health (NIHAG08702 and NS15076), the Wallace Foundation for Research, and the Taub Foundation.

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Rapid, Irregular Heartbeat May Be Linked to Problems With Memory and Thinking

June 25, 2013

People who develop a type of irregular heartbeat common in old age called atrial fibrillation may also be more likely to develop problems with memory and thinking, according to new research published in the June 5, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Problems with memory and thinking are common for people as they get older. Our study shows that on average, problems with memory and thinking may start earlier or get worse more quickly in people who have atrial fibrillation,” said study author Evan L. Thacker, PhD, of the University of Alabama at Birmingham. “This means that heart health is an important factor related to brain health.”

The study involved people age 65 and older from four communities in the United States who were enrolled in the Cardiovascular Health Study. Participants did not have a history of atrial fibrillation or stroke at the start of the study. They were followed for an average of seven years, and received a 100-point memory and thinking test every year. People who had a stroke were not included in this analysis after the stroke. Of the 5,150 participants, 552, or about 11 percent, developed atrial fibrillation during the study.

The study found that people with atrial fibrillation were more likely to experience lower memory and thinking scores at earlier ages than people with no history of atrial fibrillation. For example, from age 80 to age 85 the average score on the 100-point test went down by about 6 points for people without atrial fibrillation, but it went down by about 10 points for people with atrial fibrillation.

For participants ages 75 and older, the average rate of decline was about three to four points faster per five years of aging with atrial fibrillation compared to those without the condition.

“This suggests that on average, people with atrial fibrillation may be more likely to develop cognitive impairment or dementia at earlier ages than people with no history of atrial fibrillation,” Thacker said.

Thacker noted that scores below 78 points on the 100-point test are suggestive of dementia. People without atrial fibrillation in the study were predicted on average to score below 78 points at age 87, while people with atrial fibrillation were predicted to score below 78 points at age 85, two years earlier.

“If there is indeed a link between atrial fibrillation and memory and thinking decline, the next steps are to learn why that decline happens and how we can prevent that decline,” said Thacker.

The study was supported by the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke and the National Institute on Aging.

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2013 Alzheimer’s Disease Plan Update and Lewy Body Dementia (LBD)

June 24, 2013

U.S. Department of Health and Human Services today released the National Plan to Address Alzheimer’s Disease: 2013 Update, a follow-up to the initial plan released in May 2012. The update reflects progress made towards goals set a year ago, as well as new and revised action steps. While the title specifically refers to Alzheimer’s disease, both the legislation requiring the plan and the plan itself are inclusive of related dementias, including LBD, frontotemporal, mixed and vascular dementia.

The plan, ordered under the 2011 National Alzheimer’s Project Act, includes: finding ways to prevent and effectively treat Alzheimer’s disease by 2025; enhancing care for Alzheimer’s patients; expanding support for people with dementia and their families; improving public awareness; and carefully tracking data to support these efforts. The Plan was developed collaboratively by experts in aging and Alzheimer’s disease from federal, state, private and non-profit organizations.

The Lewy Body Dementia Association (LBDA) applauds the progress being made on the National Alzheimer’s Plan. The 2013 plan highlights ongoing or planned activities of governmental agencies and collaborating organizations to address the enormity of the problem caused by dementia. Highlights of some of the past year’s accomplishments include the following:

  • creation of a comprehensive web-based portal of Alzheimer’s research portfolios in the United States and abroad;
  • strengthening of the direct care workforce’s ability to provide high quality person-centered care, by distributing training videos to every nursing home in the country;
  • delivering programs to educate aging and legal professionals about dementia and public resources available;
  • launching public awareness initiatives about Alzheimer’s disease and an educational website for the general public on Alzheimer’s disease;
  • identifying and disseminating best practices for caregiver assessment and referral through the long-term services and supports system;

A significant step forward for Lewy body dementias (LBD) came in the form of a scientific conference in March of 2013, to solicit input on special research priorities and timelines for addressing dementias related to Alzheimer’s disease. LBDA advocates were on hand to provide their experiences with LBD, as well as input on recommendations for research.

The 2013 plan also includes new strategies, such as creating a timeline to prevent and effectively treat Alzheimer’s by 2025, developing a unified curriculum for primary care physicians on Alzheimer’s disease, identify and review measures on high quality dementia care, convening an expert panel on advanced dementia, and efforts to understand and reduce avoidable hospitalizations in dementia.

“While this plan makes significant inroads in strategy, collaboration and coordination of federal resources,” says Angela Taylor, Director of Programs LBDA, “without a staunch commitment of funding from Congress, dementia will remain the most expensive malady in the country, costing families and society $157 billion to $215 billion a year in the United States alone. Congress must set its sights on dementia now, much like it did with HIV/AIDS 20 years ago.”

To read the National Plan to Address Alzheimer’s Disease: 2013 Update, visit http://aspe.hhs.gov/daltcp/napa/NatlPlan2013.shtml

The Lewy Body Dementia Association

the Lewy Body Dementia Association (LBDA) is a 501(c)(3) nonprofit organization dedicated to raising awareness of the Lewy body dementias (LBD), supporting patients, their families and caregivers, and promoting scientific advances. Through outreach, education and research, LBDA supports those affected by Lewy body dementias. To learn more about LBD and LBDA please visit www.lbda.org.

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How Pets Help Dementia Patients

June 24, 2013

Therapy dogs and other animals can stimulate social interaction and ease agitation in dementia patients. But it takes specially trained pets to bring the full benefit of animal therapy into elder care settings. Talk to animal therapy practitioners and researchers and you will hear stories about therapy dogs and dementia patients that bring tears to your eyes.

You may hear of Diva, a German shepherd, who sought out an elderly, non-communicative man sitting alone and let him wind his fingers in her fur and hug her. Then there is the resident golden retriever-lab mix in an Alzheimer’s care unit who found his favorite patient agitated in a hallway — and gently took him by the sleeve to lead him back to his room. Or you’ll hear about Leonardo, a cat who curls up on the bed next to end-stage Alzheimer’s patients in hospice units.

But behind every successful animal-assisted therapy visit, there is also a lot of planning, training, and work to be done so that animal therapy is safe for people living in elder care settings.

The Benefits of Animal Therapy

“Even people with Alzheimer’s recognize a dog and they see that the dog is someone new in their environment. I think they see it as someone with whom they can interact without any worry,” explains Mara M. Baun, DNSc, a coordinator of the PhD in nursing program at the University of Texas Health Sciences Center at the Houston School of Nursing in Houston.

Baun has been researching the benefits of therapy animals for over a decade. In one of her studies, she and her team compared degrees of social interaction of adults in an Alzheimer’s unit with and without the presence of a dog.

“When they had the pet with them, they had more interactive behaviors, although some of them were aimed at the dog, not at the person,” she says. Her work has shown this effect is consistent whether the dog and dementia patients interact one-on-one or in a group setting.

In addition to stimulating a social response, dementia patients may benefit from the presence of therapy animals because of:

  • Reduced agitation. Agitation behaviors, common among dementia patients, are reduced in the presence of a dog.
  • Physical activity. Depending on a patient’s mobility, they may be able to groom the animal, toss a ball, or even go for a short walk.
  • Improved eating. Dementia patients have been shown to eat more following a dog’s visit.
  • Pleasure. Some patients simply enjoy the presence of the dog and its human companion, as well as the tricks therapy dogs can do.

Making Animal Therapy Work in Elder Care Settings

If the idea of animal therapy is appealing, it’s worth knowing that there is a lot of work that goes into matching the right animal and human handler team with the right patients. Here are some of the issues involved:

  • Temperament. An animal’s personality will dictate whether they can be a good therapy animal. You want an animal that is not easily startled and is comfortable interacting with unpredictable strangers in a calm manner. Dogs are the easiest to train for these types of situations, says Cheri Weston Swenson, MSN, a therapy animal handler and an evaluator for Delta Society Pet Partners Teams in Minneapolis-St Paul, Minn. Still, she knows teams that work with Delta Society-registered guinea pigs, rabbits, horses, and even chickens.
  • Individual strengths. Each animal has their own strengths. Swenson says her cat, Leonardo, does best when he is interacting one-on-one — but her dog, Victor, is fine in group situations. Some animals are better suited to children than dementia patients.
  • Training. Swenson trains her dogs to be comfortable with hospital equipment, tubing, wheelchairs, and the crowded situations they might encounter in an Alzheimer’s unit. Therapy animals should also be able to sit, stay, do tricks on command, introduce themselves nicely (such as putting their head gently on a knee), and pass over tantalizing smells. At the same time, human companions must cultivate their ability to be good advocates for their pets in difficult situations.
  • Registration or certification. “I am almost never asked about our qualifications and that bothers me,” says Swenson. “We want to uphold a high standard for therapy animals and their handlers.” She recommends seeking out therapy animals and human companions who are registered with the Delta Society, Pet Therapy International, or Therapy Dogs International. Delta Society, for which she is an evaluator, retests both humans and pets every two years — a good thing, says Swenson, who has observed that even the most committed teams can become lax during that time.
  • Cleanliness. Swenson bathes her indoor animals at least once a month and spends about 30 minutes grooming them before a visit — this includes cleaning their ears and mouth, clipping their nails, washing their feet, and brushing them thoroughly.
  • Infection control. Infectious agents such as MRSA, C. difficile, E. coli, and Salmonella are a concern in elderly care settings, affecting both dementia patients and the therapy dog teams that visit them. In addition to properly cleaning the therapy animals before and after a visit, infection control measures include:
    • Cleaning the hands of everyone who will touch the animal before and after contact.
    • Preventing animals that eat a raw foods diet from being therapy animals.
    • Avoiding contact with the animal’s mouths.
    • Using sheets and barriers, such as rolled towels, to keep some distance between the animals and the dementia patients’ bedding or furniture. Fresh sheets and towels must be used in each room.
  • Giving treats. Swenson says feeding is a universal bonding behavior, and many of the people her animals visit want to give a treat. She carries small hand-held shovels into which they can place a treat (which she provides) for the animal to retrieve — but then the therapy dogs are required to do some kind of trick in exchange. Other animal and pet teams do not allow treats, however.
  • Flexibility. With dementia patients, visits can be unpredictable, says Swenson. She has seen her dog surprised to find that a patient he knows well may, on occasion, push him away. Both human and animal have to be able to adjust to changing situations.

Baun adds that some facilities try to have a resident animal. This can work, she says, but the animal must have off-time — just like every other worker — as well as a place of its own to rest and a clear understanding at the staff-level about who is responsible for the animal’s well-being. The best situations occur when a staff member brings a suitable animal in with him during the day and then they go home together at night.

Properly trained and prepared therapy animals can be a real blessing to dementia patients in elder care settings — it’s a great option to look into for your loved one. Start with the national organizations recommended by Swenson to learn about local options.

Find more information in the Everyday Health Alzheimer’s Disease Center.

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‘Forrest Gump’ Mice Show Too Much of a Good Thing, Can Be Bad for Memory

June 24, 2013

A line of genetically modified mice that Western University scientists call “Forrest Gump” because, like the movie character, they can run far but they aren’t smart, is furthering the understanding of a key neurotransmitter called acetylcholine (ACh).

Marco Prado, PhD, and his team at Robarts Research Institute say the mice show what happens when too much of this neurotransmitter becomes available in the brain. Boosting ACh is a therapeutic target for Alzheimer’s disease because it’s found in reduced amounts when there’s cognitive failure.

Prado’s research is published in the Journal of Neuroscience.

“We wanted to know what happens if you have more of the gene which controls how much acetylcholine is secreted by neurons,”

says Prado, a Robarts scientist and professor in the Departments of Physiology and Pharmacology and Anatomy and Cell Biology at Western’s Schulich School of Medicine & Dentistry.

“The response was the complete opposite of what we expected. It’s not a good thing. Acetylcholine release was increased threefold in these mice, which seemed to disturb cognitive function. But put them on a treadmill and they can run twice as far as normal mice before tiring. They’re super-athletes.”

In addition to its function in modulating cognitive abilities, ACh drives muscle contraction which allowed for the marked improvement in motor endurance.

One of the tests the scientists, including first author Benjamin Kolisnyk, used is called the touch screen test for mice (video is available showing the test) which uses technology similar to a tablet.

After initiating the test, the mice have to scan five different spots on the touch screen to see a light flash, and then run and touch that area. If they get it right they get a reward.

Compared to the control mice, the “Forrest Gump” mice failed miserably at the task. The researchers found the mice, which have the scientific name ChAT-ChR2-EYFP, had terrible attention spans, as well as dysfunction in working memory and spatial memory.

Prado interprets the research as showing ACh is very important for differentiating cues. So if your brain is presented with a lot of simultaneous information, it helps to pick what’s important. But when you flood the brain with ACh, your brain loses the ability to discern what’s relevant. This study was funded mainly by the Canadian Institutes of Health Research.

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Association Between Hypoglycemia, Dementia in Older Adults with Diabetes

June 24, 2013

A study of older adults with diabetes mellitus (DM) suggests a bidirectional association between hypoglycemic (low blood glucose) events and dementia, according to a report published Online First by JAMA Internal Medicine, a JAMA Network publication.

There is a growing body of evidence that DM may increase the risk for developing cognitive impairment, including Alzheimer disease and vascular dementia, and there is research interest in whether DM treatment can prevent cognitive decline. When blood glucose declines to low levels, cognitive function is impaired and severe hypoglycemia may cause neuronal damage. Previous research on the potential association between hypoglycemia and cognitive impairment has produced conflicting results, the authors write in the study background.

Kristine Yaffe, M.D., of the University of California, San Francisco, and colleagues studied 783 older adults with DM (average age 74 years). During a 12-year follow-up, 61 patients (7.8 percent) had a reported hypoglycemic event and 148 (18.9 percent) developed dementia.

“Hypoglycemia commonly occurs in patients with diabetes mellitus (DM) and may negatively influence cognitive performance. Cognitive impairment in turn can compromise DM management and lead to hypoglycemia,” according to the study.

Patients who experienced a hypoglycemic event had a two-fold increased risk for developing dementia compared with those who did not have a hypoglycemic event (34.4 percent vs. 17.6 percent). Older adults with DM who developed dementia had a greater risk for having a subsequent hypoglycemic event compared with patients who did not develop dementia (14.2 percent vs. 6.3 percent), according to the study results.

“Among older adults with DM who were without evidence of cognitive impairment at study baseline, we found that clinically significant hypoglycemia was associated with a two-fold increased risk for developing dementia … Similarly, participants with dementia were more likely to experience a severe hypoglycemic event,” the authors conclude.

“The association remained even after adjustment for age, sex, educational level, race/ethnicity, comorbidities and other covariates. These results provide evidence for a reciprocal association between hypoglycemia and dementia among older adults with DM.”

Commentary: Glucose Control in Older Adults with Diabetes – More Harm Than Good?

In an invited commentary, Kasia J. Lipska, M.D., M.H.S. of the Yale University School of Medicine, New Haven, Conn., and Victor M. Montori, M.D., of the Mayo Clinic, Rochester, Minn., write: “Hypoglycemia is a major adverse consequence of glucose-lowering therapy in patients with type 2 diabetes mellitus (DM). … Older patients are at higher risk of hypoglycemia. Aging-related changes in renal function and drug clearance may contribute to this vulnerability.”

“Efforts to mitigate the risk of hypoglycemia are clearly warranted to improve quality of life and potentially prevent the associated adverse events,” they continue.

“Hypoglycemia in the course of type 2 DM treatment is both common and associated with poor outcomes. Therefore, decisions about the intensity and type of antihyperglycemic therapy must take into account the harms of hypoglycemia. Involving patients in these treatment decisions may favorably shift the current glucose-centric paradigm to a more holistic patient-centered one,” they conclude.

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Too Much Saturated Fat Tied to Alzheimer’s Risk?

June 23, 2013

Researchers say a small, new study shows that fat cut the body’s level of a chemical that keeps Alzheimer’s at bay

A diet high in saturated fat can quickly rob the brain of a key chemical that helps protect against Alzheimer’s disease, according to new research.

In a small study published online Monday in the journal JAMA Neurology, researchers found that dietary saturated fat cut the body’s levels of the chemical apolipoprotein E, also called ApoE, which helps “chaperone” amyloid beta proteins out of the brain.

“People who received a high-saturated-fat, high-sugar diet showed a change in their ApoE, such that the ApoE would be less able to help clear the amyloid,” said research team member Suzanne Craft, a professor of medicine at Wake Forest School of Medicine.

Amyloid beta proteins left loose in the brain are more likely to form plaques that interfere with neuron function, the kind of plaques found in the brains of people with Alzheimer’s disease.

Diet also directly affected the amount of loose amyloid beta found in cerebrospinal fluid, Craft said. Those on a high-saturated-fat diet had higher levels of amyloid beta in their spinal fluid, while people on a low-saturated-fat diet actually saw a decline in such levels, she said.

“An amyloid that is not cleared — or attached to ApoE to get cleared — has a greater likelihood of becoming this toxic form,” Craft said.

The clinical trial, led by Dr. Angela Hanson of the Veterans Affairs Puget Sound Health Care System in Seattle, involved 20 seniors with normal cognition and 27 with mild thinking impairment, a precursor to Alzheimer’s disease.

The patients, all in their late 60s, were randomly assigned to diets that contained the same amount of calories but were either high or low in saturated fat. The high-saturated-fat diets had 45 percent of total energy coming from fat, and more than a quarter of the total fat came from saturated fats. The low-saturated-fat diets had 25 percent of energy coming from fat, with saturated fat contributing less than 7 percent to total fat.

After just a month, the diets caused changes in the amounts of amyloid beta and ApoE in the study participants’ cerebrospinal fluid, researchers said.

“Diet can really change levels of these toxic proteins and of these mediators that help clear these amyloids,” Craft said. “Diets that are very high in bad cholesterol seem to interfere with ApoE’s ability to clear amyloid.”

One gerontology expert, who wrote an editorial accompanying the study in the journal, didn’t think the link was quite that clear.

Although the study shows that diet can affect brain chemistry, it does not definitely tie diet to a person’s risk for Alzheimer’s disease, said Dr. Deborah Blacker, director of the Gerontology Research Unit at Massachusetts General Hospital in Boston.

“Is it plausible to say this could affect the risk of having Alzheimer’s pathology in your brain? It’s not showing that,” said Blacker, who also is with the Harvard School of Public Health. “It’s showing that some of the chemicals related to Alzheimer’s pathology can shift in response to dietary factors.”

The study does, however, offer important insight into the value of good nutrition, she said.

“The important lesson from the study is that dietary intervention can change brain amyloid chemistry in largely consistent and apparently meaningful ways, in a short period of time,” Blacker wrote in the editorial. “Does this change clinical practice for those advising patients who want to avoid dementia? Probably not, but it adds another small piece to the growing evidence that taking good care of your heart is probably good for your brain too.”

People focus on diet in terms of weight and heart health, but they overlook that nutrition can be key to cognitive function as well, Craft said.

“Diet is a very underappreciated factor in terms of brain function,” she said. “It’s quite well accepted for your heart and your cholesterol and your blood, but diet is critical for a healthy brain aging. Many of the things the brain needs to function properly — fatty acids, certain amino acids — come only from food.”

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