Archives for May 2016

Will Heart Medication Help Treat Alzheimer’s Disease?

(Örebro Universitet) A new study from Örebro University, published in Science Signaling today, shows that heart medication reduces the build-up of plaque in the brain’s blood vessels in mice. The question is if this is true also in humans? If the answer is yes, it might bring scientists a step closer to developing a medicine against Alzheimer’s disease.

Together with German and Italian colleagues, the Örebro researchers have uncovered how a previously unknown mechanism is the cause of rapid build-up of plaque in in the brain. Trials involving mice have therefore been performed to establish whether a specific heart drug is able to reduce .

“You should be careful not to draw any major conclusions from experimental studies, but we have certainly identified an interesting approach worth taking further,” says Professor Magnus Grenegård at Örebro University, who together with Knut Fälker and Liza Ljungberg has been working on the study led by German Professor Margitta Elvers.

The study shows how the protein beta-amyloid sticks to the surface of blood platelets, also known as thrombocytes, initiating a rapid chain reaction. The result is an incredibly fast-paced build-up of plaque.

 “Plaque causes nerve cells to die at too fast a rate, causing the symptoms indicative of Alzheimer’s disease, such as memory loss,” says Magnus Grenegård.

“Our study is an example of solid biomedical basic research at the cell and molecular levels which points to a link that was previously unknown. What is shown is that cells in the blood may play a significant role in the development of plaque, which is found in patients with Alzheimer’s disease.”

Researchers therefore tested a widely used heart drug which today is used to prevent blood clots and decrease the risk of a heart attack. The trials in mice showed that the lumps of protein, the plaque, were reduced when the rodents were treated with heart medication. The medication thus slows the process down. It is certainly true for the plaque in the blood vessels, but possibly also in the brain tissue itself.

“In deep structures of the brain, where certain memory functions are controlled, there was a clear trend of reduced plaque presence.”

“We do not know if this is transferrable to humans; if the effect would be the same. To find out, new follow-up studies are required. Unfortunately, this is a lengthy process – it will be years before we know. But at least we have identified a new, interesting approach with respect to formation.”

Alzheimer’s disease is characterised by the damage of brain tissue. Early symptoms are a decline in memory and the ability to complete daily tasks, but ultimately the whole brain is affected.

“More than 100,000 Swedes have been diagnosed with Alzheimer’s disease and it brings great suffering to the patient, but also to family members. New medication would naturally be most welcome,” says Magnus Grenegård.


L. Donner et al. Platelets contribute to amyloid- aggregation in cerebral vessels through integrin IIb 3-induced outside-in signaling and clusterin release, Science Signaling (2016). DOI: 10.1126/scisignal.aaf6240


Study Links High Blood Pressure and Risk of Dementia Researchers analysing the health records of over 4 million people in the UK have confirmed a previously-reported link between high blood pressure and the risk of vascular dementia– the second most common cause of dementia after Alzheimer’s disease. The study is published today (Wednesday) in the journal Stroke.

Vascular dementia is caused by a reduction in blood flow to the brain resulting from a stroke or changes to small blood vessels. The condition is thought to affect around 150,000 people in the UK and causes symptoms like memory loss, communication problems and personality changes.

The team, led by researchers at the University of Oxford, analysed the electronic health records of 4.28 million people between 30 and 90. These people did not have a diagnosis of vascular disease or dementia, but the researchers were able to study their blood pressure measurements. Of these people 11,114 went on to receive a diagnosis of vascular dementia in an average follow-up period of seven years.

The results showed that people between the ages of 30 and 50 were at a 62% greater risk of developing vascular dementia per 20mmHg above usual systolic blood pressure. For people between 51 and70 there was a smaller, 26% increased risk, and there was no evidence of high blood pressure affecting the risk of vascular dementia in those between 71 and 90.

The findings were followed up in a study in Oxford that has been following a group of people who had a stroke or transient ischaemic attack (sometimes called a ‘mini-stroke’). The team examined data from 1,680 people in the group who did not have dementia. Over a five-year period, 314 developed dementia. The researchers found that the risk of dementia was associated with the volunteer’s blood pressure five or more years prior to their stroke. This link was highest in those participants who were under the age of 75.

Dr Rosa Sancho, Head of Research at Alzheimer’s Research UK, said:

“There is mounting evidence to suggest that what’s good for the heart is good for the brain and maintaining good vascular health is one of the key things people can do to reduce their risk of dementia.

This study has capitalised on the rich data held in electronic medical records to strengthen the link between high blood pressure and dementia risk, and suggest that midlife could be a particularly important window for reducing the risk of future vascular dementia.

While it’s important that treatments are given to help control high blood pressure, this study doesn’t suggest that people without high blood pressure should be taking these medications specifically to reduce the risk of vascular dementia. Anyone with concerns about their vascular health should seek out the advice of their GP.”

As well as maintaining a healthy blood pressure, there are other steps people can take to reduce their risk of dementia. The best current evidence suggests that not smoking, only drinking in moderation, staying mentally and physically active, eating a balanced diet, and keeping cholesterol levels in check can all help to keep our brains healthy as we age.”

Citation study-links-high-blood-pressure-risk-dementia/

Copyright Alzheimer’s Research UK


Caregivers Often Sacrifice for Alzheimer’s Costs

(WebMD) Many skip food and health care, cut back work hours or quit jobs to care for loved ones, survey shows.

Caring for someone with Alzheimer’s disease means caregivers often skimp on their own food and medical care, and even sell their belongings to support their loved one, a new report released Wednesday shows.

The centerpiece of the Alzheimer’s Association’s annual report was a nationwide survey detailing the heavy financial and emotional toll caregivers endure.

According to the survey, caregivers were 28 percent more likely to eat less or go hungry, and one-fifth cut back on doctor visits. Nearly half of them cut back on their own expenses to afford dementia-related care. And more than one-third reduced their hours at work or quit their job to care for a loved one, losing an average of $15,000 in income.

“Care contributors are making enormous personal and financial sacrifices, and these sacrifices are jeopardizing their own and their family’s financial security,” Beth Kallmyer, vice president of constituent services at the Alzheimer’s Association, said at a press briefing Tuesday on the annual report.

Approximately 5.4 million Americans now suffer from Alzheimer’s disease, according to the Alzheimer’s Association, and nearly 16 million family members and friends provide financial, physical and emotional support. In 2016, it is estimated, those caregivers will give 18 billion hours of unpaid care.

But many people caring for an Alzheimer’s patient have no clue about the financial side of their commitment. About two out of three people incorrectly assume that Medicare will help them cover nursing home costs or are not sure if the costs will be covered.

Currently, only 3 percent of American adults have long-term care insurance that could help them cover these costs, the researchers said.

In fact, 13 percent of those surveyed sold personal belongings, such as a car, to help pay for dementia-related costs, and nearly half dipped into savings or retirement accounts.

On average, the caregivers spent more than $5,000 a year of their own money for care. Many spend tens of thousands of dollars a year, the researchers found.

Much of that money was spent on nursing home care and home care, Kallmyer said.

Many caregivers saw their income decline by 20 percent and their spending on education for their kids dropped 11 percent, Kallmyer said.

Other highlights of the report include:

  • Without new treatments, the number of Americans with Alzheimer’s disease will rise to 13.8 million by 2050.
  • Nearly 500,000 Americans aged 65 or older will develop Alzheimer’s in 2016.
    Two-thirds of Americans over 65 with Alzheimer’s are women.
  • Alzheimer’s is the sixth-leading cause of death in the United States, and the fifth-leading cause for those 65 and older.
  • From 2000 to 2013, Alzheimer’s deaths increased 71 percent.
  • The yearly cost of caring for Alzheimer’s patients and other dementias in the United States is estimated at $236 billion (excludes unpaid caregiving), of which $160 billion is paid by Medicare and Medicaid.
  • Payments for health care, long-term care and hospice for people with Alzheimer’s and other dementias are expected to increase to more than $1 trillion in 2050.
  • Annual Medicaid spending for people with Alzheimer’s is $43 billion, while out-of-pocket spending is estimated at $46 billion.

The data for the report comes from 500 responders to a phone survey who are caring for a relative or friend with Alzheimer’s.

To help lessen the money woes, the Alzheimer’s Association suggests:

  • Use retirement planning to prepare for long-term medical costs.
  • Figure out all your financial resources including savings, insurance, retirement benefits, government assistance, VA benefits, etc. A financial planner or elder care attorney can help.
  • Investigate long-term care services in your area.
  • Call the local Agency on Aging to determine what services and support programs are available.

“The toll of all serious, chronic diseases extends out from the patient in concentric rings to affect family and friends, too,” said Dr. David Katz, director of the Yale University Prevention Research Center and president of the American College of Lifestyle Medicine.

“That toll is physical, emotional and financial. The news is really rather grim,” he added.

“But as a preventive medicine specialist, I do see opportunity, and a silver lining,” Katz said.

Dementia is substantially preventable through early lifestyle interventions, he said.

“We are all in this together, and compelled to work together to improve systems of care to accommodate this tremendous and growing burden,” he said.


By Steven Reinberg

Copyright © 2013-2016 HealthDay.



Antimicrobial Mechanism Gone Rogue May Play Role in Alzheimer’s Disease

(Scientific American) A new study finds that a key protein implicated in Alzheimer’s may normally protect the brain from infection.

General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s.

Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes.

“The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “

These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.”

Just as amyloid beta is known to do, these antimicrobial proteins can build up and form fibrils that, when not properly regulated, have harmful effects. Yet unlike amyloid beta, their role in the immune system has been widely accepted: They prevent microbes from adhering to host cells, and ultimately trap them.

So five years ago the pair of researchers set out to determine whether amyloid beta could also act as a natural antibiotic. They had previously explored their hypothesis in vitro, but in this new study they used worms and mice. For these animal models they compared what happened when amyloid beta was overexpressed to when it was not produced, and found that the former led to increased resistance to infection and longer survival rates.

The team first infected cultured human and hamster cells with a type of fungus called Candida albicans and found that high expression of amyloid beta had a protective effect, doubling the number of cells that were not infected. The researchers then moved on to roundworms, or nematodes, which usually do not survive for more than two to three days once the fungus takes hold. The nematodes with overexpressed amyloid beta, however, were still going strong five to six days after they were infected. Finally, the researchers infected the brains of mice with a strain of salmonella to cause meningitis. Mice that were genetically altered to overproduce human amyloid beta survived nearly twice as long as mice that did not have the protein at all.

Most shocking of all, according to Tanzi and Moir, was that when they injected bacteria into the brains of Alzheimer’s mouse models, amyloid plaques—the hallmark of the disease—formed within 48 hours.

“We didn’t know this was even possible,” Tanzi says, “that amyloid plaques would form rapidly overnight.”

And in the middle of each plaque was one Salmonella bacterium, supporting the theory that the amyloid deposition had formed around the microbe as an entrapment mechanism—just like LL37 and other established antimicrobial proteins.

“These results are particularly intriguing,” says Anna Palamara, a microbiologist at the Sapienza University of Rome who was not involved in the study.

“Previous [research] shows that several infectious agents, including viruses, trigger amyloid beta production and accumulation.”

Herpes and influenza are just two of the infections that have been tested by other research teams.

The Harvard team’s new findings provide further evidence that Alzheimer’s could be inadvertently spurred by an infection that causes the formation of too much amyloid. As people get older the immune system and blood-brain barrier become increasingly compromised, making it easier for microbes to sneak into the brain. It wouldn’t take many of these pathogens, according to Tanzi, to cause amyloid buildup. “And that could rapidly start the cascade toward the disease,” he says, “causing tangles and inflammation. You’ve got all three pillars of Alzheimer’s right there.”

“It is possible to speculate that during a mild infection the production of amyloid beta may help,” Palamara says.

“But in the presence of persistent or repeated infections, amyloid beta levels may accumulate, exceeding a threshold. In this case its protective role might change to the well-known neurotoxic one.”

The idea that amyloid beta has a positive function in the body could potentially change how scientists approach potential treatments. Instead of attempting to completely eliminate the protein, “we might want to think about just dialing it down,” Tanzi says. Moreover, Moir adds, the drugs in trials now are for the most part designed to reduce inflammation by targeting pathways in the adaptive immune system. But if amyloid production and deposition are innate immune responses, then targeting pathways of innate immunity or the microbes themselves may be the way to go.

They do not expect convincing the scientific community of this to be easy.

“This is really going to cause a lot of unrest in the field,” Tanzi says.

“Any new revolutionary discovery is first ridiculed, then violently opposed, and finally taken to be self-evident. We’re ready for the ridicule and the violent opposition, and we think we have enough data so that we can look forward to self-evident.”

But the pair has a long way to go. They are now moving forward with a plan to systematically characterize the microbes found in the aging brain. From there they hope to identify the pathogens that may be involved in the onset of Alzheimer’s—as well as those that potentially play a role in other amyloid diseases, such as diabetes.

“We’re at the top of a mountain with a freshly formed layer of snow,” Moir says.

“Where you go is where you choose. There’s so much to explore.”


Jordana Cepelewicz

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


A New Challenge For Caregivers: The Internet

(Northwestern University) What should caregivers do when their loved one is checking in on social media at the bank, essentially announcing their whereabouts? What if they are posting too often or don’t remember making online purchases?

In the age of online living, caregivers lack support, resources and guidelines to help the vulnerable people who rely on them, according to an initial study, to be presented May 12, at the Association for Computing Machinery Human Computer Interaction (ACM-CHI) conference in San Jose, California.

The study is one of the first to examine the role of caregivers in the online lives of adults with cognitive impairments from Alzheimer’s disease and other conditions. In a world where many everyday activities have moved online, caregivers face a new challenge: finding a balance between autonomy and protection of care recipients.

“We want people to stay independent and engaged online, but current online systems make it difficult to help people in a way that empowers them without reducing their access,”

said lead researcher Anne Marie Piper, assistant professor in the department of communication studies at Northwestern’s School of Communication.

“E-mail and social media sites aren’t designed to have a caregiver come alongside someone with cognitive impairments and help them stay active online.”

The researchers used focus groups consisting of 20 people informally caring for loved ones with Alzheimer’s, dementia and other brain-related conditions. They detailed four main ways caregivers currently help people with cognitive impairments use the Internet — “guiding, stimulating, connecting, and protecting,” with guidelines about how to improve those dynamics.

Caregivers could set up family accounts to support home computer use among family members. They also should learn how to recognize when vulnerability may be transitional, such as a gradual recovery after a stroke or a progression from early to late stage dementia.

Finally, the researchers recommended implementing a system that would allow caregivers to detect risky online situations. For example, if a password or credit card were disclosed, a transaction would be held for review by the primary caregiver. These ideas, however, raise new ethical questions about who has control over a person’s online life, Piper said.

“Technological caregiving is a new form of work,” Piper said.

“We hear about the physical, financial and social stress of caregiving, but no one ever talks about the burden caregivers feel to keep people active online, which we feel is a fundamental part of participating in society.”

According to the study, caregivers support online activity in the following ways:

Guiding: Caregivers may help someone type words into a search engine or operate a mouse. Even previously tech-savvy care recipients may need to re-learn how to use a specific technology.

“What’s challenging is that cognitive impairment is dynamic, and an individual’s needs may shift day-to-day or even moment-to-moment,” Piper said.

Stimulating: Social media can be a form of entertainment or stimulation. Caregivers play “brain games,” read news sites or view online photos of family members.

“This interaction can help alleviate some of the burden of caregiving and provide a mutual source of enjoyment,” the researchers found.

It also means caregivers have to spend time searching for content, identifying meaningful photos or videos and working it into a conversation.

Connecting: Facebook is a particularly important site for social support, caregivers said. In the study, they mentioned posting weekly updates on Facebook, Instagram, and The ways caregivers post online information “introduces tensions around surrogacy, privacy and information sharing for vulnerable populations,” the researchers wrote.

Protecting: Caregivers use spam filters and set restrictive privacy settings to help avoid phishing and to block harmful websites, friend requests or potentially upsetting information. They vigilantly watch for online financial threats.

“The challenge is deciding when and under what circumstances a care recipient should not have access to credit card information required for online purchases,” the researchers wrote.

“Sometimes it’s not until an adverse event like identity theft or overspending that the caregiver realizes they need to protect their care recipient online.”


by Julie Deardorff

Copyright Northwestern University


Assistive Tech to Tackle Dementia Isolation

(Manchester Metropolitan University) Mobile and wearable technology used to support independent living for people with dementia could hold the key to cutting social isolation.
Mobile tech

KMS Solutions’ wearable device

Wearable technology, satellite tracking and mobile phone apps are the latest tools in the fight against social isolation from dementia, unlocking the potential for increased independence.

Researchers at Manchester Metropolitan University, working with Stockport Memory Clinic and KMS Solutions, are analysing these technologies to establish their best use for people with dementia and for their carers.

The project was offically launched today as part of Dementia Awareness Week.

Josie Tetley, Professor of Nursing in ageing and long-term conditions at Manchester Metropolitan University, said: “We will work closely with the end people living with dementia and their carers. The use of the different technology options will be studied in the daily lives of a small group of research participants to analyse the potential acceptability and usability of them.

“Based on this, the project will analyse the potential of these technologies to reduce social isolation and improve health outcomes.”

John Hearns, Managing Director of KMS Solutions Ltd, said:

“The technologies we have developed can support independent living in the community by enabling the person living with dementia to move independently in safe areas, the carer to locate them using GPS tracking and the person with dementia or their carer to contact each other in case of an emergency.”

Carol Rushton, Clinical Lead from Stockport Memory Clinic at Pennine NHS Foundation Trust, added: “Going for a walk can sometimes be a challenge for people with dementia because of memory issues and confusion related to their dementia which can lead to people getting lost or disorientated even in familiar surroundings.

“These distressing experiences for some can result in reduced activity, increased social isolation and increased carer stress, so any form of technology that can support people get out and about more safely and confidently would be a great help.”

In 2015, it was estimated that there were 850,000 people living with dementia in the UK. As a result of the memory, physical and communication challenges, people with dementia and their unpaid carers may experience social isolation and loneliness.

It is part of a series of technical health projects at the University designed to employ new technologies to cut loneliness and isolation.

This project is led by Professor Josie Tetley and Dr Emma Koivunen, from the Department of Nursing, Dr Jenny Fisher, from the Department of Social Care and Social Work, and Dr Matthew Sullivan, from the School of Science and the Environment. It is funded from Greater Manchester Academic Health Science Network’s Technology Innovation Challenge.

KMS Solutions provide a range of new, easy-to-use mobile technologies that can support people living with dementia and their carers, comprising of an Android smartphone application ‘MyTrav’ App, and two wearable and portable GSM/GPS based wristbands.


© 2016 Manchester Metropolitan University

Distinguishing Differences in Dementia Using Brain Scans

(University of Leiden) Neuroscientist Anne Hafkemeijer is able to distinguish two different forms of dementia using advanced imaging techniques. This is the first step towards early recognition of dementia in patients on the basis of brain networks.

Early Diagnosis

In her PhD research Hafkemeijer used MRI scans to detect changes in brain networks that occur as a result of ageing and dementia. She studied both the structure and the function of these networks. What do these brains look like and how does their function change as people age or suffer from dementia?

Previously, people looked mainly at separate areas of the brain, but cognitive functions, such as memory, are not located in one area of the brain. As these functions are the result of brain areas working together, it is very important to be able to study the areas in detail. The research findings help us make a distinction between different forms of dementia. Early detection is important for the patient, his environment, the treatment plan and the prognosis.

Using Advanced Techniques

Hafkemeijer is a specialist in the methodology and statistics of psychology and she conducted her research in partnership with the LUMC, the Amsterdam VUmc and the Erasmus MC Rotterdam.

‘Each specific form of dementia has its own development course and symptoms,’ Hafkemeijer explains. She studied two of these forms.

‘With Alzheimer’s, memory declines whereas frontotemporal dementia affects the front part of the brain. These changes cause a noticeable change in behaviour. We used new advanced imaging techniques to show these changes in the brain.’

Differences in Dementia are Hard to Distinguish

Hafkemeijer explains: ‘Although each form of dementia has its own symptoms, there is a lot of overlap between them. We wanted to use brain scans to study whether the brain networks are different in these two forms. Particularly in the early stages of the condition it is difficult to distinguish between them. That’s why it is currently not possible to make an early diagnosis.’

Dementia Patients Classified Individually

This research makes it possible to distinguish the group of Alzheimer’s patients from those with frontotemporal dementia. Individual recognition is not always possible. Hafkemeijer sees her research findings as a first step towards an individual classification of dementia and an earlier diagnosis for dementia patients.

She will shortly be applying these advanced imaging techniques in the clinical environment, advising brain researchers within Leiden University, the Leiden Institute for Brain and Cognition and the LUMC and supporting them with their MRI research and analyses.


Copyright University of Leiden

Men’s Y Chromosome Loss Tied to Alzheimer’s Risk

(WebMD) Men who lose Y chromosomes from their blood cells as they age may have an increased risk of developing Alzheimer’s disease, a new study suggests.

The study of more than 3,200 men found those who already had Alzheimer’s were nearly three times more likely to show a loss of the Y chromosome in some of their blood cells. What’s more, older men with that “loss of Y” faced a higher risk of developing Alzheimer’s over the next eight years.

Experts said the study doesn’t prove that loss of the Y chromosome directly contributes to Alzheimer’s disease.

But it adds to evidence tying loss of Y to disease risk, said study co-author Lars Forsberg.

It also raises the possibility of one day testing men’s blood for loss of Y, to predict their risk of developing Alzheimer’s, said Forsberg, a researcher at Uppsala University in Sweden.

The findings were reported online May 23 in the American Journal of Human Genetics.

Men have an X and a Y chromosome, while women have two X chromosomes. Researchers used to think that the Y did little more than determine male sex and ensure normal sperm production.

But recent studies have shown that the Y chromosome contains a large number of genes, whose jobs are not fully understood yet.

Similarly, researchers have long known that as men age, they can lose the Y chromosome from some of their body cells. It was seen as a normal part of aging. Some recent studies, however, have suggested otherwise.

In a 2014 study, for example, Forsberg and his team found that older men with a loss of Y had a higher cancer risk and shorter lives than other men.

These latest findings on Alzheimer’s are “very interesting and provocative,” said Dr. Luca Giliberto, a neurologist and researcher with the Feinstein Institute for Medical Research, in Manhasset, N.Y.

Giliberto, who was not involved with the study, said the researchers accounted for other factors tied to Alzheimer’s risk — including older age, education levels, high blood pressure and diabetes.

And still, men who had a loss of Y in their blood cells were nearly seven times more likely to develop Alzheimer’s, versus other men.

“It seems that the loss of Y is, per se, an independent risk factor for Alzheimer’s disease,” Giliberto said.

That opens up many more questions, Giliberto noted. One is, which genes on the Y chromosome — when lost — might leave a man more vulnerable to Alzheimer’s?

Another question is, when does loss of Y begin?

“We speculate that whatever cellular mechanisms fail and lead to Alzheimer’s, they start in our young adult life, not in our 70s,” Giliberto said. “Is loss of Y a process that starts that early?”

If loss of Y does not begin until late in life, he added, then it may only make an “ancillary” contribution to Alzheimer’s risk.

The findings are based on blood samples from more than 3,200 European men, average age 73. Overall, 17 percent had a detectable loss of Y in some of their blood cells.

When the researchers focused on men free from Alzheimer’s at the outset, they found that loss of Y predicted a higher risk of developing the disease. And the greater the loss, the higher the risk: Men missing the chromosome from around 35 percent of their blood cells were more likely to develop Alzheimer’s than those with loss of Y in 10 percent of their cells.

Since scientists do not fully understand the workings of Y, the reasons for the link are unclear.

But Forsberg speculated that impaired immune function could play a role — since loss of Y has been tied to cancer risk as well.

Giliberto agreed. He noted that loss of Y has also been seen in certain autoimmune diseases — where the immune system mistakenly attacks the body’s own tissue. And some researchers suspect immune function may affect Alzheimer’s risk.

“A faulty brain immune system has been proposed as a possible ‘soft spot’ for Alzheimer’s disease, allowing for the abnormal accumulation of proteins and consequent (brain cell) degeneration,” Giliberto said.

For now, though, researchers have much to learn about the connection between the Y chromosome and disease. And more studies will be needed before loss of Y can be used as a “biomarker” of Alzheimer’s risk, Giliberto said.


By Amy Norton

Copyright © 2013-2016 HealthDay. All rights reserved.