Concussions double veterans' risk for Alzheimer's, study says

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Los Angeles Times

For veterans coming home from Iraq and Afghanistan with head injuries, the wounds of war may eventually include dementia. In a study reported at a July 18 meeting in Paris of the Alzheimer's Assn., researchers found that older veterans who had suffered concussions were more than twice as likely as other veterans to develop Alzheimer's disease or other forms of dementia.

Doctors have suspected for many years that a blow to the head could set the stage for dementia. But the new study — involving more than 281,000 veterans 55 and over — was one of the largest to ever look at the long-term effects on a group that suffers more than its share of head injuries.

The researchers looked at veterans who had visited a doctor at least once between 1997 and 2000 and had a follow-up visit between 2001 and 2007. The study found that almost 16% of veterans with a history of head trauma had developed dementia during that time. By comparison, only 7% of those who hadn't suffered a head injury were diagnosed with dementia.

With the widespread reliance by insurgents on roadside bombs and rocket-propelled grenades, the wars in Iraq and Afghanistan have been especially rife with head injuries, making the latest study findings especially relevant and disconcerting. Army doctors estimate that 15% to 25% of soldiers deployed to these countries end up with "mild traumatic brain injury," caused by direct blows to the head and/or exposures to blasts. For those seriously wounded in combat, the list of injuries generally includes head trauma. A 2006 study found that two-thirds of soldiers sent to Walter Reed Army Medical Center from Iraq had brain injuries.

Head injuries can leave long-lasting psychological wounds, too. A study in the New England Journal of Medicine in 2008 found that a serious head injury quadrupled the risk of post-traumatic stress disorder. Of 2,500 infantry soldiers studied who had just finished serving a year in Iraq, 5% had received a blow to the head that was severe enough to knock them out. More than 40% of these soldiers showed the classic signs of PTSD. For those who weren't injured, the rate of PTSD was less than 10%.

PTSD can be overcome with counseling, medication and time. For now, though, there is no real treatment for Alzheimer's. Unless that changes, many veterans from Iraq and Afghanistan will be facing a new battle in 30 to 40 years.

Study: Two antidepressants given to dementia patients ineffective

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USA Today

The antidepressants most often prescribed to treat depression in dementia patients provide no appreciable relief, and may raise the risk for serious side effects, new British research suggests.

"The two classes of antidepressants most likely to be prescribed for depression in Alzheimer's disease are no more effective than placebo," the study authors said.

The drugs in question are Zoloft (sertraline), and Remeron (mirtazapine).

"In our study, there were more adverse reactions in individuals treated with antidepressants than there were with placebo," the research team added. "Clinicians and investigators need to reframe the way they think about the treatment of people with Alzheimer's disease who are depressed, and reconsider routine prescription of antidepressants."

Led by Sube Banerjee of the Institute of Psychiatry at Kings College London in England, the authors reported their findings online July 19 in The Lancet.

Banerjee and his colleagues focused on 325 patients being treated at any of nine health centers across England for probable or possible Alzheimer's disease. The patients were also subject to bouts of depression lasting at least a month, and all registered above a minimum threshold during dementia-related depression exams.

None had been prescribed antidepressants prior to the study launch, nor were any in a critical stage of depression involving suicidal thoughts.

The patients were divided into three 13-week treatment groups. One group received 150 milligrams (mg) a day of sertraline; a second group received 45 mg a day of mirtazapine; and a third took sugar pills (placebos).

After three months, the authors found no difference in the incidence of depression among the three groups. The lack of an apparent benefit attributable to either sertraline or mirtazapine continued almost 10 months after the study's start, according to a journal news release.

Also, while about a quarter of those given placebos experienced adverse reactions as a result of treatment, that figure rose to between 41 percent and 43 percent in the groups given an antidepressant. Such side effects were also more likely to be serious among the antidepressant recipients than among the placebo group.

Dr. Henry Brodaty, an aging and dementia specialist at the University of New South Wales in Sydney, Australia, and author of an accompanying journal editorial, said the trial "has underscored the need for clinicians to think about creative alternatives to drug treatment for management of depression in people with dementia." It is important to use evidence-based techniques and to work in partnership with family caregivers, he wrote in the news release.






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Ensuring proper denture fit may reduce individuals' risk of developing dementia

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DentalPlans.com

While maintaining an active social life and good nutrition has been associated with a lower risk of developing dementia in old age, other factors such as denture fit and ear health may also play a role in staving off cognitive impairment.

A recent study published in the journal Neurology found that 19 health factors that had not previously been associated with dementia may increase the risk of the condition when left unaddressed. The researchers said this finding may indicate that maintaining good overall health is essential to avoiding brain diseases like Alzheimer's.

The research involved more than 7,200 dementia-free adults who were questioned about the fit of their dentures, whether they had arthritis pain, had trouble seeing, and numerous other things.

The study's results showed that each health factor increased the participants' risk of developing dementia by 3.2 percent.

"Our study suggests that rather than just paying attention to already known risk factors for dementia, such as diabetes or heart disease, keeping up with your general health may help reduce the risk for dementia," said study author Kenneth Rockwood, M.D.

The American Dental Association states that poor-fitting dentures may lead to irritation or sores in the mouth.

ICAD: Biomarkers Take Center Stage in Alzheimer's Field

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By John Gever, Senior Editor, MedPage Today

PARIS – Although disease-modifying treatments for Alzheimer's disease are still years away, research on biomarkers and imaging techniques for identifying individuals most likely to benefit from them is making great strides.

That's the view of William Thies, PhD, chief medical and scientific officer of the Alzheimer's Association, sponsor of the International Conference on Alzheimer's Disease (ICAD) that starts here today.

In an exclusive interview with MedPage Today senior editor John Gever, Thies said that new results on diagnostic and prognostic markers would be among the major highlights of this year's meeting.

A major trend in the field, he said, has been "increasing interest in biomarkers and increased understanding of biomarkers – they're not created equal, there may be different biomarkers that are going to be useful in different parts of the disease."

"It's certainly true that the progress in biomarkers and the progress in new treatments almost has to go hand in hand," Thies added.

Indeed, another trend receiving significant attention at this year's ICAD is early treatment of Alzheimer's disease, before dementia becomes severe.

The recently updated diagnostic criteria for the disease are facilitating early intervention, he said, because they better describe what he called "the continuum of Alzheimer's disease."

These trends are interrelated and will become more so when disease-modifying therapies finally become available, Thies predicted.

"As new medications are developed and [approved], they'll probably receive labeling with some careful instructions about biomarkers used during the diagnostic procedure," he suggested.

Whether those medications will be directed against beta-amyloid protein is still unclear, he conceded.

But Thies said the recent negative results with anti-amyloid drugs did not yet mean the approach was a dead end.

"There are several anti-amyloid therapies that are still in phase III testing. These are the monoclonal antibodies that bind to beta-amyloid," he said.

"I think we're going to see very important data coming out of those trials. I think it's too early to declare the amyloid hypothesis dead."

Those data will not be reported here, but the ICAD agenda does feature results from other studies that will shed light on other aspects of the disease, including:

•Modifiable risk factors
•Traumatic brain injury as a cause of Alzheimer's disease
•Safety of anti-amyloid therapies
•Cerebrospinal fluid proteins and imaging results early in the disease

Thies also mentioned that a critical need for future research is recruitment of potential research participants.

The Alzheimer's Association has launched a service called TrialMatch to place volunteers into research studies – including cognitively healthy and mildly impaired individuals as well as those with overt Alzheimer's disease.

"The hope is to increase the number of people in trials," he said, noting that about 10,000 people are now available in the pool.

"We hope that eventually this will drastically speed the recruitment of people in trials," alleviating a major obstacle to progress.

"Currently, to recruit a full cohort for a phase III clinical trial in Alzheimer's disease, it takes somewhere between a year and a year and a half. That's just wasted time," Thies declared.

'Prevention is better than cure for Alzheimer's disease

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By Robert Bazell
Chief science and health correspondent

NBC News NBC News

Curing Alzheimer’s disease may be impossible and the best hope to control the disease may require beginning treatments as much as 20 years before the onset of symptoms. It could take decades to find effective therapies for the brain-wasting disease.

That is the view of Dr. Sam Gandy, a highly respected Alzheimer's expert at Mount Sinai Medical Center in New York. Writing a perspective article titled “Prevention is Better than Cure” in this week’s issue of the journal Nature, Gandy offers an argument that will likely dominate much of the discussion next week when 4,000 researchers gather in Paris for the Alzheimer’s Association’s Annual International Conference.

Gandy notes it has been more than a century since the German psychiatrist Alois Alzheimer described the condition that bears his name. Dr. Alzheimer discovered the disease in a 51-year-old woman called Auguste D. After her death, Alzheimer noticed her brain was speckled with plaques of a protein now known as amyloid-beta peptide.

In recent decades, on the basis of sound evidence, many scientists have concluded that amyloid plaques play a key role in causing the devastation of Alzheimer’s disease. The pharmaceutical industry has produced drugs and vaccines designed to clear the plaques from the brain. The problem is, in a few large studies the plaque goes away, but the symptoms of the disease continue to worsen.

One camp among Alzheimer’s researchers believes this shows that amyloid is simply not the cause. But the majority of researchers, like Gandy, believe that once the plaque appears the damage to the brain is too great to undo and the only hope is to prevent it. Recent studies using brain scans, spinal fluid and blood samples have been searching for signs that appear before the psychological tests reveal the onset of dementia. Much of this work is centered on the handful of families where some members carry a dominant gene variation that causes them to get Alzheimer’s in their 30s, 40s or 50s, but that type of screening is expected to become more common.

It is increasingly apparent from these studies that many of these changes occur as much as 20 years before the symptoms of the disease. Alzheimer's can progress at different rates but typically develops through different stages, beginning with mild cognitive impairment — forgetting familiar words or losing common objects — to difficulty performing tasks to severe dementia and the inability to carry on a conversation or control movements.

Scientists believe it might be necessary to administer amyloid-lowering drugs early in the course of the disease — long before it is anything that could be called a disease. It also seems likely that it will take years to prove whether any drugs work.

However, getting started with any course of treatment quickly is vital. By 2050, it's estimated that as many as 16 million Americans will have the disease. Most people survive about four to eight years after diagnosis, but some can live as long as 20 years with the disease, according to the Alzheimer's Association.

Gandy writes that “we should not be discouraged by the prospect of another decade or two of work” to know whether controlling amyloid is the key to controlling Alzheimer’s disease. “Prophylactic intervention,” he writes, “is now the best hope.”

Alzheimer's disease research advances

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ScienceDaily Advances in research into Alzheimer's disease: transporter proteins at the blood CSF barrier and vitamin D may help prevent amyloid β build up in the brain.

Advancing age is a major risk factor for Alzheimer's disease and is associated with build- up of the peptide amyloid β in the brain. New research published in BioMed Central's open access journal Fluids and Barriers of the CNS shows that removal of amyloid β from the brain depends on vitamin D and also on an age-related alteration in the production of transporter proteins which move amyloid β in and out of the brain.

Low levels of vitamin D are thought to be involved in age-related decline in memory and cognition and are also associated with Alzheimer's disease. Researchers from Tohoku University, Japan, looked at the mechanism behind this and found that vitamin D injections improved the removal of amyloid β from the brain of mice.

Prof Tetsuya Terasaki said, "Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway. These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer's disease."

The transport of amyloid β across the BBB is known to be orchestrated by transporter proteins such as LRP-1 and P-gp, which move amyloid β out of the brain, and RAGE, which controls influx. Looking at the transport of amyloid β from blood to cerebrospinal fluid (CSF), and from CSF to blood, researchers from Rhode Island Hospital and The Warren Alpert Medical School, found that , and P-gp at the blood-cerebrospinal fluid barrier (BCSFB), increased with age so increasing removal of amyloid β from the CSF and brain.

Prof Gerald Silverberg said, "While increased production of transporter proteins at the blood CSF barrier may help amyloid β removal from the older brain, production of these proteins eventually fails. This failure may be an important event in brain function as we age and for people with Alzheimer's disease."

Overlooked Peptide Reveals Clues to Causes of Alzheimer's Disease

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hly aggregative and neurotoxic amyloid peptide Abeta43 points the way to new approaches for AD diagnosis and treatment

Tokyo, - (JCN Newswire) - Researchers at the RIKEN Brain Science Institute (BSI) and their collaborators have shed light on the function of a little-studied amyloid peptide in promoting Alzheimer's disease (AD). Their surprising findings reveal that the peptide is more abundant, more neurotoxic, and exhibits a higher propensity to aggregate than amyloidogenic agents studied in earlier research, suggesting a potential role in new approaches for preventing AD-causing amyloidosis.

An irreversible, progressive brain disease affecting millions worldwide, Alzheimer's disease is devastating for its victims, robbing them of their memory and cognitive skills and ultimately of their lives. Even after decades of research, however, the causes of AD remain elusive. Two features in the brain, abnormal clumps (senile plaques) and tangled bundles of fibers (neurofibrillary tangles), are known to characterize AD, but there is little consensus on the link between these features and the underlying roots of the disease.

One hypothesis that has attracted widespread support proposes that AD is caused by the buildup of the senile plaques, and in particular of their main constituent, beta amyloid peptides (Abeta). Two major forms of Abeta, Abeta40 and Abeta42, have been associated with genetic mutations causing early-onset AD, and have thus received considerable research attention. The role of longer Abeta species, in contrast, which also exist in the brains of Alzheimer's patients, has not yet been fully investigated.

In their current work, the researchers focused on Abeta43, an beta amyloid peptide found just as often in patient brains as Abeta42, but about which relatively little is known. To study the peptide's role in AD, they generated mice with a mutation causing overproduction of Abeta43, and used a highly sensitive system to distinguish between concentrations of Abeta40, A42 and Abeta43.

Their surprising results reveal that Abeta43 is even more abundant in the brains of AD patients than Abeta40, and more neurotoxic than Abeta42. Abeta43 also exhibits the highest propensity to aggregate and considerably accelerates amyloid pathology. Moreover, unlike the other two Abeta species, which exist in human and mouse brains at birth, Abeta43 levels appear to increase with age, consistent with the pattern of AD onset.

Published in the journal Nature Neuroscience, the findings thus reveal the possible value of Abeta43 as a biomarker for diagnosis of AD and suggest a potential role in new approaches for preventing AD-causing amyloidosis, promising hope to AD sufferers around the world.

Reference:
Takashi Saito, Takahiro Suemoto, Nathalie Brouwers, Kristel Sleegers, Satoru Funamoto, Naomi Mihira, Yukio Matsuba, Kazuyuki Yamada, Per Nilsson, Jiro Takano, Masaki Nishimura, Nobuhisa Iwata, Christine Van Broeckhoven, Yasuo Ihara, and Takaomi C. Saido. Potent amyloidogenicity and pathogenicity of Abeta43. Nature Neuroscience, doi: 10.1038/nn.2858.

Salk study shows strawberries may help those with Alzheimer's disease

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Fox News
Sandiego.com

Strawberries are similar to blueberries and red wine in having multiple health benefits, thanks to a compound called fisetin, the Salk Institute for Biological Studies reported recently.

Fisetin helps combat juvenile diabetes and protects neurons in the brain, according to a study by Salk researchers David Schubert, Ph.D., and Pam Maher, Ph.D., appearing in the journal, PLoS ONE.

Strawberries are the best source of fisetin, which appear to a lesser extent in other fruits and vegetables, according Maher.

Salk Institute Strawberry Study
The researchers gave Akita mice, which are afflicted with unusually high blood sugar, a fisetin-high enriched diet, and the medical effects of diabetes were eased, according to the study. There is also evidence that fisetin can protect neurons and could help slow or prevent neurological disorders such as Alzheimer's disease and Huntington's Disease, Maher said.
It would take 37 strawberries daily to equal the dosage given to the lab mice, so researchers envision fisetin not as a dietary change, but as a supplement that would be taken in pill form. Although dietary supplements containing fisetin are available in the U.S., the dose is generally lower than the equivalent dose given to the mice in the study, Maher said.

Maher said the Salk researchers have had preliminary discussion with pharmaceutical companies about fisetin. Their also plan to see if fisetin is effective in treating type 2 diabetes.

Natural Estrogen May Improve Cognition for Alzheimer's Disease Patients

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Madison, Wisconsin - Post-menopausal women who had mild to moderate Alzheimer's disease and who wore a skin patch with natural estrogen for three months did better on cognitive tests than women who did not wear the patch, according to new findings by the University of Wisconsin School of Medicine and Public Health (SMPH).

The findings are published as an early online version of the Journal of Alzheimer's Disease and are scheduled for publication in the September issue

The study shows that using a natural form of estrogen called estradiol, for short periods of time, may be cognitively beneficial for post-menopausal women with mild to moderate Alzheimer's disease," said Whitney Wharton, lead author and researcher at the UW School of Medicine and Public Health's Alzheimer's Disease Research Center (ADRC).



In the study, 43 post-menopausal women with mild to moderate Alzheimer's disease were enrolled at the University of Wisconsin SMPH ADRC or the University of Washington in Seattle.



Women were randomly assigned to one of five different treatment plans in the randomized, placebo-controlled, double-blind parallel group study: low dose estradiol patch with a placebo tablet or a 2.5 mg tablet of progesterone (medroxyprogesterone); high dose patch with placebo tablet or 2.5 mg tablet of progesterone; placebo skin patch with a placebo tablet.



The study participants underwent cognitive testing before, and at various intervals during, the study. The main result of the study was that women who received estradiol performed better on multiple cognitive tests than women who were assigned to the placebo group.



Also, the cognitive improvements were directly related to estradiol levels. Estradiol is a naturally occurring estrogen predominant in women before menopause. Wharton says estrogen is likely associated with the hippocampus, an area of the brain that has many estrogen receptors and is associated with Alzheimer's disease.




Video: Wharton talks about what we can learn from the study.


Wharton said it's important to realize that estradiol is different from a popular hormone-replacement drug that contains a compound called conjugated equine estrogen (CEE). The compound is not naturally occurring in humans like estradiol.

CEE, the most widely used estrogen used for hormone therapy in the U.S., was the estrogen studied in the landmark Women's Health Initiative (WHI) study and the Women's Health Initiative Memory Study (WHIMS).

The WHI and WHIMS found that hormone replacement therapies using CEE might be associated with increased risk of cardiovascular disease and dementia.

"We know that Alzheimer's is associated with a build-up of amyloid plaques in the brain and we know from basic science studies, that estradiol interacts with, and breaks down, those plaques," said Wharton.

In contrast to the currently FDA-approved Alzheimer's disease drugs, estradiol may actually affect the neuropathology of Alzheimer's disease. Wharton says current drugs treat symptoms like memory loss and mood, but do not change brain mechanisms involved in the disease, such as amyloid plaques.

Wharton says because there are different types of estrogens, the findings about CEE should not be generalized to all forms of estrogen, including estradiol. Wharton says the next step for the research is to replicate the findings.

"We can say that an estradiol skin patch, used for three months or less, appears to improve cognition in post-menopausal women with mild to moderate Alzheimer's disease," said Wharton. "But there is a need for larger trials with more women over longer periods of time to see if estradiol could serve as an alternative therapy for Alzheimer's disease, or one day help scientists learn how to prevent the disease."

The study was funded by the National Institutes of Health and used the resources of the universities of Wisconsin and Washington Department of Medicine Division of Geriatrics and Gerontology, and the Geriatric Research Education and Clinical Center (GRECC) of the William S. Middleton Memorial Veterans Hospital in Madison and the Veterans Affairs Puget Sound Health Care System in Seattle

Why chronic stress hastens progression of Alzheimer's disease

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Daily News and Analysis

Previous studies have pinpointed the role of stress in Alzheimer's disease and other neurodegenerative disorders.

Now, scientists at the USC have discovered why.

Corresponding author Kelvin JA Davies, the James E Birren Chair at the USC Davis School of Gerontology, and professor of Molecular and Computational Biology in the USC Dornsife College, examined the brains of rats that had experienced psychological stresses and found high levels of the RCAN1 gene.

Davies and his colleagues suggest that chronic stress — physical or mental — causes overexpression of RCAN1, in turn leading to neurodegenerative disease.

Think of a gene as a pattern or mold that generates specific proteins. For example, if 200 RCAN1 proteins are built where only 100 were needed, scientists would describe this as "overexpression" of the RCAN1 gene.

In a healthy person, the RCAN1 gene helps cells cope with stress. Overproduction, however, can eventually damage neurons, preventing the brain's signals from traveling and causing disease.

Currently, there are two competing theories about the leading cause of neurodegeneration in Alzheimer's disease: overproduction of the Amyloid Beta peptide and tau hyperphosphorylation. Research in the Davies lab suggests that overexpression of RCAN1 is connected to both, and appears to unite the Amyloid Beta and tau theories of neurodegeneration.

"Both are clearly important, and RCAN1 could be the link," Davies said.

The study has tremendous implications for understanding and treating Alzheimer's disease, the authors say.

The study has been published in the Journal of the Federation of American Societies for Experimental Biology.

Over the counter drugs can increase risk of dementia

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HealthAim

by LeslieD

A study conducted by researchers at the University of East Anglia (UAE) discovered that common over the counter and prescription drugs may increase the risk of dementia and death in the elderly.

The study involved 13,000 people aged 65 and over from across the UK. Researchers analyzed over 80 drugs including antihistamines, anti-depressants, incontinence drugs, blood thinners, painkillers, heartburn medications and eye drops taken for glaucoma.

The drugs were analyzed for a potential side effect called “anticholinergic activity” which affects the brain by blocking a key neurotransmitter called acetylcholine.

The risk for anticholinergic activity increases when taking a combination of the drugs, causing a cumulative effect.

The drugs in question include the antihistamines chlorphenamine (used in Piriton) and promethazine (used in Phenergan), anti-depressants amitriptyline (used in several brands) and paroxetine (used in Seroxat), the incontinence drug oxybutynin (used in Ditropan), the blood thinner warfarin, the heartburn drug ranitidine (used in the brand Zantac), alongside painkiller codeine and timolol maleate eye drops taken for glaucoma.

“This is the first large-scale study into the long-term impact of medicines which block acetylcholine – a common brain neurotransmitter – on humans, and our results show a potentially serious effect on mortality,” said Dr. Chris Fox, clinical senior lecturer at Norwich Medical School, UEA.

It is strongly recommended that patients with any concerns about their OTC or prescription medication consult their pharmacist and/or family physician.

5 Signs of Alzheimer's That Sometimes Show up Before Memory Loss

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Caring.com

Paula Spencer

Memory loss is the symptom everybody worried about Alzheimer's disease or other forms of dementia seems to focus on. After all, it's distressing -- and increasingly obvious. Yet there are other common symptoms of Alzheimer's or dementia that can turn up even earlier, researchers say.

Sometimes, according to memory experts, even doctors miss early dementia signs because they're focused on memory loss to the exclusion of other symptoms.

In fact, in 2011 Spanish researchers found that more than a third of adults who go on to develop early-onset Alzheimer's (the kind that appears before age 65) have the following symptoms early in the disease, even before memory loss is apparent. These symptoms can also be the first to appear among adults who develop Alzheimer's after age 65.

Of course, if you notice any of these symptoms, it's important to have them checked out by a doctor, psychologist, or other expert in cognition and the brain.

Early sign of dementia #1: Personality change
A warm, friendly loved one may seem to morph into a bit of a grouch -- at first occasionally, and then increasingly. A gregarious person still jokes and talks a lot but begins to say inappropriate things or make odd accusations. A mild-mannered loved one begins cursing. All of these are examples of the kinds of personality changes that can predate memory loss in someone with dementia. Often, it's only later that friends and family look back and realize that behaviors they found off-putting or upsetting weren't intentional but related to the Alzheimer's.

Early sign of dementia #2: Problems with executive functioning
Trouble carrying out basic, familiar tasks can creep up slowly but surely. The person may, for example, have difficulty doing something that involves multiple steps, like following written directions or instructions. A longtime cook may avoid complicated recipes. A hobbyist may simplify the form of his or her craft.

Other hallmark trouble areas: making plans and not following through, whether for a vacation or an activity. Not tracking bills. Not being able to solve simple problems, such as mending a broken piece of machinery he or she could once fix easily.

Early sign of dementia #3: Vision problems
Problems with depth perception or visual-spatial coordination can precede memory problems. The person may have trouble driving or even walking well without tripping on stairs. It can be hard to judge distances or see contrasts between like colors, which can lead to accidents. In a more severe example of a perception problem, the person may not recognize himself or herself in a mirror or when passing his or her reflection in a building or window on the street.

Early sign of dementia #4: Language problems
Word retrieval and getting out the right words can become apparent before friends and family notice the more common communication problem of repeating stories or questions. For example the person having trouble may stop in the middle of a sentence, unable to think of the next word. (This can happen to anyone, but when it's a sign of dementia, it happens with alarming frequency, and sometimes the person isn't even aware of doing it.) Or the wrong word may come out -- "mouth cleaner" for "toothbrush" or "picture stick" for "TV remote control."

Early sign of dementia #5: Social withdrawal
Early in Alzheimer's disease and other dementias, the person is often well aware that something is amiss, even if he or she isn't exactly sure of the source of the problem. It can be frightening to feel that you're not quite in control of your faculties all of the time. This can cause the person to use more and more energy to stay in self-command. That leaves less energy to interact with others. Sometimes the person isn't even aware that he or she seems to be losing interest in friends and family, because he or she is concentrating so hard on just getting through the day.

Social withdrawal can also be caused by a desire to avoid embarrassment or by depression -- which often develops alongside dementia.

Natural Alzheimer's weapon suggests better treatment

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EurekAlert

AUGUSTA, Ga. – Scientists have shown a molecular chaperone is working like a waste management company to collect and detoxify high levels of toxic amyloid beta peptide found in Alzheimer's disease.

It was known that the molecular chaperone, HspB1, was present in the hallmark plaque of Alzheimer's patients but its role remained a mystery.

"What we have found is HspB1 is a protective mechanism that tries to get rid of the toxic oligomers or aggregates of amyloid beta that occur in Alzheimer's," said Dr. Anil G. Cashikar, Biochemist at Georgia Health Sciences University's Center for Molecular Chaperones and Radiobiology. He is corresponding author of the study published in Molecular and Cellular Biology.

Amyloid beta peptide, or Abeta, is believed to start the cascade of events that leads to brain cell damage and death in Alzheimer's: as levels increase, the peptide starts clumping in the brain. In fact, high levels in the spinal fluid are a diagnostic marker for the disease. Molecular chaperones are known for their propensity to respond to disease-producing misfolded proteins, which is how the body views excessive Abeta.

While resulting plaques occupy prime real estate in the brain, it's still better than toxic Abeta killing neurons, Cashikar said. "We think maybe the system gets overwhelmed."

Acknowledging much work remains, the scientist is excited about identifying the protective mechanism and exploring its treatment potential.

Earlier this year, a paper Cashikar published in PLoS One showed deleting genes with a similar function from a mouse model of Alzheimer's worsened disease symptoms. The new study also showed neurons from HspB1-deficient mice were more sensitive to the toxic ravages of Abeta.

"HspB1 is present because its function is to protect cells. The implication is if we can elevate the levels of this molecular chaperone, we may be able to handle the situation a little better," Cashikar said.

He wants to exploit this natural system by developing a smaller version of the molecular chaperone that could be put into the bloodstream to leach excess Abeta from the brain. The brain has a natural protective mechanism that likely would prevent its direct application. However, the natural affinity of amyloid beta and HspB1 indicates a more distant approach could be effective. "We want to come up with smaller versions of HspB1 that can be put into the bloodstream so you can sop up the material from the brain into the blood where it can be cleared more efficiently." He also wants to explore a way to increase brain cells' natural production of protective HspB1.

Neurons actually also make the Abeta believed to attack them in Alzheimer's. The peptide's normal function in the brain is not clear, but early evidence suggests it could be involved in synaptic pruning, which is essential for memory formation. Synapses connect neurons and some existing connections must be cut for new connections and memories to be made. Why neurons start making too much Abeta and how its overproduction can be controlled are million-dollar questions, Cashikar said.

A related ongoing debate is whether the amyloid plaques and neurofibrillarly tangles, insoluble globs of protein also found in Alzheimer's, are a cause or result of the disease. Cashikar's work as well as new studies on the neurofibrillarly tangles, suggest both are protective mechanisms. Also, there is evidence of both in the brains of some healthy, elderly individuals.

GHSU Graduate Student Juhi Ojha is first author on the paper.

Recycling of Alzheimer’s proteins could be key to new treatments

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Aβ40 and Aβ42 Amyloid Fibrils Exhibit Distinct Molecular Recycling Properties”

Journal of the American Chemical Society

The formation of abnormal strands of protein called amyloid fibrils — associated with two dozen diseases ranging from Alzheimer’s to type-2 diabetes — may not be permanent and irreversible as previously thought, scientists are reporting in the Journal of the American Chemical Society. Rather, protein molecules are constantly attaching and detaching from the fibrils, in a recycling process that could be manipulated to yield new treatments for Alzheimer’s and other diseases.

In a study that focused on the fibrils associated with Alzheimer’s disease (AD), Natàlia Carulla and colleagues explain that scientists once believed that the fibrils themselves caused the memory loss and other symptoms of AD. During the last 10 years, however, suspicion has fallen on some toxic intermediate of the process through which those fibrils form in the brain. This study suggests that fibrils could be a source of those toxic intermediates.

The new study used laboratory techniques to detail molecular recycling within fibrils formed by two proteins, Aβ40 and Aβ42, which is most associated with AD. After monitoring recycling for 40 days, they found that both Aβ40 and Aβ42 molecules recycle within the fibril population, although to different extents. After 40 days, 80 percent of the molecules making up Aβ40 fibrils underwent recycling while only 30 percent did so in Aβ42 fibrils. These observations imply that Aβ42 recycles more slowly.

“In the context of AD, demonstrating that recycling occurs in the fibrils is a step forward but it is also crucial to identify the recycling species involved; whether they are individual Aβ units or small aggregates made of several units,” explains Carulla.

“It will be important to address if differences in the recycling species within Aβ40 and Aβ42 fibrils are relevant in the development of Alzheimer’s disease. We are now working towards this aim. Once we have this information, we will be in a position to devise new therapeutic strategies that can modulate recycling.”