Can Stabilizing Amyloid Stop Alzheimer's?

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Alzheimer's and Dementia Weekly

BREAKTHROUGH: Never-before-seen images have exposed a missing link in the early-Alzheimer's cascade. Taken by the world's largest synchrotron, they imply new drugs may do better stabilizing amyloid than eliminating it. Learn more about this course-changing discovery. 

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Researchers at Lund University in Sweden have used the MAX IV synchrotron in Lund - the strongest of its kind in the world - to produce images that predate the formation of toxic clumps of beta-amyloid, the protein believed to be at the root of Alzheimer's disease. 

The unique images appear to contradict a previously unchallenged consensus. Instead of attempting to eliminate beta-amyloid, or so-called plaques, the researchers now suggest stabilizing the protein. 

It is a long-held belief in the scientific community that the beta-amyloid plaques appear almost instantaneously. Hence the term "popcorn plaques". The infrared spectroscopy images, however, revealed something entirely different. 


The researchers could now see structural, molecular changes in the brain. 

"No one has used this method to look at Alzheimer's development before. The images tell us that the progression is slower than we thought and that there are steps in the development of Alzheimer's disease that we know little about. This, of course, sparked our curiosity," says Gunnar Gouras, professor in experimental neurology at Lund University and senior author of the study. 

What was happening at this previously unknown phase? Through biochemical identification the first author of the study, Oxana Klementieva, was able to look closer at these early brain changes. 

The results revealed another discovery. Namely, that the beta-amyloid did not appear as a single peptide, a widely held belief in the field, but as a unit of four peptides sticking together, a tetramer. 

This breakthrough offers a new hypothesis to the cause of the disease. The abnormal separation of these four peptides could be the start of the beta-amyloid aggregation that later turns into plaques. 

"This is very, very exciting. In another amyloid disease, transthyretin amyloidosis, the breaking up of the tetramer has been identified as key in disease development. For this disease, there is already a drug in the clinic that stabilizes the tetramers, consequently slowing down disease progression. We hope that stabilizing beta-amyloid in a similar fashion may be the way forward in developing future therapies" says Gunnar Gouras. 

The discovery could therefore alter the direction of therapy development for the disease. The aim of most clinical trials today is to eliminate plaques. 

Researchers at Lund University will now try to understand the interaction patterns of beta-amyloid preceding the aggregation process. Finding the antidote to whatever breaks the beta-amyloid protein apart could open doors towards a major shift in­ the development of therapies for Alzheimer's disease. 

Why exercise slows memory loss in Alzheimer’s

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Futurity

A stress hormone produced during moderate exercise may protect the brain from memory changes related to Alzheimer’s disease.

The findings, published in the Journal of Alzheimer’s Disease by researchers from the University of Nottingham, may also explain why people who are susceptible to stress are at more risk of developing the disease.

Increasingly there is evidence that physical and mental activity can reduce people’s chances of developing the disease or can slow down its progression but until now it has been unclear how this happens.

A research team, led by Marie-Christine Pardon in the School of Biomedical Sciences, discovered that the stress hormone CRF—or corticotrophin-releasing factor—may have a protective effect on the brain from the memory changes brought on by Alzheimer’s disease.

CRF is most associated with producing stress and is found in high levels in people experiencing some forms of anxiety and depressive diseases. Normal levels of CRF, however, are beneficial to the brain, keeping the mental faculties sharp and aiding the survival of nerve cells.

Studies have shown that people with Alzheimer’s disease have a reduced level of CRF.

Researchers used an experimental drug to prevent the hormone from binding to a brain receptor called CRFR1 in mice with Alzheimer’s disease that were free from memory impairments, therefore blocking the effects of the hormone.

They discovered that the mice had an abnormal stress response with reduced anxiety but increased behavioral inhibition when confronted by a stressful situation—in this case being placed in a new environment—and this is was due to the abnormal functioning of the CRFR1.

This abnormal stress response before the onset of symptoms may explain why people susceptible to stress are more at risk of developing Alzheimer’s.

Pardon and her team also found that interrupting the hormone from binding on to the CRFR1 receptor blocked the improvement of memory normally promoted by exercise. However, in mice with Alzheimer’s a repeated regime of moderate exercise restored the normal function of the CRF system allowing its memory enhancing effects.

The results are in line with the idea that regular exercise is a means of improving one’s ability to deal with everyday stress in addition to keeping mental abilities keen.

The switching on of this particular brain receptor during exercise increased the density of synapses, which makes the connection between nerve cells, the loss of which is thought to be responsible for the early memory loss seen in Alzheimer’s patients.

“This is the first time that researchers have been able to identify a brain process directly responsible for the beneficial effects of exercise in slowing down the progression of the early memory decline characteristics of Alzheimer’s disease,” says Pardon.

“Overall, this research provides further evidence that a healthy lifestyle involving exercise slows down the risk of Alzheimer’s disease and opens avenues for the new interventions targeting the altered CRFR1 function associated with the early stages of the disease.”

Research into Aging (Age UK) and the University of Nottingham funded the study.

Source: University of Nottingham

New Model Of Alzheimer's Derived From Skin Cells Of People With The Disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

PR Newswire

VANCOUVER, British Columbia, July 16, 2012 /PRNewswire via COMTEX/ -- Researchers at the Alzheimer's Association International Conference® 2012 (AAIC® 2012) today reported the creation of a new model of Alzheimer's derived from the skin cells of people with the disease that were reprogramed into Alzheimer's brain cells.

This new Alzheimer's model may prove to be more accurate than current mouse models of the disease and therefore can be used (a) to generate important new insights into the biology of Alzheimer's and related disorders and (b) for early stage testing of new therapies.


"Current animal models of Alzheimer's are highly engineered to express elements of the disease, and, while valuable for research, incompletely represent how the disease forms and progresses in people," said William Thies, PhD, Alzheimer's Association® Chief Medical and Scientific Officer. "In order to develop better therapies and eventually prevent Alzheimer's, we need better, more accurate animal and cellular models of the disease. This newly reported research is a significant step forward in that direction."


Most of the current Alzheimer's mouse models incorporate genetic changes found in familial young-onset forms of Alzheimer's. Although these mice have taught us about many valuable aspects of the disease, the hallmark amyloid plaques found in the brains of people with Alzheimer's do not form in the same way as in the brains of mice expressing mutant forms of the most common young-onset Alzheimer's gene, and significant brain cell death does not occur. New approaches are needed.


Andrew Sproul, PhD, a postdoctoral associate, and colleagues working at The New York Stem Cell Foundation (NYSCF) in the laboratory of Scott Noggle, PhD, the NYSCF-Charles Evans Senior Research Fellow for Alzheimer's Disease, pursued an induced pluripotent stem cell (iPSC) approach to model Alzheimer's, and reported their results for the first time today at AAIC 2012. This involves taking cells from people with the disease and their unaffected family members, typically skin cells, and reprogramming them by adding genetic factors. The resulting iPSCs can be used to model Alzheimer's in a dish.


"One advantage of this technology is that we get a near infinite supply of disease and control patient stem cells," Sproul said. "Another is that we can then turn the iPSCs into any tissue in the body. This allows us to investigate the role of various cells in Alzheimer's disease progression by manipulating the iPSCs to form different types of brain cells (forebrain nerve cells, neural stem cells, glial cells) that we and others believe are involved in Alzheimer's."


The researchers generated iPSCs from a total of 12 people with Alzheimer's and healthy controls from two young-onset, genetic Alzheimer's families. The iPSC lines have been quality-controlled, including ensuring pluripotency, which is the ability to make all kinds of cells from the endoderm (interior stomach lining, gastrointestinal tract, lungs), mesoderm (muscle, bone, blood, urogenital), or ectoderm (skin and nervous system).


"We have made both the control and Alzheimer's iPSCs into brain cells and have demonstrated that they are electrically active. These new brain cells include forebrain cholinergic neurons, which are particularly vulnerable in Alzheimer's disease," Sproul said.


"We have also begun to use the iPSC-derived neurons and neural stem cells to compare differences in cellular function between people with Alzheimer's and their unaffected relatives. For example, we, in conjunction with Dr. Sam Gandy's group at Mount Sinai School of Medicine, have demonstrated that Alzheimer's neurons produce more of the toxic form of beta amyloid, the protein fragment that makes up amyloid plaques, though this aspect of the research is preliminary," Sproul added.


The research reported at AAIC 2012 focuses on people with presenilin-1 (PSEN1) mutations, which are responsible for the most common form of rare, inherited, young-onset Alzheimer's (estimated to be less than two percent of total cases). According to Sproul, this work may provide a platform to screen new drugs that could alleviate defects caused by the faulty gene.


However, because the overwhelming majority of people with Alzheimer's have the late onset "sporadic" form of the disease, the scientists say they plan to expand their research to include large-scale production of iPSCs from people with different types of Alzheimer's.


"We have begun to extend this work by collaborating with four different institutions in New York City - the Mount Sinai School of Medicine, Columbia University, New York University, and Rockefeller University. Over the next few years, we expect to provide substantial insight into Alzheimer's and valuable tools to help create the next generation of therapeutics," Sproul said.


About AAICThe Alzheimer's Association International Conference (AAIC) is the world's largest conference of its kind, bringing together researchers from around the world to report and discuss groundbreaking research and information on the cause, diagnosis, treatment and prevention of Alzheimer's disease and related disorders. As a part of the Alzheimer's Association's research program, AAIC serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community.


About the Alzheimer's Association The Alzheimer's Association is the world's leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research, to provide and enhance care and support for all affected, and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's. For more information, visit www.alz.org or call 800-272-3900.


\\\SOURCE Alzheimer's Association

Will the new Alzheimer's drugs work

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Forbes


Michael Waldholz, 

In the coming months researchers will release results of several drug studies that will impact millions of Alzheimer’s victims and their families, as well as the fortunes of drugmakers,  Merck, Pfizer, Lilly and Johnson & Johnson  among others. Just as important, maybe even more so, the studies may finally provide evidence to support a controversial 20-year old theory of how the mind-robbing and lethal illness works.

But there’s plenty of reason to believe these studies tests will be inconclusive. The biggest worry is that even if the drugs work, the studies may show that to be effective, the medicines must be used much like anti-cholesterol pills, well  before the disease begins to show debilitating symptoms. If that’s true it will mean years of uncertainty about an effective treatment or cure. Alternately, the 

drugs may turn out to be complete busts, or only improve memory and thinking in a statistically negligible manner that will spark conflicting interpretations. And since there is nothing in drugmakers’ pipeline to replace the drugs being tested, negative results will force Alzheimer’s research back to square one for a disease that is already costing untold suffering and adding hundreds of millions of dollars a year in health costs that will explode as the population ages.

What follows is a review, a scorecard of sorts, of what is at stake. Much of this conversation will be front and center at an international research meeting beginning this weekend in Vancouver.

A primer: The experimental medicines all focus on attacking beta amyloid, a protein autopsies show masses in the brains of Alzheimer’s victims. According to the amyloid theory, these packets of plaque destroy brain cells over time, though exactly how they do this is still unknown. One school of scientists believes the plaques, which collect in small amounts in nearly all people as they reach old age, arise earlier and in much larger amounts in people with a predisposing genetic makeup. Another group argues that the clumping is merely the residue of some other unknown chain of events, so drugs designed to prevent or destroy amyloid will provide little if any benefit.

Alzheimer’s researchers, doctors and victims are literally holding their collective breath, hoping the studies will not only provide relief, but give scientists the kind of clear roadmap needed to fuel future investigations

A gene discovery backing the amyloid theory:  Just this week, a well-regarded research team in Icelandreported in the journal Nature that they had identified a gene that, when mutated, slows the body’s production an enzyme called beta secretase. This is a valuable discovery because beta secretase appears to play an important role in amyloid formation. Merck, Lilly and Esai are in advanced clinical studies of drugs that mimic the protective action of the gene by blocking the action of the enzyme. The Iceland group, under the direction of the gene-hunting company DeCode and its charismatic founder, Kari Stefansson, found that people with an unusual variant of the gene either don’t have the disease or don’t amass plaque in large amounts. Because the study involved a small number of people in Iceland, there is reason to be cautious about broader application.

• The garbage collectors:  Perhaps the most important advanced study, whose results will be reported in October, involves the drug bapineuzumab, being developed by Pfizer and Johnson & Johnson and a similar drug called solanezumab from Lilly. These medicines are laboratory produced antibodies that, given through infusions, have been shown to attack and clear amyloid from the brain. Early results of another drug, Gammagard from Baxter, a combination of plaque-clearing antibodies, will also be released at the week the Alzheimer’s Association International Conference. Even a slight increase in cognition from these drugs will likely result in FDA approval and annual sales of billions of dollars. The worry is that even there though the drugs can sterilize amyloid clumps from the brain, the patient population studied may be too far advanced in their disease to be helped, or the study not be sensitive enough to detect benefits.

Still another antibody, crenezumab, being developed by Roche’s Genentech unit, is being tested in a $100 million trial in a family in Colombia where an early-onset form of the disease is common. That trial, involving about 300 relatives, won’t be completed for years.

• The gatekeepers: Merck and Lilly are in the second of three phases of clinical trials of drugs called beta-secretase inhibitors, also referred to as BACE drugs. Unlike the antibody medicines, these drugs are being tested in pill form. The science underlying these drugs got a boost from the Iceland gene study. The idea behind these medicines is to inhibit the formation of amyloid plaque before it can cause havoc. As with the amyloid clearing drugs, there is concern that the studies underway involve patients too far into their disease.

• The takeaway: It is clear that all the drugs in development will be most effective if used early in the disease, meaning the ability to identify those at risk is critical. Even then, the health profession and policymakers will face a dilemma. Conducting population-wide screening will be enormously expensive. Giving these medicines as long-term preventive treatments will cost many billions of dollars more. This is just one of many example of why the nation’s health bill will continue to rise sharply, with or without success in battling Alzheimer’s disease.

Could a Diabetes Drug and a Supplement Work Together to Treat Alzheimer's Disease

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AC Content

Metformin is a medication used to treat diabetes. Resveratrol is a supplement that has the benefits of drinking concentrated red wine. Doctors at Dundee University say that taking both of these things together may stop
Alzheimer's disease in its tracks.

The doctors report that metformin interferes with the development of tau which are neurofibratory tangles. Neurofibratory tangles severly limit communication between brain cells in Alzheimer's disease. They also say that Resveratrol limits the formation of these neurofibratory tangles. This research could help millions of people from getting Alzheimer's disease.

Resveratrol is a type of natural phenol, and is produced naturally by several plants when they are under the attack of harmful bacteria or fungi. Resveratrol is found in the skin of red grapes. Red wine seems to contains a high level of it.

Resveratrol was added to the cells that produce abnormal proteins called amyloid-beta. The research scientists who did this found that the levels of this abnormal protein were much lower in the cells treated with resveratrol over the untreated cells. While the scientists do not think that the amounts of resveratrol found in grapes and wine could produce the results they found in their studies using larger amounts of resveratrol. These research scientists think that grapes and wine contain molecules that, like resveratrol, are strong antioxidants. The scientists feel that resveratrol can work with other drugs like metformin to fight Alzheimer's disease.

Some experts say that it is read all of..... Could a Diabetes Drug and a Supplement Work Together to Treat Alzheimer's Disease

Is Alzheimer's Disease Contageous?

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Alzheimer's disease is caused partly by the build-up of abnormal proteins in the brain. Scientists already know that one of these abnormal proteins, amyloid peptides also called beta amyloids, can be infectious.
It seems that Alzheimer’s disease is easier to catch than first thought.

Neurologist Yvonne S. Eisele and her team of fellow scientists had already proved that mice could catch Alzheimer’s disease from each other; however this only happened when the brain of a healthy mouse was injected with amyloid peptides from mice that already had Alzheimer's disease symptoms.
Now a new study shows about Is Alzheimer's Diseaase Contageous

Sydney scientists make Alzheimer's breakthrough

Sudney Morrning herald
Louise Hall

Scientists in Sydney have discovered a way to stimulate the brain's own stem cells, which has the potential to lead to a new treatment for neurological disorders such as Parkinson's and Alzheimer's disease.

Bryce Vissel and Andrea Abdipranoto at the Garvan Institute of Medical Research identified a chemical, called activin A, that is essential for the brain's own stem cells to form new nerve cells, and to repair the brain, following neurodegeneration.

Using a mouse model, the researchers showed that, following acute nerve cell damage, the brain immediately acts to repair itself by replacing the damaged nerve cells with new cells.

The researchers then showed that the brain does this by releasing activin A. But when the chemical was blocked, regeneration stopped.

After five years of laboratory testing, the researchers made the surprising finding that activin A has an essential but indirect role in regeneration: it works by inhibiting the replication and activation of inflammatory cells.

Both Parkinson's and Alzheimer's disease are associated with a severe inflammation that occurs in response to a loss of nerve cells, said Dr Vissel, Garvan's Head of Research into Neural Plasticity and Regeneration.

"If this inflammation is not properly controlled, it blocks nerve regeneration from the brain's own stem cells," he said.

Activin A appeared to keep the immune system in check so it did not become overactive, allowing regeneration to occur.

"The idea that the brain itself produces an anti-inflammatory that is in turn necessary for regeneration and repair is a very new finding, a finding with significant implications for repair of the brain in chronic neurodegenerative diseases."

Parkinson's and Alzheimer's disease result from steady ongoing nerve cell damage in the parts of the brain that control movement and memory, respectively.

At least 300,000 Australians are affected but there is no treatment that will repair the brain or even slow the progression of these devastating diseases.

Dr Vissel said: "We know the brain has the capacity to regenerate. The question is, why do killed or injured nerve cells not get replaced with new nerve cells in Alzheimer's or Parkinson's disease?"

The team's breakthrough, published online yesterday in Stem Cells, suggests regeneration could be promoted with anti-inflammatory treatments such as activin A, or other anti-inflammatory drugs.

Dr Vissel said that this..........read the whole article

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