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.”


By Jon Hamilton


Why Do People with Alzheimer’s Stop Recognizing Their Loved Ones?

(Journal of Alzheimer’s Disease) Alzheimer’s not only steals people’s memories but also their ability to recognize faces, which widens the gulf between people with this disease and their loved ones. A recent study has demonstrated that, beyond causing memory problems, Alzheimer’s disease also impairs visual face perception.

This finding may help families better understand their loved one’s inevitable difficulties and lead to new avenues to postpone this painful aspect of the disease. Research in this area by the team of Dr. Sven Joubert, PhD, a researcher at the Centre de recherche de l’Institut universitaire de gériatrie de Montréal of the CIUSSS du Centre-Sud-de-l’Île-de-Montréal and a professor with the Department of Psychology at Université de Montréal, has just been published in the Journal of Alzheimer’s Disease.

Face perception plays a fundamental role in human communication, which is why humans have evolved into experts at quickly detecting and identifying faces. This faculty is thought to depend on the ability to perceive a face as a whole.

Also known as “holistic perception,” this ability is in contrast to the local and detailed analysis required to perceive individual facial features, such as the eyes, nose or mouth. Dr. Joubert’s study has demonstrated that the holistic ability to perceive faces is impaired by Alzheimer’s disease.

For the study, the Montreal team recruited people with Alzheimer’s along with healthy seniors to study their ability to perceive faces and cars in photos that were either upright or upside down (see the figure below for examples of different displays/trials of stimuli).

Dr. Joubert explains the team’s findings:

“The results for people with Alzheimer’s were similar to those in the control group in terms of answer accuracy and the time to process the upside-down faces and cars. To perform these tasks, the brain must perform a local analysis of the various image components perceived by the eye.

However, with the upright faces, people with Alzheimer’s were much slower and made more mistakes than the healthy individuals. This leads us to believe that holistic face recognition in particular becomes impaired.

Subjects with Alzheimer’s disease also demonstrated normal recognition of the upright cars, a task that in theory does not require holistic processing. This suggests that Alzheimer’s leads to visual perception problems specifically with faces.”

What’s also surprising about this impairment is that it is observed in the early stages of the disease.


Overall, Dr. Joubert’s study better explains the mechanism involved in the problem that people with Alzheimer’s have with recognizing the faces of family members or celebrities. The fact that impaired facial recognition might stem from a holistic perception problem—and not just a general memory problem—opens the door to different strategies (such as the recognition of particular facial traits or voice recognition) to help patients recognize their loved ones for longer.


A qualitative impairment in face perception in Alzheimer’s disease: Evidence from a reduced face inversion effect. Journal of Alzheimer’s Disease JAD 51(4), April 12, 2016 DOI: 10.3233/JAD-151027

Sven Joubert is supported by a Chercheur-boursier senior award from the Fonds de recherche du Québec – Santé (FRQ-S). Sven Joubert and Isabelle Rouleau are supported by the Alzheimer Society of Canada. Delphine Gandini was supported by a CIHR postdoctoral award and Guillaume Vallet is supported by a FRQ-S postdoctoral award. Bruno Rossion is supported by the Belgian National Fund for Scientific research and a BELSPO grant.

About the Institut universitaire de gériatrie de Montréal (IUGM)
The IUGM has 446 short-term and long-term beds and an ambulatory centre. It has what is considered to be the largest Francophone research centre in the field of aging. A member of Université de Montréal’s larger excellence in health network, the IUGM opens its doors every year to hundreds of students, trainees and researchers. Since April 1, 2015, the IUGM has been part of the CIUSSS du Centre-Sud-de-l’Île-de-Montréal.

About the Centre intégré universitaire de santé et de services sociaux du Centre-Sud-de-l’Île-de-Montréal (CIUSSS-CSMTL)
The Centre intégré universitaire de santé et de services sociaux du Centre-Sud-de-l’Île-de-Montréal (CIUSSS-CSMTL) was created on April 1, 2015, from the merger of ten health and social services institutions on the Island of Montreal. It provides services to a population of nearly 300,000 Montrealers who live on the southern part of the island in the boroughs of Ville-Marie, Verdun, Le Sud-Ouest, Le Plateau-Mont-Royal and part of Rosemont–La Petite-Patrie. It also has a regional responsibility for such services as rehabilitation, youth services, public health and emergency measures. With four institutes and two university-affiliated centres in different health and social services sectors, the CIUSSS-CSMTL fulfills a significant academic mission.

Geneviève Desrosiers
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Journal of Alzheimer’s Disease is published by IOS Press

Copyright © 2016


Almost Half of Alzheimer’s Cases are Due to Hyperinsulinemia

(MedicalNewsToday) Scientists have long known that there is a strong association between diabetes and Alzheimer’s, but the nature of that relationship – and how to treat it – was unclear. Now Melissa Schilling, an innovation professor at NYU, has discovered the pathway between diabetes and Alzheimer’s, and it has big implications for how Alzheimer’s can be prevented.

Professor Schilling compared and integrated decades of research on diabetes, Alzheimer’s, and molecular chemistry, focusing in particular on results that seemed to yield conflicting results.

It turns out that routine practices in research – like excluding all patients with known medical problems such as diabetes from an Alzheimer’s study, for example – had obscured the mechanisms that connect the two diseases. Those main mechanisms turn out to be insulin and the enzymes that break it down.

The same enzymes that break down insulin also break down amyloid-beta, the protein that forms tangles and plaques in the brains of people with Alzheimer’s. When people have hyperinsulinemia (i.e., they secrete too much insulin due to a poor diet, pre-diabetes, early diabetes, obesity, etc.) the enzymes are too busy breaking down insulin to break down amyloid-beta, causing amyloid-beta to accumulate.

The American Diabetes Association estimates that roughly 8.1 million Americans have undiagnosed diabetes and 86 million have pre-diabetes and have no idea. The good news is that hyperinsulinemia is preventable and treatable through changes in diet, exercise, and medication.

Schilling notes,

“If we can raise awareness and get more people tested and treated for hyperinsulinemia, we could significantly reduce the incidence of Alzheimer’s disease, as well as other diabetes-related health problems. Everyone should be tested, early and often, preferably with the A1C test that doesn’t require fasting. Dementia patients should especially be tested – some studies have shown that treating the underlying hyperinsulinemia can slow or even reverse Alzheimer’s.”

Professor Schilling’s research has been published in Journal of Alzheimer’s Disease.



Unraveling Alzheimer’s: Making Sense of the Relationship between Diabetes and Alzheimer’s Disease, Schilling, Melissa A., Journal of Alzheimer’s Disease, doi: 10.3233/JAD-150980, published 12 April 2016.

Source: Professor Melissa A. Schilling, New York University

MediLexicon International Ltd, Bexhill-on-Sea, UK

© 2004-2016 All rights reserved.


Re-energizing the Aging Brain

(MedicalNewsToday) The human brain has a prodigious demand for energy — 20 to 30% of the body’s energy budget. In the course of normal aging, in people with neurodegenerative diseases or mental disorders, or in periods of physiological stress, the supply of sugars to the brain may be reduced. This leads to a reduction in the brain’s energy reserves, which in turn can lead to cognitive decline and loss of memory.

But new research on mice shows that the brain’s energy reserves can be increased with a daily dose of pyruvate, a small energy-rich molecule that sits at the hub of most of the energy pathways inside the cell. These results need to be replicated in human subjects, but could ultimately lead to clinical applications.

“In our new study, we show that long-term dietary supplementation with pyruvate increases the energy reserves in the brain, at least in mice, in the form of the molecules glycogen, creatine and lactate,”

says lead author Heikki Tanila, Professor of Molecular Neurobiology at the A. I. Virtanen Institute of the University of Eastern Finland.

What’s more, dietary supplementation with pyruvate didn’t only increase the brain’s energy stores: it also changed the behavior of the mice in positive ways, show the researchers.

“The mice became more energetic and increased their explorative activity. It appears that these behavioral changes are directly due to the effect of pyruvate on brain function, since we didn’t find that these mice had developed greater muscle force or endurance,” says Tanila.

For example, chronic supplementation with pyruvate facilitated the spatial learning of middle-aged (6- to 12-months-old) mice, made them more interested in the odor of unfamiliar mice, and stimulated them to perform so-called “rearing”, an exploratory behavior where mice stand on their hind legs and investigate their surroundings.

The dose necessary to achieve these effects was about 800 mg pyruvate per day – which corresponds to about 10 g per day in humans — given to the mice in normal chow over a period of 2.5 to 6 months. A single large dose of pyruvate injected directly into the blood stream had no detectable effect.

Interestingly, the positive response to dietary supplementation with pyruvate was also found in a strain of transgenic mice called APPswe/PS1dE9, often used as an animal model for the study of Alzheimer’s disease.

These mice exhibit many of the same symptoms as people with Alzheimer’s, such as the deposition of protein plaques in the brain, neurodegeneration, and cognitive decline. These results raise hopes that pyruvate might also benefit people with neurodegenerative disorders such as Alzheimer’s and Parkinson’s.

“Pyruvate supplementation may prove beneficial as an activating treatment for the elderly and in therapies for alleviating cognitive decline due to aging, neurodegenerative disease, or mental disorders. It is well tolerated and warrants further studies in humans,” says Tanila.

The study, which was supported by the Alzheimer Association, is published in the open-access journal Frontiers in Aging Neuroscience.


Chronic Pyruvate Supplementation Increases Exploratory Activity and Brain Energy Reserves in Young and Middle-Aged Mice

Hennariikka Koivisto, Henri Leinonen, Mari Puurula, Hani Sayed Hafez, Glenda Alquicer Barrera, Malin H. Stridh, Helle S. Waagepetersen, Mika Tiainen, Pasi Soininen, Yuri Zilberter and Heikki Tanila

Frontiers in Aging Neuroscience

DOI. 10.3389/fnagi.2016.00041

Published online 16 March 2016

The study was supported by the Alzheimer Association.

Source: Frontiers

Additional source: EurekAlert!, the online, global news service operated by AAAS, the science society

© 2004-2016 All rights reserved.

New Gene Responsible for Stroke Discovered

(Boston University School of Medicine) Researchers have identified a new set of genes that may be responsible for the two most common and disabling neurological conditions, stroke and dementia.

The study, which appears in the journal Lancet Neurology, may help researchers better understand, treat and prevent ischemic and hemorrhagic stroke, and perhaps Alzheimer’s disease and other dementias.

Stroke is the leading neurological cause of death and disability worldwide. Previous studies have looked mainly at genes causing atherosclerosis and genes affecting the function of platelets and clotting processes as risk factors for ischemic stroke (clot obstructing blood flow to the brain). A different set of genes have been associated with hemorrhagic stroke (bleeding into the brain).

Researchers from Boston University School of Medicine looked for new stroke genes using genome wide association as well as meta-analysis. They identified a new gene called FOXF2 which increased the risk of having a stroke due to small vessel disease in the brain. No previous study has identified a gene for the common type of small vessel disease stroke although some genes associated with familial small vessel diseases such as CADASIL are known.

“Our research has identified a gene affecting another type of ischemic stroke, due to small vessel disease, and also suggests some genes may be associated with both ischemic and hemorrhagic stroke and may act through a novel pathway affecting pericytes, a type of cell in the wall of small arteries and capillaries.

Unraveling the mechanisms of small vessel disease is essential for the development of therapeutic and preventive strategies for this major cause of stroke,” explained corresponding author Sudha Seshadri, MD, professor of neurology at BUSM.

According to the researchers small vessel disease not only causes stroke but is also a major contributor to dementia risk, and is associated with gait problems and depression.

“Hence, it is exciting that we are beginning to better understand the cause of this very important and poorly understood type of stroke,” she added.

The study was carried out in collaboration between researchers at Boston University School of Medicine, Bordeaux University, Washington University, the University of Calgary, Gothenburg University and many others.

Funding for this study was provided by the National Institute of Neurological Disorders and Stroke: NS017950, the National Institute on Aging: AG033193 and the National Heart, Lung and Blood Institute.


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


An Implant to Prevent Alzheimer’s

(École Polytechnique Fédérale de Lausanne) One of the hypothesized causes of Alzheimer’s is the over-accumulation of the protein amyloid beta (Abeta) in different areas of the brain. This results in the deposition of aggregated protein plaques, which are toxic to neurons.

One of the most promising ways to fight the plaques is to “tag” the Abeta proteins with antibodies that signal the patient’s own immune system to attack and clear them. To be most effective, this treatment has to be given as early as possible, before the first signs of cognitive decline. But this requires repeated vaccine injections, which can cause side effects. EPFL scientists have now solved the problem with an implant that can deliver a steady and safe flow of antibodies to the patient’s brain to clear Abeta proteins. The work is published in the journal Brain.

The lab of Patrick Aebischer at EPFL has developed a bioactive capsule containing cells that have been genetically engineered to produce antibodies against Abeta. The capsule is implanted in the tissue under the skin, and over time the cells produce and release a steady flow of antibodies into the bloodstream, from where they cross over into the brain to target the Abeta plaques.

The capsule itself is based on a design from Aebischer’s lab published in 2014. It is referred to as a “macroencapsulation device” and it is made of two permeable membranes sealed together with a polypropylene frame. The complete device is 27-mm long, 12-mm wide and 1.2-mm thick, and contains a hydrogel that facilitates cell growth. All the materials used are biocompatible, and the lab specifically used a method that is easily reproducible for large-scale manufacturing.

The cells inside the capsule are important. Not only must they be able to produce antibodies, but they also have to be compatible with the patient, so as to not trigger the immune system against them, like a transplant can. This is where the capsule’s membranes come into play, shielding the cells from being identified and attacked by the immune system. This protection also means that cells from a single donor can be used on multiple patients.

Before going into capsule, the cells are first genetically engineered to produce antibodies that specifically recognize and target Abeta. The cells of choice are taken from muscle tissue, and the permeable membranes let them interact with the surrounding tissue to get all the nutrients and molecules they need.


In Alzheimer’s mouse models, the implantable capsule significantly reduced levels of beta-amyloid protein and plaques in mice. Image credit: Patrick Aebischer (EPFL)

The researchers tested the device on mice with great success. The mice – a genetic line that is commonly used to simulate Alzheimer’s disease – showed dramatic reduction of Abeta plaque load. Indeed, the constant flow of antibodies produced by the capsule over a course of 39 weeks prevented the formation of Abeta plaques in the brain. The treatment also reduced the phosphorylation of the protein tau, another sign of Alzheimer’s observed in these mice.

The proof-of-concept work is a landmark. It demonstrates clearly that encapsulated cell implants can be used successfully and safely to deliver antibodies to treat Alzheimer’s disease and other neurodegenerative disorders that feature defective proteins.

This work involved a collaboration between EPFL’s Neurodegenerative Studies Laboratory (Brain Mind Institute), the Swiss Light Source (Paul Scherrer Institute) and F. Hoffmann-La Roche. It was funded by the Swiss Commission for Technology and Innovation and F. Hoffmann-La Roche Ltd.


Written by Nik Papageorgiou


Lathuilière A, Laversenne V, Astolfo A, Kopetzki E, Jacobsen H, Stampanoni M, Bohrmann B, Schneider BL, Aebischer P. A subcutaneous cellular implant for passive immunization against amyloid-β reduces brain amyloid and tau pathologies.Brain 08 March 2016. DOI: 10.1093/brain/aww036

© 2016 EPFL all rights reserved


Scientists Discover a Missing Link Between Tau and Memory Loss

(ScienceDaily) Scientists have long known that the protein tau is involved in dementia, but how it hinders cognitive function has remained uncertain. In a study published in the journal Neuron, researchers at the Gladstone Institutes reveal how tau disrupts the ability of brain cells to strengthen connections with other brain cells, preventing new memories from forming.

“Understanding why and how tau is toxic to neurons is the first step in repairing or preventing the damage it causes in Alzheimer’s disease,” said senior author Li Gan, PhD, a senior investigator at Gladstone.

“We learned that tau disrupts memory in models of Alzheimer’s disease by depleting another protein, KIBRA, which is critical for memory formation. With this knowledge, we can explore ways to increase KIBRA with drugs that block the harmful effects of tau.”

Memories are formed when chemical signals strengthen the connection between neurons. To maintain the memories, neurons physically change, recruiting more chemical receptors to the surface where the connections are made (the synapse) to increase the strength of incoming signals. If the connections among neurons weaken or are lost, so is the memory.

In the current study, the scientists discovered that, in a mouse model of Alzheimer’s disease, the accumulation of tau in neurons disrupts the cells’ ability to strengthen their connections with other neurons, preventing them from stabilizing new memories. This is because a natural chemical modification of tau called acetylation that is exacerbated in Alzheimer’s disease results in tau moving from its normal location in the neuron to the synapse.

At the synapse, tau depletes another protein called KIBRA (KIdney/BRAin protein), a process that prevents neurons from adapting and strengthening their connections. Increasing KIBRA levels reversed the harmful effects of acetylated tau and restored the cells’ ability to form memories.

Supporting the clinical relevance of this finding, the researchers also found that KIBRA is decreased in the brains of patients with Alzheimer’s disease, which correlated with an increase in acetylated tau.

“Our findings suggest that KIBRA may be the missing link between tau and memory loss in Alzheimer’s disease,” said first author Tara Tracy, PhD, a postdoctoral scholar at Gladstone.

“The next step is to determine precisely how acetylated tau causes KIBRA levels to drop, and to explore whether our findings may help develop better treatments for Alzheimer’s disease.”

Other Gladstone scientists on the study include Peter Sohn, S. Sakaura Minami, Chao Wang, Sang-Won Min, Yaqiao Li, Yungui Zhou, David Le, Iris Lo, and Ravikumar Ponnusamy. Researchers from the Buck Institute for Research on Aging and John Hopkins University School of Medicine also contributed to the research.


Story Source:

The above post is reprinted from materials provided by Gladstone Institutes. Note: Materials may be edited for content and length.

Journal Reference:

Tara E. Tracy, Peter Dongmin Sohn, S. Sakura Minami, Chao Wang, Sang-Won Min, Yaqiao Li, Yungui Zhou, David Le, Iris Lo, Ravikumar Ponnusamy, Xin Cong, Birgit Schilling, Lisa M. Ellerby, Richard L. Huganir, Li Gan. Acetylated Tau Obstructs KIBRA-Mediated Signaling in Synaptic Plasticity and Promotes Tauopathy-Related Memory Loss. Neuron, 2016 DOI: 10.1016/j.neuron.2016.03.005

Gladstone Institutes. (2016, March 31). Scientists discover a missing link between tau and memory loss: Increasing levels of a protein involved in memory formation may reverse the cognitive deficits caused by tau. ScienceDaily. Retrieved April 2, 2016 from

Copyright 2015 ScienceDaily or by third parties, where indicated.


Omega-3 Fatty Acids Shown to Exert a Positive Effect on the Aging Brain

(Eureka Alert) Changes in cognitive function and memory decline form a normal part of aging. However, in neurodegenerative diseases such as Alzheimer’s disease or mild cognitive impairment (the pre-dementia phase of Alzheimer’s disease), these changes occur more quickly. There are currently no effective treatments for these diseases.

Physicians and researchers are constantly looking for new treatment methods that will maintain their patients’ cognitive performance and independence for as long as possible. Targeted prevention is another essential component when trying to preserve cognitive function for as long as possible.

“Ideally, any measures used should be aimed at long-term prevention. This means that measures must be suitable for use in healthy older adults, and should be easy to integrate into day-to-day life,”says Dr. Nadine Külzow, a researcher at Charité’s Department of Neurology. Nutritional supplements represent one such option.

“A number of different dietary components, including omega-3 fatty acids, are currently thought to have a direct effect on nerve cell function. This is why we decided to study the effects on memory function of a daily dose of 2,200 milligrams taken for a duration of six months,” says Dr. Külzow.

Study participants who received omega-3 fatty acids showed greater improvements on an object location memory task than participants who received a placebo containing sunflower oil. However, there was no evidence of improved performance on a verbal learning test.

“Results from this study suggest that a long-term approach to prevention is particularly effective in preserving cognitive function in older individuals. A targeted approach involving dietary supplements can play a central role in this regard,”

concluded the researchers.

Whether or not the improvements recorded can make a noticeable difference in day-to-day life will need to be investigated as part of a larger clinical study.

As a next step, however, the researchers are planning to test the effect of supplementation with a combination of omega-3 fatty acids and vitamin B. According to research conducted at Oxford, this combination may be associated with synergistic effects.


*Nadine Külzow, Veronica Witte, Lucia Kerti, Ulrike Grittner, Jan Philipp Schuchardt, Andreas Hahn and Agnes Flöel. Impact of Omega-3 Fatty Acid Supplementation on Memory Functions in Healthy Older Adults. Journ. Alzheimers Dis. 2016 Feb 10. doi: 10.3233/JAD-150886.

Study participants wanted

We are currently recruiting for additional studies aimed at testing the effects of regular dietary supplementation on cognitive abilities such as memory and learning. Participants must be aged between 60 and 80 years, and suffer from impaired memory. For further details, please refer to the following page:

Department of Neurology and Experimental Neurology

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