Abnormally Low Blood Flow Indicates Damage to NFL Players’ Brains

(IOS Press) The discovery of brain pathology through autopsy in former National Football League (NFL) players called chronic traumatic encephalopathy (CTE) has raised substantial concern among players, medical professionals, and the general public about the impact of repetitive head trauma.

Using sophisticated neuroimaging and analytics, researchers have now identified abnormal areas of low blood flow in living professional football players. These findings, published in the Journal of Alzheimer’s Disease, raises the potential for better diagnosis and treatment for persons with football related head trauma.

“This report opens the study of traumatic brain injury to well established brain imaging approaches,” commented George Perry, PhD, Editor in Chief of the Journal of Alzheimer’s Disease.

“The findings suggest that brain hypoperfusion may play a role in the development of the clinical changes seen in NFL players.”

This study used cerebral perfusion imaging with single photon emission computed emission tomography (SPECT) to examine the brains of the largest group of retired and current NFL players investigated to date, a total of 161 individuals with an average age of 52.

Looking at blood flow to every region of the brain, researchers were able to identify areas of abnormally low blood flow. Combining this information with a leading-edge quantitative approach called machine learning allowed them to distinguish NFL players with abnormal brain patterns compared to health controls with 92-94% accuracy.

“Without functional imaging studies like SPECT, it is very difficult to know if brain trauma is present and which areas are affected,” explained lead author Daniel G. Amen, MD, Amen Clinics, Inc, Costa Mesa, CA.

“Structural studies often appear normal but what we can do better with functional neuroimaging with SPECT is not only pinpoint specific areas of the brain that are unhealthy with low blood flow, but also demonstrate their improvement with successful brain rehabilitation treatments in persons like football players.”

Co-author Dr. Bennet Omalu, who originally described CTE as depicted in the movie Concussion featuring Will Smith, added,

“What our current work is doing in addition to other imaging modalities builds the foundation between identifying the negative effects of head trauma on the brain while the patient is still alive so that we can intervene with better treatments.”

Investigators determined that on average the NFL players had lower blood flow in 36 areas of the brain. The decreased blood flow in the following six regions of the brain were the most important in determining who had football related health trauma: anterior superior temporal lobes, rolandic operculum, insula, superior temporal poles, precuneus and, cerebellar vermis.

These same regions function in memory, mood, and learning. When damaged, they can produce cognitive and psychiatric problems as evidenced by the fact that 83% of players in this study had memory problems and 29% of them had history of depression.

According to lead investigator Cyrus A. Raji, MD, PhD, University of California Los Angeles Medical Center,

“This convergence of a critical research question of high national interest, functional neuroimaging, and new computer-based predictive analytics makes this study both intriguing and impactful. It is of key importance not only for the neurological safety of football players, but for the general public as well.”

Citation

http://www.iospress.nl /ios_news/abnormally-low-blood-flow-indicates-damage-to-nfl-players-brains/

Journal Reference:

Daniel G. Amen, Kristen Willeumier, Bennet Omalu, Andrew Newberg, Cauligi Raghavendra, and Cyrus A. Raji. Perfusion Neuroimaging Abnormalities Alone Distinguish National Football League Players from a Healthy Population. Journal of Alzheimer’s Disease, April 2016 DOI: 10.3233/JAD-160207

Copyright 2016 ScienceDaily or by third parties, where indicated.

 

Social Clubs Fill Gap in Dementia Support

(University of British Columbia) Community-based social groups could play a crucial role in empowering people with early-onset dementia, according to new UBC research.

The study, led by UBC nursing professor Alison Phinney, focused on an independently run program known as Paul’s Club, which offers social and recreational activities three days a week out of a hotel in downtown Vancouver. Members range in age from mid-40s to late 60s.

“Of the estimated 1.4 million Canadians living with Alzheimer’s and other forms of dementia by 2031, a few thousand in every major city will be diagnosed before age 65,” noted Phinney.

“The question is how we can support them so that they can continue to live at home for as long as possible.”

The answer, according to Phinney’s research, could be day programs like Paul’s Club.

The club, founded in 2012 by retired Vancouver nurse Nita Levy and her husband, Michael, provides members a friendly environment without medical or hospital associations–hence the “club” monicker and the choice of a hotel for a meeting place. The focus is on having fun, so dementia is rarely mentioned or discussed.

The club runs from 10 a.m. to 4 p.m. to give members’ families a break from caring from their loved ones. Each day starts with morning coffee, often followed by chair yoga, a dance or other light workout before the group heads out for lunch and a walk in the neighbourhood. Ice cream at a local gelato shop caps off the day.

While the club doesn’t follow a strict schedule, the one constant is the group walk. Linking arms or holding hands with the Levys or club volunteers, members stroll in groups of twos or threes, stopping frequently to admire the scenery or talk to other people.

“By observing and talking to the members, we found that walking in the neighbourhood and interacting with others kept them connected to the community,” said Phinney, a researcher with Vancouver Coastal Health Research Institute.

“They felt that they still belonged–something that wouldn’t have been possible had they stayed at home.”

The Levys founded the club following the death of a beloved brother-in-law as a result of early-onset dementia. They saw a need for services for younger people with dementia as most programs are suitable for older people, and very few are targeted to those with dementia.

“Young-onset dementia is incredibly challenging because they’re still fairly active and healthy and suddenly they’re no longer able to work,” said Phinney.

“Being part of the club keeps them busy and healthy and gives their family respite, making it more feasible for members to stay at home longer.”

Phinney’s research is funded by the Alzheimer’s Society of Canada. Its next stage will examine a more traditional adult day program for older people, including some living with dementia.

“Walking in the Neighbourhood: Performing Social Citizenship in Dementia,” has been accepted for publication in Dementia: The International Journal of Social Research and Practice. It can be found here: https://open.library.ubc.ca/cIRcle/collections/facultyresearchandpublications/52383/items/1.0300370

Citation

http://news.ubc.ca/2016/05/03/social-clubs-fill-gap-in-dementia-support/

Copyright The University of British Columbia

 

Group Activities Reduced Depressive Symptoms Among Older People with Dementia

(Umeå universitet) Both a high-intensity functional exercise programme and a non-exercise group activity, conducted among older care facility residents with dementia, reduced high levels of depressive symptoms. However, exercise had no superior effect on depression, according to a dissertation from Umeå University.

“Unfortunately, depression is common among older people, especially in people with dementia,” says Gustaf Boström, doctoral student at the Department of Community Medicine and Rehabilitation and author of the dissertation.

“Treatment with antidepressant drugs is often ineffective in older people and people with dementia. In addition, the risk of drug-related side effects increases with higher age and poor health, which is yet another reason to find other treatments.”

In his dissertation, Gustaf Boström investigated whether 45 minutes of high-intensity exercise, every other weekday for four months, had a better effect on depressive symptoms than a seated group activity, performed with the same duration and frequency, in older people with dementia.

The exercise programme included balance- and leg strengthening exercises that mimicked everyday movements, e.g. rising up from a chair, step up and down from a step board, or walking on a path with obstacles. Participants in the seated group conversed, sang, or listened to readings, all with varying themes such as season, wild animals or well-known authors. There was no difference in effect between activities, but high levels of depressive symptoms were reduced in both groups.

“Previous studies have shown that people with dementia at residential care facilities have few social interactions, which can negatively affect a person’s well-being. The positive effects could therefore be the results of social interactions in these kinds of group activities. However, more research is needed to confirm this,” says Gustaf Boström.

Gustaf Boström also investigated if there is a connection between impaired balance, general dependency in activities of daily living, and depression in older age. The study involved 392 participants and results suggest that there is a correlation between impaired balance and depressive symptoms. Regarding dependency in activities of daily living, two specific tasks were related to increases in depressive symptoms — dependency in transfer and dressing.

“The link between impaired balance, dependency in transfer or dressing, and depression is an important finding and may be the subject of future studies focusing on prevention or treatment of depression among people in older age,” says Gustaf Boström.

Finally, Gustaf Boström analysed if people with dementia or people over the age of 85 had an increased risk of death with ongoing treatment with antidepressants. Previous studies have shown an increased risk of death with antidepressant use in older people with depression.

For very old people or people with dementia, who are expected to have a higher risk of drug-related side effects, the knowledge of potential mortality risk associated with antidepressant use is limited.

The study showed no significantly increased risk in these groups, but did find gender differences. Among very old people, women had a higher mortality risk with antidepressant use in comparison to men. Among people with dementia, antidepressant use was associated with a reduced mortality risk in men. These differences and the potential risk of initial treatment need to be investigated further in future studies.

Citation

http://www.medfak.umu.se/english/about-the-faculty/news/newsdetailpage/group-activities-reduced-depressive-symptoms-among-older-people-with-dementia.cid268388

Copyright 2016 Umeå universitet

 

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.

 

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

Big Financial Costs are Part of Alzheimer’s Toll on Families

(NPR) First, Alzheimer’s takes a person’s memory. Then it takes their family’s money.

That’s the central finding of a report published Wednesday by the Alzheimer’s Association on the financial burden friends and families bear when they care for someone with dementia.

“What we found was really startling,” says Beth Kallmyer, vice president of constituent services for the organization.

“The cost of paying for care was putting people in a situation where they had to make really difficult choices around basic necessities — things like food, medical care, transportation.”

The report, based on a survey of more than 3,500 Americans contributing to the care of someone with dementia, also found that:

  • Friends and family spent, on average, more than $5,000 a year of their own money on the expenses of their loved one with dementia, ranging from food to adult diapers.
  • More than one-third of these contributors to care who had jobs had to reduce their hours or quit.
  • To make ends meet, about 13 percent had to raise money by selling personal belongings, such as a car.
  • Nearly half of the care contributors surveyed had to dip into their savings or retirement funds.

The Alzheimer’s Association decided to conduct the survey, Kallmyer says, after hearing lots of stories of financial hardship from friends and family members of people with Alzheimer’s. One of those stories came from Paul and Sarah Hornback, who live in central Kentucky.

Paul Hornback was a senior engineer and analyst for the U.S. Army when was diagnosed with Alzheimer’s six years ago. He was just 55.

“I was kind of at the height of my career and then this dreadful diagnosis came and it just wiped out every plan I had for my career,” he says.

Hornback and his wife, Sarah, had to re-imagine their future. Then they began to consider the financial implications.

The Hornbacks had borrowed a lot of money to put three children through college. Now Paul was being forced to retire early and they wouldn’t have his salary to pay off the debt.

“We had to sell basically everything but my wife’s car and an old truck that I kept to drive around here on the farm,” he says.

At first, Sarah Hornback kept working as a school administrator. But about 18 months ago, she also had to retire early — to care for her husband.

“It got to the point where it just wasn’t safe for him to stay alone just because of memory and decision making,” she says.

“He might leave the stove on or he might decide that there was a tree branch bothering him and he should get out the chain saw.”

The Hornbacks are getting by on their early retirement income. But Sarah Hornback says the real financial problems will start when she can no longer care for her husband on her own.

“When he has to go into full-time care, I’m going to be at the poverty level, basically,” she says.

The financial burden is greatest for people like the Hornbacks, who have to pay more while working less, Kallmyer says.

“It’s really a double whammy,” she says.

“People are sometimes not able to work as much or not able to work at all in order to provide care, and then they’re paying money out of pocket on top of that.”

The survey also found that about two-thirds of Americans believe Medicare will help cover nursing home costs, or aren’t sure whether it will. It won’t.

“What that tells us is that families are ultimately unprepared for that really, really significant cost of long-term care,” Kallmyer says.

Clinics that specialize in Alzheimer’s often try to help family members navigate the financial aspects of care.

“It’s a challenge for almost every family that we see,” says Dr. Pierre Tariot, a geriatric psychiatrist and director of the Banner Alzheimer’s Institute in Phoenix.

“We do see folks who are lucky and have considerable resources. But even for those families it’s a major financial obligation.”

And it’s not realistic to expect every family to absorb the cost, Tariot says.

“Ultimately,” he says, “society will need to think of other ways of funding care for our elders as they become vulnerable.”

Citation

http://www.npr.org/sections/health-shots/2016/03/30/472295791/big-financial-costs-are-part-of-alzheimers-toll-on-families

By Jon Hamilton