Archives for April 2016

New Cases of Dementia in UK Fall by 20% Over Two Decades

(University of Cambridge) The UK has seen a 20% fall in the incidence of dementia over the past two decades, according to new research from England, led by the University of Cambridge, leading to an estimated 40,000 fewer cases of dementia than previously predicted. However, the study, published in Nature Communications, suggests that the dramatic change has been observed mainly in men.

Reports in both the media and from governments have suggested that the world is facing a dementia ‘tsunami’ of ever-increasing numbers, particularly as populations age. However, several recent studies have begun to suggest that the picture is far more complex.

Although changing diagnostic methods and criteria are identifying more people as having dementia, societal measures which improve health such as education, early- and mid-life health promotion including smoking reduction and attention to diet and exercise may be driving a reduction in risk in some countries.

Prevalence (the proportion of people with dementia) has been reported to have dropped in some European countries but it is incidence (the proportion of people developing dementia in a given time period) that provides by far the most robust evidence of fundamental change in populations.

As part of the Medical Research Council Cognitive Function and Ageing Study (CFAS), researchers at the University of Cambridge, Newcastle University, Nottingham University and the University of East Anglia interviewed a baseline of 7,500 people in three regions of the UK (Cambridgeshire, Newcastle and Nottingham) between 1991 and 1994 with repeat interviews at two years to estimate incidence.

Then 20 years later a new sample of over 7,500 people from the same localities aged 65 and over was interviewed with a two year repeat interview again. This is the first time that a direct comparison of incidence across time in multiple areas, using identical methodological approaches, has been conducted in the world.

The researchers found that dementia incidence across the two decades has dropped by 20% and that this fall is driven by a reduction in incidence among men at all ages. These findings suggest that in the UK there are just under 210,000 new cases per year: 74,000 men and 135,000 women – this is compared to an anticipated 250,000 new cases based on previous levels. Incidence rates are higher in more deprived areas.

Even in the presence of an ageing population, this means that the number of people estimated to develop dementia in any year has remained relatively stable, providing evidence that dementia in whole populations can change. It is not clear why rates among men have declined faster than those among women, though it is possible that it is related to the drop in smoking and vascular health improving in men.

Professor Carol Brayne, Director of the Cambridge Institute of Public Health, University of Cambridge, says:

“Our findings suggest that brain health is improving significantly in the UK across generations, particularly among men, but that deprivation is still putting people at a disadvantage.

The UK in earlier eras has seen major societal investments into improving population health and this appears to be helping protect older people from dementia. It is vital that policies take potential long term benefits into account.”

Professor Fiona Matthews from the Institute of Health and Society, Newcastle University and the MRC Biostatistics Unit, Cambridge adds:

“Public health measures aimed at reducing people’s risk of developing dementia are vital and potentially more cost effective in the long run than relying on early detection and treating dementia once it is present.

Our findings support a public health approach for long term dementia prevention, although clearly this does not reduce the need for alternative approaches for at-risk groups and for those who develop dementia.”

The researchers argue that while influential reports continue to promote future scenarios of huge increases of people with dementia across the globe, their study shows that global attention and investment in reducing the risk of dementia can help prevent such increases.

“While we’ve seen investment in Europe and many other countries, the lack of progress in access to education, malnutrition in childhood and persistent inequalities within and across other countries means that dementia will continue to have a major impact globally,” says Professor Brayne.

“Our evidence shows that the so-called dementia ‘tsunami’ is not an inevitability: we can help turn the tide if we take action now.”

Dr Rob Buckle, director of science programmes at the Medical Research Council, which funded the study, added:

“It is promising news that dementia rates, especially amongst men, have dropped by such a significant amount over the last twenty years, and testament to the benefits of an increased awareness of a brain-healthy lifestyle.

However, the burden of dementia will continue to have significant societal impact given the growing proportion of elderly people within the UK population and it is therefore as important as ever that we continue to search for new ways of preventing and treating the disease.

This study does, however, reinforce the importance of long-term, quality studies that create a wealth of data of invaluable resource for researchers.”

Citation

http://www.cam.ac.uk/research/news/new-cases-of-dementia-in-the-uk-fall-by-20-over-two-decades

Reference

target=”_blank”>A two decade comparison of incidence of dementia in individuals aged 65 years and older from three geographical areas of England: results of the Cognitive Function Ageing Study I and II. Nature Communications; 19 April 2016; DOI 10.1038/ncomms11398

© 2016 University of Cambridge

 

10 Real-Life Strategies for Dementia Caregiving

(Family Caregiver Alliance) As caregivers, we often use intuition to help us decide what to do. No one ever gave us lessons on how to relate to someone with memory loss. Unfortunately, dealing with Alzheimer’s disease and other dementias is counter-intuitive; i.e., often the right thing to do is exactly opposite that which seems like the right thing to do. Here is some practical advice:

  1. Being Reasonable, Rational and Logical Will Just Get You into Trouble. When someone is acting in ways that don’t make sense, we tend to carefully explain the situation, calling on his or her sense of appropriateness to get compliance. However, the person with dementia doesn’t have a “boss” in his brain any longer, so he does not respond to our arguments, no matter how logical. Straightforward, simple sentences about what is going to happen are usually the best.
  2. People With Dementia Do Not Need to Be Grounded in Reality. When someone has memory loss, he often forgets important things, e.g., that his mother is deceased. When we remind him of this loss, we remind him about the pain of that loss also. When someone wants to go home, reassuring him that he is at home often leads to an argument.  Redirecting and asking someone to tell you about the person he has asked about or about his home is a better way to calm a person with dementia.
  3. You Cannot Be a Perfect Caregiver. Just as there is no such thing as a perfect parent, there is no such thing as a perfect caregiver. You have the right to the full range of human emotions, and sometimes you are going to be impatient or frustrated. Learning to forgive your loved one as well as yourself is essential in the caregiving journey.
  4. Therapeutic Lying Reduces Stress. We tend to be meticulously honest with people. However, when someone has dementia, honesty can lead to distress both for us and the one we are caring for. Does it really matter that your loved one thinks she is the volunteer at the day care center? Is it okay to tell your loved one that the two of you are going out to lunch and then “coincidentally” stop by the doctor’s office on the way home to pick something up as a way to get her to the doctor?
  5. Making Agreements Doesn’t Work. If you ask your loved one to not do something ever again, or to remember to do something, it will soon be forgotten. For people in early stage dementia, leaving notes as reminders can sometimes help, but as the disease progresses, this will not work. Taking action, rearranging the environment, rather than talking and discussing, is usually a more successful approach. For example, getting a teakettle with an automatic “off” switch is better than warning someone of the dangers of leaving the stove on.
  6. Doctors Often Need to Be Educated By You. Telling the doctor what you see at home is important. The doctor can’t tell during an examination that your loved one has been up all night pacing. Sometimes doctors, too, need to deal with therapeutic lying; e.g., telling the patient that an antidepressant is for memory rather than depression.
  7. You Can’t Do It All.  It’s OK to Accept Help Before You Get Desperate. When people offer to help, the answer should always be “YES.” Have a list of things people can do to help you, whether it is bringing a meal, picking up a prescription, helping trim the roses or staying with your loved one while you run an errand. This will reinforce offers of help. It is harder to ask for help than to accept it when it is offered, so don’t wait until you “really need it” to get support.
  8. It Is Easy to Both Overestimate and Underestimate What Your Loved One Can Do. It is often easier to do something for our loved ones than to let them do it for themselves. However, if we do it for them, they will lose the ability to be independent in that skill. On the other hand, if we insist individuals do something for themselves and they get frustrated, we just make our loved one’s agitated and probably haven’t increased their abilities to perform tasks. Not only is it a constant juggle to find the balance, but be aware that the balance may shift from day to day.
  9. Tell, Don’t Ask. Asking “What would you like for dinner?” may have been a perfectly normal question at another time. But now we are asking our loved one to come up with an answer when he or she might not have the words for what they want, might not be hungry, and even if they answer, might not want the food when it is served after all. Saying “We are going to eat now” encourages the person to eat and doesn’t put them in the dilemma of having failed to respond.
  10. It Is Perfectly Normal to Question the Diagnosis When Someone Has Moments of Lucidity. One of the hardest things to do is to remember that we are responding to a disease, not the person who once was.  Everyone with dementia has times when they make perfect sense and can respond appropriately. We often feel like that person has been faking it or that we have been exaggerating the problem when these moments occur. We are not imagining things—they are just having one of those moments, to be treasured when they occur.

Read more on this subject here:  Caregiver’s Guide to Understanding Dementia Behaviors

Citation

https://www.caregiver.org/ten-real-life-strategies-dementia-caregiving

Copyright © 2016 Family Caregiver Alliance.

All rights reserved.

Problems Finding Your Way Around May Be Earliest Sign of Alzheimer’s Disease

(Washington University in St. Louis) Long before Alzheimer’s disease can be diagnosed clinically, increasing difficulties building cognitive maps of new surroundings may herald the eventual clinical onset of the disorder, finds new research from Washington University in St. Louis.

“These findings suggest that navigational tasks designed to assess a cognitive mapping strategy could represent a powerful new tool for detecting the very earliest Alzheimer’s disease-related changes in cognition,” said senior author Denise Head, associate professor of psychological and brain sciences in Arts & Sciences.

“The spatial navigation task used in this study to assess cognitive map skills was more sensitive at detecting preclinical Alzheimer’s disease than the standard psychometric task of episodic memory,” she said.

Preclinical Alzheimer’s disease denotes the presence of Alzheimer-related changes in the brain that occur prior to the development of symptoms that lead to the diagnosis.

The cognitive findings from this study, published in the April issue of the Journal of Alzheimer’s Disease, are consistent with where in the brain the ill effects of Alzheimer’s disease first surface, as well as with the progression of the disease to other brain regions.

Previous research has shown that navigation problems crop up early in individuals with Alzheimer’s disease. These deficits may be associated with the build up of amyloid plaques and tau tangles and other signs of deterioration and shrinkage in the brain’s prefrontal cortex, hippocampus and caudate.

The hippocampus, which is associated with long-term memory storage, the recognition of new surroundings and the creation of cognitive maps, is well-established as an early target for Alzheimer’s-related damage. Similar damage also turns up in the caudate, which is associated with learning as well as voluntary movement.

“Our observations suggest a progression such that preclinical Alzheimer’s disease is characterized by hippocampal atrophy and associated cognitive mapping difficulties, particularly during the learning phase,” said first author Samantha Allison, a psychology doctoral student at Washington University.

“As the disease progresses, cognitive mapping deficits worsen, the caudate becomes involved, and route learning deficits emerge.”

Making a Mental Map

While these deficits are well documented in patients with early stage Alzheimer’s disease, they have not been well studied in seemingly normal patients who may be progressing toward identifiable early stages of the disease, a status known as preclinical Alzheimer’s disease.

In this study, researchers used a virtual maze navigation experiment to examine whether specific problems with route learning and cognitive map building, which involve the caudate and the hippocampus, respectively, could be detected in preclinical Alzheimer’s. The experiment’s design plays on the fact that humans generally find their way in life using two distinct forms of spatial representation and navigation.

With egocentric navigation, people rely on past knowledge to follow well-worn routes, moving sequentially from one landmark to another until they reach their target destination. In allocentric navigation, people become familiar with their big picture surroundings and create a mental map of existing landmarks, allowing them to plot best available routes and find shortcuts to new destinations.

Participants in this study were separated into three groups based on a test of brain and spinal fluids that can detect biomarkers shown to predict the future development of Alzheimer’s-related plaques and tangles in the brain. People who are clinically normal with these markers are considered to have preclinical Alzheimer’s disease.

This study included 42 clinically normal individuals who lacked the cerebrospinal fluid markers for Alzheimer’s, 13 clinically normal individuals who were positive for these markers and thus had preclinical Alzheimer’s, and 16 individuals with documented behavioral symptoms of early stage Alzheimer’s.

All 71 study participants spent about two hours on a desktop computer being tested on their ability to navigate a virtual maze consisting of a series of interconnected hallways with four wallpaper patterns and 20 landmarks. Participants were tested on two navigation skills: how well they could learn and follow a pre-set route, and how well they could form and use a cognitive map of the environment. Participants were given 20 minutes to either learn a specified route, or to study and explore the maze with a navigation joystick. They were then tested on their ability to recreate the route or find their way to specific landmarks in the environment.

“People with cerebrospinal markers for preclinical Alzheimer’s disease demonstrated significant difficulties only when they had to form a cognitive map of the environment — an allocentric, place-learning navigation process associated with hippocampal function,” Head said.

“This same preclinical Alzheimer’s disease group showed little or no impairment on route learning tasks — an egocentric navigation process more closely associated with caudate function.”

When compared with cognitively normal study participants who lacked the cerebrospinal fluid markers of Alzheimer’s, those with preclinical Alzheimer’s disease scored lower on their ability to learn the locations of objects in the environment in relation to each other during the initial study phase.

While these results suggest deficits in the ability to form a cognitive map, preclinical Alzheimer’s disease participants eventually managed to overcome these map-learning deficits, performing almost as well as cognitively normal participants during a subsequent wayfinding navigation task.

“These findings suggest that the wayfinding difficulties experienced by people with preclinical Alzheimer’s disease are in part related to trouble acquiring the environmental information,” Head said.

“While they may require additional training to learn new environments, the good news here is that they seem to retain sufficient information to use a cognitive map almost as well as their cognitively normal counterparts.”

A More Sensitive Diagnostic?

Head cautions that the current study has several limitations, including a relatively small sample size and a lack of direct information about brain regions and networks that have a role in spatial navigation and wayfinding.

However, Allison notes, “We are currently investigating how brain regions impacted early during the course of the disease are related to cognitive mapping deficits in a larger sample of individuals with preclinical Alzheimer’s disease.”

Within the context of these limitations, the current investigation demonstrates significant preclinical Alzheimer’s disease-related deficits in aspects of cognitive mapping with relative preservation in route learning. In contrast, people experiencing memory lapses and other behavioral problems associated with early stage Alzheimer’s disease had clear difficulties both in learning an established route and in finding their own way to new landmarks.

“This pattern is consistent with decrements in hippocampal integrity prior to changes in the caudate,” Head said.

“These findings suggest that navigational tasks designed to assess a cognitive mapping strategy could represent a powerful tool for detecting the very earliest Alzheimer’s disease-related changes in cognition.”

Participants in the study came from an ongoing study at Washington University’s Charles F. and Joanne Knight Alzheimer’s Disease Research Center. Scientists have been following participants with and without a family history of the disease, with the aim of identifying Alzheimer’s disease biomarkers most closely associated with the development of full-blown disease years later.

The research team notes that the presence of cerebrospinal fluid markers for preclinical Alzheimer’s does not guarantee that a person will go on to develop full blown Alzheimer’s. “Future research should examine whether cognitive mapping deficits in individuals in preclinical Alzheimer’s are associated with an increased risk of developing symptomatic Alzheimer’s,” they said.

Citation

https://source.wustl.edu/2016/04/ problems-finding-way-around-may-earliest-sign-alzheimers-disease-study-suggests/

Other study co-authors, both from Washington University School of Medicine, include Anne M. Fagan, professor of neurology, and John C. Morris, MD, director of the Charles F. and Joanne Knight Alzheimer’s Disease Research Center and the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology.

This work was supported by NIH grants P50 AG05861, P01 AG03991, and P01 AG026276. Samantha Allison was supported by National Institute on Aging 5T32AG00030.

©2016 Washington University in St. Louis

 

Fructose Alters Hundreds of Brain Genes, Which Can Lead to a Wide Range of Diseases

(UCLA) A range of diseases — from diabetes to cardiovascular disease, and from Alzheimer’s disease to attention deficit hyperactivity disorder — are linked to changes to genes in the brain. A new study by UCLA life scientists has found that hundreds of those genes can be damaged by fructose, a sugar that’s common in the Western diet, in a way that could lead to those diseases.

However, the researchers discovered good news as well: An omega-3 fatty acid known as docosahexaenoic acid, or DHA, seems to reverse the harmful changes produced by fructose.

“DHA changes not just one or two genes; it seems to push the entire gene pattern back to normal, which is remarkable,” said Xia Yang, a senior author of the study and a UCLA assistant professor of integrative biology and physiology.

“And we can see why it has such a powerful effect.”

DHA occurs naturally in the membranes of our brain cells, but not in a large enough quantity to help fight diseases.

“The brain and the body are deficient in the machinery to make DHA; it has to come through our diet,” said Fernando Gomez-Pinilla, a UCLA professor of neurosurgery and of integrative biology and physiology, and co-senior author of the paper.

DHA strengthens synapses in the brain and enhances learning and memory. It is abundant in wild salmon (but not in farmed salmon) and, to a lesser extent, in other fish and fish oil, as well as walnuts, flaxseed, and fruits and vegetables, said Gomez-Pinilla, who also is a member of UCLA’s Brain Injury Research Center.

Americans get most of their fructose in foods that are sweetened with high-fructose corn syrup, an inexpensive liquid sweetener made from corn starch, and from sweetened drinks, syrups, honey and desserts. The Department of Agriculture estimates that Americans consumed an average of about 27 pounds of high-fructose corn syrup in 2014. Fructose is also found is in most baby food and in fruit, although the fiber in fruit substantially slows the body’s absorption of the sugar — and fruit contains other healthy components that protect the brain and body, Yang said.

To test the effects of fructose and DHA, the researchers trained rats to escape from a maze, and then randomly divided the animals into three groups. For the next six weeks, one group of rats drank water with an amount of fructose that would be roughly equivalent to a person drinking a liter of soda per day. The second group was given fructose water and a diet rich in DHA. The third received water without fructose and no DHA.

After the six weeks, the rats were put through the maze again. The animals that had been given only the fructose navigated the maze about half as fast than the rats that drank only water — indicating that the fructose diet had impaired their memory. The rats that had been given fructose and DHA, however, showed very similar results to those that only drank water — which strongly suggests that the DHA eliminated fructose’s harmful effects.

Other tests on the rats revealed more major differences: The rats receiving a high-fructose diet had much higher blood glucose, triglycerides and insulin levels than the other two groups. Those results are significant because in humans, elevated glucose, triglycerides and insulin are linked to obesity, diabetes and many other diseases.

The research team sequenced more than 20,000 genes in the rats’ brains, and identified more than 700 genes in the hypothalamus (the brain’s major metabolic control center) and more than 200 genes in the hippocampus (which helps regulate learning and memory) that were altered by the fructose.

The altered genes they identified, the vast majority of which are comparable to genes in humans, are among those that interact to regulate metabolism, cell communication and inflammation. Among the conditions that can be caused by alterations to those genes are Parkinson’s disease, depression, bipolar disorder, and other brain diseases, said Yang, who also is a member of UCLA’s Institute for Quantitative and Computational Biosciences.

Of the 900 genes they identified, the researchers found that two in particular, called Bgn and Fmod, appear to be among the first genes in the brain that are affected by fructose. Once those genes are altered, they can set off a cascade effect that eventually alters hundreds of others, Yang said.

That could mean that Bgn and Fmod would be potential targets for new drugs to treat diseases that are caused by altered genes in the brain, she added.

The research also uncovered new details about the mechanism fructose uses to disrupt genes. The scientists found that fructose removes or adds a biochemical group to cytosine, one of the four nucleotides that make up DNA. (The others are adenine, thymine and guanine.) This type of modification plays a critical role in turning genes “on” or “off.”

The research is published online in EBioMedicine, a journal published jointly by Cell and The Lancet. It is the first genomics study of all the genes, pathways and gene networks affected by fructose consumption in the regions of the brain that control metabolism and brain function.

Previous research led by Gomez-Pinilla found that fructose damages communication between brain cells and increases toxic molecules in the brain; and that a long-term high-fructose diet diminishes the brain’s ability to learn and remember information.

“Food is like a pharmaceutical compound that affects the brain,” said Gomez-Pinilla.

He recommends avoiding sugary soft drinks, cutting down on desserts and generally consuming less sugar and saturated fat.

Although DHA appears to be quite beneficial, Yang said it is not a magic bullet for curing diseases. Additional research will be needed to determine the extent of its ability to reverse damage to human genes.

The paper’s lead author is Qingying Meng, a postdoctoral scholar in Yang’s laboratory. Other co-authors are Zhe Ying, a staff research associate in Gomez-Pinilla’s laboratory, and colleagues from UCLA, the National Institutes of Health and Icahn School of Medicine at Mount Sinai in New York.

Yang’s research is supported by the National Institutes of Health (grant R01DK104363), as is Gomez-Pinilla’s (R01DK104363 and R01NS050465).

Citation

http://newsroom.ucla.edu/releases/fructose-alters-hundreds-of-brain-genes-which-can-lead-to-a-wide-range-of-diseases

© 2016 UCLA All Rights Reserved.

 

What is The Key to Healthy Aging? New Gene Study Sheds Light

(MedicalNewsToday) A new study may bring us closer to unlocking the secret to healthy aging, after uncovering an array of genetic variants among healthy, elderly individuals that may protect against Alzheimer’s and heart disease.

The findings come from the ongoing “Wellderly” study, in which researchers have so far applied whole genome sequencing to the DNA of more than 1,400 healthy individuals from the US aged 80-105 years.

Launched in 2007, the study aims to pinpoint certain genetic variants that may contribute to lifelong health.

“This study is exciting because it is the first large one using genetic sequencing to focus on health,” says Michael Snyder, PhD, chairman of the Department of Genetics at Stanford University in California, who was not involved with the research.

“Most of the world’s scientists are studying disease, but what we really want to understand is what keeps us healthy. That is what the Wellderly study is all about.”

Lower Genetic Risks for Alzheimer’s, Heart Disease for the Wellderly

To reach the new findings – published in the journal Cell – co-senior study author Dr. Eric Topol, director of the Scripps Translational Science Institute (STSI) in La Jolla, CA, and colleagues used the Complete Genomics sequencing platform to analyze the genomes of 600 Wellderly participants.

All subjects were free of cancer, stroke, Alzheimer’s disease, Parkinson’s disease, diabetes, heart attack and any other chronic disease or illness.

Their genomes were compared with those of 1,507 adults who represented the general population and who were part of a study conducted by the Inova Translational Medicine Institute (ITMI) in Falls Church, VA.

After controlling for blood relatedness and ethnic differences among the participants, the researchers were left with 511 individuals from the Wellderly study and 686 people from the ITMI cohort for whom they conducted downstream DNA analyses.

All in all, the researchers analyzed 24,205,551 specific gene variants across both groups.

Compared with the ITMI cohort, participants from the Wellderly study had lower genetic risks for Alzheimer’s disease and coronary artery disease – the most common form of heart disease.

However, the team identified no difference in genetic risks for cancer, stroke or type 2 diabetes between the two groups, suggesting that participants of the Wellderly study possess other genetic characteristics or protective behaviors that prevent them from developing these diseases.

“We didn’t find a silver bullet for healthy longevity,” notes study co-author Ali Torkamani, PhD, director of genome informatics at STSI.

“Instead, we found weaker signals among common as well as rare variant sites, which collectively suggest that protection against cognitive decline contributes to healthy aging.”

COL25A1 Gene Variant Discovery May Lead to New Alzheimer’s Treatments

Interestingly, the researchers identified a number of very rare variants in the COL25A1 gene of 10 individuals who were part of the Wellderly study. Such variants were not found in the ITMI cohort.

The team explains that COL25A1 encodes for a key component of amyloid plaques, which are clumps of beta-amyloid protein that are found in the brains of people with Alzheimer’s.

“Those gene variants might offer a pathway for the development of new treatments for Alzheimer’s,” notes Torkamani.

The Wellderly study is set to continue and, based on the findings to date, the researchers are confident that the study will offer much-needed insight into the genetics behind healthy aging.

Commenting on the research, Eric Schadt, PhD, director of the Icahn Institute for Genomics and Multiscale Biology at Mount Sinai in New York, NY, says:

“For many decades, we have searched for the genetic causes of disease in sick individuals. The Wellderly study presents an attractive alternative by studying those who are well in order to uncover the solutions nature has provided to protect us against disease.

The initial discoveries around protective factors for Alzheimer’s disease and coronary artery disease demonstrate the keys the Wellderly may hold in unlocking ways in which we all may live healthier lives.”

Citation

http://www.medicalnewstoday.com/articles/309346.php

Written by Honor Whiteman

MediLexicon International Ltd, Bexhill-on-Sea, UK
© 2004-2016 All rights reserved.

 

Physical Activity, Diet, and Risk of Alzheimer Disease

JAMA. 2009 Aug 12;302(6):627-37. doi: 10.1001/jama.2009.1144.

Physical activity, diet, and risk of Alzheimer disease.

Scarmeas N1, Luchsinger JA, Schupf N, Brickman AM, Cosentino S, Tang MX, Stern Y.

Abstract

Context

Both higher adherence to a Mediterranean-type diet and more physical activity have been independently associated with lower Alzheimer disease (AD) risk but their combined association has not been investigated.

Objective

To investigate the combined association of diet and physical activity with AD risk.

Design, Setting, and Patients

Prospective cohort study of 2 cohorts comprising 1880 community-dwelling elders without dementia living in New York, New York, with both diet and physical activity information available. Standardized neurological and neuropsychological measures were administered approximately every 1.5 years from 1992 through 2006. Adherence to a Mediterranean-type diet (scale of 0-9; trichotomized into low, middle, or high; and dichotomized into low or high) and physical activity (sum of weekly participation in various physical activities, weighted by the type of physical activity [light, moderate, vigorous]; trichotomized into no physical activity, some, or much; and dichotomized into low or high), separately and combined, were the main predictors in Cox models. Models were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, body mass index, smoking status, depression, leisure activities, a comorbidity index, and baseline Clinical Dementia Rating score.

Main Outcome Measure

Time to incident AD.

Results

A total of 282 incident AD cases occurred during a mean (SD) of 5.4 (3.3) years of follow-up. When considered simultaneously, both Mediterranean-type diet adherence (compared with low diet score, hazard ratio [HR] for middle diet score was 0.98 [95% confidence interval {CI}, 0.72-1.33]; the HR for high diet score was 0.60 [95% CI, 0.42-0.87]; P = .008 for trend) and physical activity (compared with no physical activity, the HR for some physical activity was 0.75 [95% CI, 0.54-1.04]; the HR for much physical activity was 0.67 [95% CI, 0.47-0.95]; P = .03 for trend) were associated with lower AD risk. Compared with individuals neither adhering to the diet nor participating in physical activity (low diet score and no physical activity; absolute AD risk of 19%), those both adhering to the diet and participating in physical activity (high diet score and high physical activity) had a lower risk of AD (absolute risk, 12%; HR, 0.65 [95% CI, 0.44-0.96]; P = .03 for trend).

Conclusion

In this study, both higher Mediterranean-type diet adherence and higher physical activity were independently associated with reduced risk.

Citation

http://www.ncbi.nlm.nih.gov/pubmed/19671904

 

Mother’s Day is May 8: Gifts for People with Alzheimer’s and Their Caregivers

(Alzheimer’s Association) If you have a caregiver or a person with Alzheimer’s on your gift-giving list, we’ve got some suggestions to make your shopping a bit easier.

Gifts for People with Alzheimer’s

In the early stages

Items to help remember things

  • magnetic reminder refrigerator pads
  • Post-It notes
  • baskets or trays that can be labeled within cabinets or drawers
  • a small pocket-sized diary or notebook
  • erasable white boards for key rooms in the house
  • a memorable calendar featuring family photos – write special family occasions such as birthdays and anniversaries

Items to help with everyday tasks

  • a memory phone that can store up to eight pictures with the names and contact information of family and friends automatic medication dispenser that can help the person living with Alzheimer’s remember to take medicine
  • nightlights that come on automatically when it gets dark
  • a clock with the date and time in large type

Items to help keep the person engaged  

  • an outing to a movie, play or concert, sporting event, museum or possibly an organized holiday shopping trip with friends and family
  • favorite musical CDs or CD with compilation of favorite tunes
  • VHS/DVD collection of favorite movies
  • activities such as scrapbooking or other craft projects

In the middle-to-late stages 

Sensory stimulation gifts. Stimulating the five senses may bring back pleasant memories. Give gifts such as:

  • scented lotions
  • a fluffy bathrobe in a favorite color
  • a soft blanket or afghan to keep warm

Clothes. Get comfortable, easy to remove, easily washable clothes such as:

  • sweat suits
  • knits
  • large banded socks
  • shoes with Velcro ties
  • wrinkle free nightgowns, nightshirts and robes

Music. Research shows that music has a positive impact on individuals with Alzheimer’s, bringing them back to good times, increasing stimulation and providing an opportunity to interact with family members. Buy favorite CDs or burn a CD full of musical favorites

Framed photographs or a photo collage. Copy photos of family members and friends at photo centers, insert the names of the people in the photo and put in frames or in a photo album created specifically for that person.

MedicAlert® + Alzheimer’s Association Safe Return®.  Enroll the person in MedicAlert + Safe Return, a 24-hour nationwide emergency response service for wandering and medical emergencies.

Gifts for Caregivers

  • The gift of time. Cost-effective and truly meaningful gifts are self-made coupons for cleaning the house, cooking a meal, mowing the lawn, shoveling the driveway, and giving time off so a caregiver can do something to meet their needs.
  • Gift cards and certificates. Give gift certificates for restaurants, laundry/dry cleaning services, lawn care services, computer/technology support, maid services, and personal pampering services such as massages and pedicures.
  • Books. In addition to giving novels on the caregiver’s “must read” list, there are also a number of books on caregiving such as “The 36-Hour Day” by N.L.Mace and P.V. Rabins; “The Best Friends Approach to Alzheimer’s Care” by V. Bell and D. Troxel; and “Alzheimer’s: A Caregiver’s Guide and Sourcebook,” by H. Gruetzner; and “Coach Broyles’ Playbook for Alzheimer’s Caregivers” by Frank Broyles. Also consider giving book on CD.
  • Digital Video Recorder (DVR). Purchase DVR/TiVo and year’s worth of service so the caregiver can record favorite shows or sports programs he or she may not be able watch in real time due to care responsibilities.
Citation

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Copyright © 2016  Alzheimer’s Association®. All rights reserved

 

Early Abnormalities of Alzheimer’s Disease: It Takes 2 (Proteins) to Tango

(McGill University) For years, neuroscientists have puzzled over how two abnormal proteins, called amyloid and tau, accumulate in the brain and damage it to cause Alzheimer’s disease (AD). Which one is the driving force behind dementia? The answer: both of them, according to a new study by researchers at the Douglas Mental Health University Institute.

In the journal Molecular Psychiatry, the team led by Dr. Pedro Rosa-Neto, a clinician scientist at the Douglas and assistant professor of Neurology, Neurosurgery and Psychiatry at McGill University, reports for the first time evidence that the interaction between amyloid and tau proteins drives brain damage in cognitively intact individuals.

“We specifically found that both proteins mutually enhance their individual toxic effects and cause a brain dysfunction considered to be a signature of AD.

This finding challenges previous polarized theories that a single protein abnormality was the major driving force of disease progression,” explains Dr. Rosa-Neto, whose team is part of the CIUSSS de l’Ouest-de-l’Île-de-Montréal research network.

Toward new therapeutic strategies

This research also points toward new therapeutic strategies to mitigate the progression of AD.

“Until now, therapeutic clinical trials have targeted a single pathological process. Our result paves the way for new therapeutic strategies for prevention or stabilization of AD. For example, combination therapies should be used simultaneously against both amyloid and tau protein accumulation,” says Dr. Tharick A. Pascoal, lead author of the study.

Rosa-Neto’s team analyzed the performances of 120 cognitively intact individuals over two years (equal gender distribution; average age 75). By measuring amyloid levels using PET scans and tau proteins through cerebrospinal fluid analysis, the researchers were able to identify the patients at risk of brain damage associated with AD.

According to the World Health Organization, Alzheimer’s disease is the most common cause of dementia, affecting more than 30 million people worldwide in 2015. In 2011, 747 000 Canadians were living with Alzheimer’s disease and other forms of dementia, and the combined direct (medical) and indirect (lost earnings) costs of dementia amounted to $33 billion (Alzheimer Society of Canada).

This work was funded by the Canadian Institutes of Health Research, the Alan Tiffin Foundation and the Alzheimer’s Association. Individuals evaluated in this study were part of the Alzheimer’s disease neuroimaging initiative study.

Citation

About the science team of Dr. Pedro Rosa-Neto

Dr. Pedro Rosa-Neto (MD, PhD) is the current deputy director of the PREVENT-AD program and leads the translational neuroimaging laboratory (TNL). The TNL conducts groundbreaking research on quantifying neurodegenerative processes using Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI) to enable preclinical diagnosis of dementing diseases.

Dr. Serge Gauthier (MD, FRCPC) is a neurologist and a full-time clinician researcher who has been conducting research on dementing disorders at the Douglas Institute since 1990. Dr. Gauthier is the director of the Alzheimer’s Disease Research Unit at the McGill Centre for Studies in Aging. In 2015, he was appointed to the Order of Canada for his contributions to advancing our understanding of Alzheimer’s disease and dementia, and for fostering the development of research networks in his specialty.

Dr. Tharick Ali Pascoal (MD) is a Brazilian neurologist who is currently conducting PhD studies on the Integrated Program in Neuroscience (IPN) at McGill University.  Dr. Pascoal is a recipient of a Stop-AD scholarship. For his thesis, he focuses on in vivo quantification of protein to protein interactions as determinants of dementia using imaging and fluid biomarkers.

About the CIUSSS de l’Ouest-de-l’Île-de-Montréal

The Centre intégré universitaire de santé et de services sociaux (CIUSSS) de l’Ouest-de-l’Île-de-Montréal is made up of the CSSS de l’Ouest-de-l’Île, the CSSS de Dorval-Lachine-LaSalle, St. Mary’s Hospital, St. Anne’s Hospital, Douglas Mental Health University Institute, West Montreal Readaptation Centre, Grace Dart Extended Care Centre, and Batshaw Youth and Family Centres.

The Douglas Mental Health University Institute is a world-class institute affiliated with McGill University and the World Health Organization. It treats people suffering from mental illness and offers them both hope and healing. Its teams of specialists and researchers are constantly increasing scientific knowledge, integrating this knowledge into patient care, and sharing it with the community in order to educate the public and eliminate prejudices surrounding mental health.

http://www.mcgill.ca/newsroom/channels/news/alzheimers-disease-it-takes-two-proteins-tango-260514

Journal Reference:

T A Pascoal, S Mathotaarachchi, S Mohades, A L Benedet, C-O Chung, M Shin, S Wang, T Beaudry, M S Kang, J-P Soucy, A Labbe, S Gauthier, P Rosa-Neto. Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer’s disease. Molecular Psychiatry, 2016; DOI: 10.1038/mp.2016.37

Source

Centre intégré universitaire de santé et de services sociaux de l’Ouest-de-l’Île-de-Montréal