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A research tool to evaluate new treatments for Alzheimer's

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A new imaging molecule that can detect and map plaques and tangles in the brains of people with Alzheimer's disease could eventually lead to earlier diagnosis of the devastating disease, researchers at the University of California, Los Angeles report in the New England Journal of Medicine. The compound, developed by UCLA and called FDDNP, also holds promise as a research tool to evaluate new treatments for Alzheimer's. FDDNP binds to plaques and tangles, enabling researchers to see these abnormal deposits that form in the brains of people with Alzheimer's disease on PET (positron emission tomography) scans. PET scans display maps of the brain that scientists use to understand brain function.

In a clinical trial with volunteers who reported memory problems, results of PET scans using FDDNP correlated well with the volunteers' clinical diagnoses measured by performance on memory tests. In this study, Gary Small, M.D., of UCLA, led a research team that compared PET scans using FDDNP, PET scans using another molecule (FDG) to measure brain activity, and magnetic resonance imaging (MRI), which can show areas losing brain tissue in Alzheimer's disease. Of 83 people who volunteered for the trial, researchers classified 25 as having Alzheimer's, 28 as having mild cognitive impairment, and 30 as healthy. The FDDNP PET scans were more accurate than FDG PET scans or MRI at detecting differences among the groups of volunteers, the study found. Two years later, follow-up testing on a subset of the volunteers showed that FDDNP PET scans continued to correlate well with their clinical symptoms and diagnoses.

"The hope is that better imaging techniques and markers will allow us to conduct clinical trials with fewer volunteers and in less time," says Susan Molchan, M.D., program officer in the NIA Neuroscience and Neuropsychology of Aging Program. "The ability to image brain changes may allow us to see how drugs affect the accumulation of proteins in the brain that cause Alzheimer's plaques and tangles, possibly preventing or delaying the progression of Alzheimer's."

The Best Pill For Preventing Alzheimer's .

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A study published in PLoS ONE addresses the impact of neuroprotection on Alzheimer's disease. Remarkably, the study shows that even very modest neuroprotective effects at the cellular level can lead to dramatic reductions in the number of cases of Alzheimer's. Based on data derived from 26 epidemiological studies worldwide (comprising over 60,000 subjects), Dr de la Fuente-Fernandez developed a simple mathematical model that will allow researchers to test the effect of new neuroprotective drugs. Perhaps not too surprisingly, the study suggests however that the most effective neuroprotective therapy for Alzheimer's disease may well not be a pill, but education and intellectual activity. Mounting evidence accumulated over the last few ye ars supports the notion that intellectual activity increases what neuroscientists call "the cognitive reserve". According to the model, a mere 5% increase in the cognitive reserve in the general population would prevent one third of Alzheimer's cases. Dr de la Fuente-Fernandez, a neurologist at the Hospital A. Marcide in Ferrol (Spain), points out that public health policies aimed at implementing higher levels of education in the general population are likely the best strategy for preventing Alzheimer's disease.

The dock-lock mechanism

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Nonfibrillar soluble oligomers, which are intermediates in the transition from monomers to amyloid fibrils, may be the toxic species in Alzheimer's disease. To monitor the early events that direct assembly of amyloidogenic peptides we probe the dynamics of formation of (A16-22)n by adding a monomer to a preformed (A16-22)n-1 (n = 4-6) oligomer in which the peptides are arranged in an antiparallel -sheet conformation. All atom molecular dynamics simulations in water and multiple long trajectories, for a cumulative time of 6.9 µs, show that the oligomer grows by a two-stage dock-lock mechanism. The largest conformational change in the added disordered monomer occurs during the rapid (50 ns) first dock stage in which the -strand content of the monomer increases substantially from a low initial value. In the second slow-lock phase, the monomer rearranges to form in register antiparallel structures. Surprisingly, the mobile structured oligomers undergo large conformational changes in order to accommodate the added monomer. The time needed to incorporate the monomer into the fluid-like oligomer grows even when n = 6, which suggests that the critical nucleus size must exceed six. Stable antiparallel structure formation exceeds hundreds of nanoseconds even though frequent interpeptide collisions occur at elevated monomer concentrations used in the simulations. The dock-lock mechanism should be a generic mechanism for growth of oligomers of amyloidogenic peptides. Institute of Physical and Theoretical Chemistry, J. W. Goethe University.

A new therapy for Alzheimer's disease

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There is no known cure or preventative treatment for Alzheimer's disease, a debilitating illness affecting one in 20 people over the age of 65 and one in five over the age of 80 in the UK. Worldwide, the disease afflicts more than 12 million people. Alzheimer's causes a distressing, irreversible and progressive loss of brain function and memory.

A team led by Dr. Emma Kidd at Cardiff University's Welsh School of Pharmacy made the discovery during research funded by the Alzheimer's Society, the UK's leading care and research charity for Alzheimer's disease and other types of dementia.

The results of the study show that it is possible to decrease production of a small protein called *-amyloid (A*), which is believed to be the main cause of the disease. Deposits of A* build up in the brain, preventing it from functioning properly.

The team has developed an antibody that binds to a naturally occurring protein in the brain, amyloid precursor protein (APP), preventing the production of A*. The antibody blocks the access to APP of an enzyme, b-secretase, crucial for the formation of Ab.

"Our results are highly encouraging at this stage," Dr. Kidd said. "We believe that our approach could lead in time to a new therapy for this distressing and debilitating disease as it should prevent or reduce the irreversible deterioration of a patient's memory and other brain functions. This would also reduce the burden on caretakers, usually family members, who look after patients in the earlier stages of the disease," she said.

"We also believe it is possible that our antibody could be used as a preventative treatment to protect people at high risk of Alzheimer's Disease through their family history or other factors," she said.

The work funded by the Alzheimer's Society research program, Quality Research In Dementia, was conducted on cultured cells in the laboratory. The team believes that a form of the antibody could be used as a treatment to reduce A* build-up in the brain, improving the patient's memory and quality of life. Any development of the antibody as a drug will take several years. The team is in the process of seeking funding for the next stage of development of the antibody.

The charity's Quality Research in Dementia program is led and steered by caretakers and people with dementia, who set the priorities. This ensures that funding only goes to projects with a potential for high impact on the lives of people with dementia and their caretakers.

Professor Clive Ballard, director of research at the Alzheimer's Society said: "We are thrilled to have been able to fund this innovative work. As a charity we rely on donations from the public and we hope people will understand how important it is to invest more in research into all types of dementia so that we eventually may have a selection of new treatments to change the lives of people with dementia and their caretakers."

MEM 3454 in Alzheimer's disease

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Memory Pharmaceuticals Corp. (Nasdaq: MEMY) today announced that the U.S. Food and Drug Administration (FDA) has completed its review of the investigational new drug application (IND) for MEM 3454 and has informed the Company that the clinical hold on the development of this drug candidate has been released. The Company now plans to commence its previously-announced Phase 2a clinical trial for MEM 3454 in Alzheimer's disease during the first quarter of 2007.

"Memory has worked diligently with the FDA since this trial was placed on clinical hold in October, and we are pleased that we will now be able to move forward with the proof-of-concept trial for this important drug candidate," stated Jim Sulat, President and Chief Executive Officer of Memory Pharmaceuticals. "Given the safety and pharmacokinetic results of the Phase 1 trial for MEM 3454 and the positive cognitive data generated in that trial, we believe that MEM 3454 may offer a new approach for the treatment of debilitating central nervous system disorders."

Blocking Apo E and Amyloid Beta

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Deposits of amyloid beta proteins in the brain are one of the defining characteristics of Alzheimer's disease. The prevention or reduction of such deposits is what researchers hope for in Alzheimer's disease research studies.

Researchers from NYU School of Medicine have reduced by around 50 percent the aggregation of toxic amyloid protein in the brains of mice by blocking the interaction between a protein called apolipoprotein E (apo E) and amyloid. (Apo E acts as a sort of biological chaperone, ferrying cholesterol and fats around the brain.)

"Our approach opens up a completely new avenue for therapy," says Dr. Wisniewski. "There is a lot of data showing that apo E is important in sporadic Alzheimer's disease. But until now no one has really addressed how you can manipulate its interaction with amyloid beta."

Alzheimer's affects some 4.6 million people in the United States, and the devastating neurodegenerative disease occurs most commonly as "sporadic," meaning it affects individuals who do not have rare genetic mutations.


Headed by Martin Sadowski, M.D., Ph. D., Assistant Professor of Neurology and Psychiatry and Dr. Thomas Wisniewski, M.D., Professor of Neurology, Pathology and Psychiatry, the research team created a nontoxic, synthetic protein fragment or peptide that binds to apo E, preventing it from latching onto amyloid. Once deprived of its biochemical chaperone, amyloid won't form deadly plaques.

Hormonal Therapy For Alzheimer’s

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Researchers tested the theory of a testosterone link to Alzheimer's on mice. One group of mice could not produce testosterone. "Mice with low testosterone showed rapid progression in the development of Alzheimer's disease," said Dr. Pike. "That suggests -- if you dare to extrapolate what's going on in mice might be going on in aged men -- is that in the absence of testosterone, the brain becomes a much more willing environment for the progression of the disease."

Scientists gave another group of mice extra testosterone. These mice didn't have as much beta amyloid brain plaques -- characteristic of Alzheimer's disease -- as other mice. The testosterone mice also had less memory impairment.

Using a mouse model of AD, in which three genes had been altered, researchers evaluated how experimental manipulation of sex hormones affected the progress of the disease. Researchers removed the testes of young adult male mice and over several months, treated some with a testosterone hormone and others with a placebo.

After the treatment period, memory-related behavior and measures of Alzheimer-like pathology were measured in the different groups of mice. The castrated models that received the placebo showed poor working memory and high brain levels of Aâ. However, both Aâ accumulation and cognitive decline were prevented in mice treated with the hormone therapy.

“Although the results of the study predict that androgen therapy has the potential to reduce the risk of AD in at least some men,” Pike said, “clinical studies will be required to determine when and how to use androgen therapy.”

Before anyone starts taking testosterone boosters, Dr. Pike says it's too soon to assume the hormone would be a good way for humans to ward off Alzheimer's disease.

"There's all this great promise of what testosterone might be able to do in men. The problem is, we don't know what the long-term efficacy is. We don't know what the safety is," said Dr. Pike. "We jumped ahead with this with women and estrogen-based hormone therapy and it's gotten us into a bit of a mess. There was increased risk for breast cancer and increased risk for stroke." Studies have linked testosterone to prostate cancer.

However, the new data does extend the body of knowledge scientists have on Alzheimer's. Dr. Pike said previous population data has suggested the link between testosterone and Alzheimer's that this study confirms. "This at least gives you the ability to have a screening tool to identify aging men who are going to benefit from any type of potential preventive therapies," he said. The information could also help scientists create testosterone-like drugs that would target the cause of Alzheimer's and not affect other conditions, like prostate cancer.

Scan Detects Alzheimer's

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Scientists have now come up with what appears to be a reliable non-invasive method of detecting these Alzheimer "markers" using a PET scan and a new tracer chemical called FDDNP that binds effectively to abnormal protein plaques and tangles.

PET stands for Positron Emission Tomography. A PET scan gives a three dimensional, computer enhanced and highly colourful "blurry-looking" image of the brain as it traces a positron emitting chemical (in this case FDDNP) after it is injected into the patient and travels through the tiny blood vessels in the brain. Any abnormal protein plaques and tangles show up because the FDDNP will stick to them.

Gary Small who led the study, and his team examined 83 volunteers who were psychiatrically evaluated and given cognitive tests (e.g. to detect memory and reasoning problems). 30 of the volunteers were classed as having no cognitive impairment (they were the "healthy controls"), 28 as having mild cognitive impairment, and 30 were classed as having Alzheimer's disease.

All of the volunteers underwent a PET scan using FDDNP, and they were also scanned using another PET method based on another chemical tracer called FDG. MRI (magnetic resonance imaging) scans were also performed on 72 of the volunteers.

The results showed that it was possible to tell which of the 83 volunteers was "healthy", which had Alzheimer's and which had the mild memory problems. The level of accuracy achieved was 98 per cent - significantly better than the FDG-PET method (87 per cent) and the MRI method (68 per cent accuracy).

Key factor in formation of Alzheimer's

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A team of South Korean scientists said Wednesday they have discovered a crucial factor in the formation of Alzheimer's disease, a finding likely to help develop a treatment for the neuro-degenerative disorder.

Alzheimer's disease causes a progressive loss of memory and impaired cognitive capabilities. It can be inherited, but more commonly strikes victims in old age.

The team led by Chung Sung-kwon, a medical professor at Seoul's Sungkyunkwan University, discovered that the density of PIP2, a type of an organic compound forming the base of brain cells, plays a crucial part in the inherited form of the disease.

The team claimed to have made the discovery for the first time in the world.

The familial type is known to be formed from an overflow of proteins called beta amyloid in brain cells among people with mutated presenilin, another protein. However, scientists in the past could not find the correlation between the two proteins.

The team discovered that the density of PIP2 plays a key role in controlling the level of the two proteins, and that mutations of presenilin led to an increase in PIP2 density, while an artificial increase in the PIP2 density caused a fall in beta amyloids.

"We believe that a cure for the disease could be produced when and if we figure out how to control the concentration of PIP2," Chung said.

"Our team is in the process of developing means to control the PIP2 density."
While the breakthrough is based on the more uncommon, familial form of Alzheimer's disease, Chung believs that the late-onset type could arise from a similar reason.

The team's feat was published in the latest edition of the Proceedings of the National Academy of Sciences, the official journal of the U.S. National Academy of Sciences.

2006 Favorite Alzheimer's Articles

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10. Turn Off the TV, Boost Your Memory
Switching off the television set to do a crossword puzzle or read a novel and eating heart-healthy foods like fish may be key to keeping the memory sharp into old age, a recent survey from Australia suggests.

9. Shedding Pounds May Be An Early Indicator of Alzheimers Disease
Many men and women tend to drop some pounds as they hit their 70s, 80s, and beyond. But the slow and steady weight loss of aging may speed up prior to the onset of Alzheimer’s disease, a new study shows.

8. Stress May Hasten Progression of Alzheimers Disease
Studies suggest that stress may play an important role in the progression of Alzheimer’s, a disease that causes damage to parts of the brain essential for thinking and memory.

7. Memory Deficits Linked to Brain Loss
Some older men and women who complain of “senior moments” may be losing brain cells along with their memory, according to a new study.

6. Drinking Juice Slashes Alzheimers Risk
Older men and women who drank fruit and vegetable juices more than three times a week were 76 percent less likely to develop Alzheimer’s disease than those who drank juices less than once a week, a new study shows.

5. Plaques Linked to Problems with “Episodic Memory”
Many individuals remain mentally alert into old age, despite brain lesions known as amyloid plaques that are otherwise characteristic of Alzheimer’s disease.

4. Getting Closer to an Alzheimer's Blood Test
There is still no diagnostic test for Alzheimer’s disease, an ailment that requires careful and often drawn out assessment by a clinician as memory and thinking skills gradually fade.

3. Death Rates from Alzheimer's Are on the Rise
American men and women are living longer — to an average age of 80.4 years for women and 75.2 years for men — the U.S. government reports. But death rates from Alzheimer's disease are on the rise.

2. Doctors May Fail to Recognize Anxiety in Alzheimer's Sufferers
Physicians who treat people with Alzheimer's disease often fail to recognize symptoms of anxiety, researchers report. In many cases, anxiety may be mistaken for other psychological or medical problems, and the confusion may lead to inappropriate treatment.

1. Medications May Be to Blame for Some Cases of Memory Loss in Seniors
Various commonly prescribed prescription medicines may impair thinking and memory in elderly men and women. Many of the seniors taking these drugs were given a diagnosis of “mild cognitive impairment,” a condition that may occur before the development of Alzheimer's disease.

SEE: http://www.alzinfo.org/newsletter/december192006.html

Protection against Alzheimer's Disease

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A number of studies have suggested that curcumin, the biologically active constituent in turmeric, protects against Alzheimer's disease by turning on a gene that codes for the production of antioxidant proteins. A study published December 2003 in the Italian Journal of Biochemistry discussed curcumin's role in the induction of the the heme oxygenase pathway, a protective system that, when triggered in brain tissue, causes the production of the potent antioxidant bilirubin, which protects the brain against oxidative (free radical) injury. Such oxidation is thought to be a major factor in aging and to be responsible for neurodegenerative disorders including dementias like Alzheimer's disease. Another study conducted jointly by an Italian and U.S. team and presented at the American Physiological Society's annual scientific conference, held April 17-21, 2004 in Washington, DC, confirmed that curcumin strongly induces expression of the gene, called hemeoxygenase-1 (HO-1) in astrocytes from the hippocampal region of the brain.
Alzheimer's disease results when a protein fragment called amyloidβ accumulates in brain cells, producing oxidative stress and inflammation, and forming plaques between nerve cells (neurons) in the brain that disrupt brain function. Amyloid is a general term for protein fragments that the body produces normally. Amyloidβ is a protein fragment snipped from another protein called amyloid precursor protein (APP). In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's disease, the fragments accumulate, forming hard, insoluble plaques between brain cells.
In persons with Alzheimer's disease, immune system cells called macrophages, which would normally ingest and destroy waste products-including the beta-amyloid proteins that deposit in the brain forming the plaques characteristic of Alzheimer's- don't work very well.

Research published in the Journal of Alzheimer's Disease, (Zhang L, Fiala M, et al), indicates that curcuminoids, phytonutrient compounds found in turmeric that give the spice its yellow color, stimulate the macrophages of Alzheimer's patients' to clear out beta-amyloid plaques.

Following up on earlier experiments that showed curcuminoids enhanced clearance of beta-amyloid in animals, researchers at the University of California-LA, studied the blood of six patients with Alzheimer's disease, ranging in age from 65 to 84, and three healthy controls.

When macrophages were extracted from the subjects' blood and exposed in the lab to curcumin, the macrophages of three of the Alzheimer's patients showed greatly improved clearance of beta-amyloid deposits. The patient's age and how far his or her Alzheimer's had progressed appeared to influence curcumin's effectiveness, with younger and early-stage Alzheimer's patients benefiting the most. For one delicious way to add more turmeric to your healthy way of eating, cut cauliflower florets in half and healthy sauté with a generous spoonful of turmeric for 5 minutes. Remove from the heat and toss with olive oil, salt and pepper to taste.
SEE: http://whfoods.org/genpage.php?tname=foodspice&dbid=78#healthbenefits

Participants for clinical trials

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The Roskamp Institute in Sarasota is screening potential candidates with the relapsing/remitting form of multiple sclerosis for a research study on an experimental MS drug called fingolimod that has shown promise in earlier clinical trials. It was developed by Novartis.

What makes fingolimod so exciting is the fact that this is a once-a-day capsule, said Dr. Richard Mullan, Roskamp's director. Currently the only treatment option available for this type of MS is a drug that must be given by injection, Mullan said.

The fingolimod study, which is part of the FDA approval process, is designed to determine the effectiveness and safety of the drug. fingolimod appears to help relapsing/remitting MS patients by causing white blood cells to move away from areas of inflammation and retreat to the lymph system, thereby lessening the symptoms. The white cells known as T-cells are responsible for immune reactions that characterize MS, Mullan said. And it's here - the trigger that causes the white cells to retreat - where one finds the connection that links one of the nation's leading research institutes in Alzheimer's disease with research on multiple sclerosis.

Roskamp scientists have found that patients with Alzheimer's disease and patients with MS have the same marker on their T-cells. This marker appears to act as a switch, directing the T-cells' response, said Mullan. In the case of Alzheimer's it triggers a decrease in T-cells. That leads to a build-up of a sticky substance, a protein called beta amyloid, in the brain. The build-up causes major damage to neurons, Mullan said. In MS patients, the marker appears to cause the T-cells to aggressively attack the body.

It's this very research in how that marker works to influence the T-cell that has Roskamp scientists excited, said Dr. Andrew Keegan, an investigator in the clinical trials division participating in the fingolimod study.

Treatment for Alzheimer's

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Physicians and scientists have not determined the exact cause of the disease, but they widely believe that Alzheimer's is caused by the build up of certain proteins in the brain. The proteins, called beta amyloid proteins, can damage nerve cells that are responsible for transmitting signals throughout the brain.

The damage to the brain's nerve cells has serious side effects. In many cases, the cells are unable to produce enough of a much-needed chemical called acetylcholine, which plays a key role in memory and judgment. Acetylcholine helps transmit information to other cells.

Most Alzheimer's research involves inhibiting the breakdown of acetylcholine, allowing the brain to transmit information.

The race to develop a better treatment for Alzheimer's disease took off about 10 years ago, just after the country's most widely used Alzheimer's treatment hit the market.

In 1996, the federal government approved the use of Aricept to treat the disease. Aricept is made by Pfizer and works by inhibiting the breakdown of acetylcholine. Other Alzheimer's treatments perform similar functions - but no drug is able to repair or prevent the basic cell degeneration believed responsible for the disease. In addition, Aricept and similar drugs can have side effects including nausea, vomiting, fatigue and even anorexia.

Now, 10 years later, that earlier research has set off a wider search to develop a better drug.

Targacept, for example, is developing a drug with the working name of TC-1734. The drug works by triggering certain receptor cells in the brain to release more acetylcholine, the chemical that helps transmit information. The drug would reduce the cognitive- impairment symptoms of the illness. It also seems to have fewer side effects than medications like Aricept, according to the company's studies. Targacept, based in the Piedmont Triad Research Park, has about 75 employees. It is developing drugs based on nicotine research to treat diseases of the central nervous system, which also include schizophrenia and cognitive impairment.

The company entered the public market in April. Its Nasdaq stock price debuted at $9 a share but has since ranged from $5.26 to $9 a share, reflecting the volatile biotechnology industry. Targacept officials are betting that their particular drug will deliver positive benefits. "The problem right now is there's a huge unmet need," in helpful Alzheimer's treatments, said Alan Musso, Targacept's chief financial officer. "It's just an area, right now, where the current therapeutics that are available aren't very effective."

The pharmaceutical industry is taking keen interest in the small company's research. AstraZeneca, Targacept's partner in the Alzheimer's research, makes the popular acid-reflux medications Prilosec and Nexium, for example.

Generally in developing drugs for the disease, "the failure rate is going to be high, but the reward is going to be higher," said Don deBethizy, Targacept's chief executive. TransTech Pharma is taking a different route. The company, which has about 80 employees, is using specific molecules to try to prevent Alzheimer's in patients, rather than treat the symptoms of the disease.

The company is developing molecules that could help prevent the buildup of the beta amyloid proteins believed responsible for the illness, TransTech Pharma officials said. Beta amyloid proteins can eventually kill healthy nerve cells in the brain, causing the debilitating symptoms common to Alzheimer's. A steadily aging population has made the need for drugs treating Alzheimer's disease and age-associated memory illnesses more vital, experts said. "There's a demographic tsunami coming our way, in terms of Alzheimer's disease," said Dr. Anton Porsteinsson, an assistant professor of psychiatry at the University of Rochester School of Medicine in New York. "It's a big problem today, and it's going to be a huge problem."

TransTech Pharma officials agreed. "The company that comes up with a drug that really does treat this is going to be viewed as a real savior out there," said Stephen Holcombe, the company's chief financial officer. "It's certainly a popular illness to go after."

Alzheimer's projects

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The amyloid plaques are found between nerve cells in the brains of Alzheimer's sufferers. They consist of amyloid protein fragments that are normally broken down by the body and removed. However, in people who suffer from Alzheimer's, the fragments, mainly beta-amyloid build up into hard deposits that can kill surrounding nerve cells.

The SupraAntigen Technology has generated a lead anti-beta-amyloid antibody that has been highly active in animal disease models for AD. The antibody changes the plaques from an insoluble to soluble form, enabling them to be removed by the body. This was directly linked to improvement of memory.

Genentech will cover all development and clinical costs of the lead antibody and subsequent antibody candidates.

Several other companies run Alzheimer's projects. Samaritan Pharmaceuticals have filed a patent for caprospinol (SP 233), a drug that appears to reduce the toxic effects of beta-amyloid and help remove plaques.

Irish pharmaceutical company Elan has developed ACC-001 in collaboration with US drug major. The drug induces an immune response designed to clear beta amyloid and is currently in Phase I clinical trials. A further study has shown that a drug previously approved for treatment of several immune disorders can also benefit patients with mild to moderate Alzheimer's. Weill Medical College of Cornell University, New York, have demonstrated that Intravenous Immunoglobulin (IVIg), a purified mixture of human antibodies, can be used to remove amyloid plaques from the brain. The antibiotics also appear to block the toxic effects of amyloid-beta.

Brain nerve cells and dendritic spines

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During learning and memory formation, the brain builds or remodels tiny structures on the surface of its nerve cells to store the new information. Now, a team led by Duke University Medical Center researchers has discovered where the brain gets the raw materials for such construction -- and has even taken "home movies" of the process.

The discovery, made in rodents, may lead to advances in understanding Alzheimer's disease, autism and age-related memory loss, and could point to potential treatments for these and other neurological conditions, said senior study investigator Michael Ehlers, M.D., Ph.D., an associate professor of neurobiology and a Howard Hughes Medical Institute investigator at Duke. The researchers published the findings in the Dec. 7, 2006, issue of the journal Neuron.

The team focused on specific structures in brain nerve cells, or neurons, called dendritic spines. These are tiny bumps that form on the surface of dendrites, which extend off neurons like tree branches and receive chemical signals from other neurons. Each dendritic spine "talks" with its counterpart on a nearby neuron, and collectively the two structures comprise the "synapse" that links the neurons.

The brain stores new information by changing the structure of the synapses, Ehlers said. "If we need to remember a name, directions to a location or how to perform certain motor tasks -- anything involving learning or memory, really -- our brain does it by changing the properties of synapses," he said.

During learning, synapses change in ways that make it easier for connected neurons to communicate with each other. This "plasticity" can occur in two ways. One way is structural, in which a synapse changes in size or shape; the other way is functional, in which connections between the synapses are strengthened by increasing the chemical signals sent or received by connected neurons.

In previous studies, Ehlers and colleagues at Duke found that certain cellular structures called recycling endosomes, which recycle used proteins within the cell, play an important role in controlling the functional type of plasticity. In the current study, the researchers sought to determine if recycling endosomes are involved in the structural type of plasticity as well.

To create a study model, the researchers transplanted neurons from rats into cell culture dishes. They then stimulated the neurons with chemicals and examined the cultures using a technique called live-cell imaging, in which a camera attached to a powerful microscope recorded the dendritic spines as they grew. This technique, Ehlers said, enabled the team to glimpse inside the internal world of the neuron to see how the recycling endosomes responded when neurons were stimulated. When the scientists triggered the neurons, they saw the recycling endosomes, labeled with a green dye, streaming up and down the neurons, dipping in and out of the dendritic spines. Inside the dendritic spines, the recycling endosomes deposited pieces of recycled proteins that grew new spines or changed the shape and size of existing spines, Ehlers said.

A variety of neurological disorders, including Alzheimer's disease, autism and early forms of age-related memory loss, are characterized by the loss of synapses or by the abnormal structural development of dendritic spines, he said.

An Alzheimer's vaccine that targets beta-amyloid

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The Austrian company Affiris GmbHproject is part of the sixth EU Framework Programme and is seeking to develop an Alzheimer's vaccine that targets specific types of beta-amyloid, the causative agent of Alzheimer's disease. "Alzheimer's is caused by deposits of beta-amyloid peptides. These deposits – also known as plaques – are formed when parts of a human protein detach from the cell membrane of nerve cells and clump together, Dr. Frank Mattner, Project Manager and CSO of Affiris GmbH, explains.

“A high proportion of these peptides, the so-called beta-amyloids, consist of 40 or 42 amino acids. The first vaccine developed by Affiris targets precisely these types of peptides and helps to break down the plaques." It was a technology from Affiris GmbH, that proved decisive in securing approval for the project. This technology enables scientists to get round a key problem posed by vaccines against degenerated human proteins such as beta-amyloid – the development of autoimmune reaction.

By selecting the correct peptides for the vaccine, Affiris GmbH's mimotope technology enables a precise immune reaction to be implemented against only the degenerated form of the protein, and for this to be done without attacking the natural form. This principle has already been proven in the first vaccine developed by Affiris. "The exceptional approval rating the Framework Programme's panel of independent experts gave the MimoVax project – 29 out of a possible 30 points – is, of course, also a great vote of confidence in Affiris' mimotope technology. And, actually, MIG-Fonds in Germany have already invested in this Affiris technology, thereby enabling us to reach the current stage of development for our first Alzheimer's vaccine.

“This will be used on the first patients in the coming months. Overall, this broad financial support demonstrates wide-ranging confidence in the use of mimotope technology as an efficient strategy for vaccinating against human rogue proteins." During the MimoVax project, both pre-clinical and the first clinical phases of development for the new vaccine will be carried out over the next three years.

Reduce Alzheimer's Disease With Certain Anti-hypertensive Drugs

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A new cardiovascular drug screening has identified existing anti-hypertensive agents capable of preventing cognitive decline and amyloid neuropathology associated with Alzheimer's disease. The research, conducted by Dr. Gulio Maria Pasinetti at the Mount Sinai School of Medicine in New York, NY, was released at the American College of Neuropsychopharmacology's (ACNP) annual conference. These findings suggest that a large number of geriatric patients currently under pharmacological treatment for high-blood pressure with certain anti-hypertensive drugs may also reap the benefits of the drug's cognitive effects.

Dr. Pasinetti's research is part of a growing push to identify and develop more effective treatments for Alzheimer's disease. This devastating, degenerative illness is of particular concern now Boomers begin to turn 60 and are at increased risk for developing cognitive impairment and Alzheimer's disease.

"There is no convincing evidence that there is any available drug presently on the market to cure Alzheimer's disease, and there are many questions surrounding the effectiveness of drugs that are available to delay or effectively alleviate symptoms of memory deterioration or dementia," said Pasinetti. Despite major breakthroughs over the past ten years in understanding the pathogenesis, molecular mechanisms and possible causes of Alzheimer's disease, limited progress has been done in the identification of novel therapeutic strategies that made a real impact in the prevention or treatment of the disease in the general population."

Over the past two years, researchers have begun screening drugs that are already commercially available for treatment of other disorders to determine their potential value in treating Alzheimer's disease and cognitive impairment.

Commonly prescribed drugs were administered in vitro to brain cells derived from animal models genetically predisposed to develop Alzheimer's disease amyloid neuropathology. The brain cells in vitro were then monitored to systematically assess the potential beneficial effect of novel drugs, especially in respect to generation of abnormally processed beta-amyloid.

Abnormally processed beta-amyloid has been identified as playing a key role in Alzheimer's disease pathogenesis, particularly in respect to cognitive deterioration.

Thus, characterization of novel drug treatments preventing abnormal beta-amyloid generation will help in the identification of future, novel pharmacological treatments for Alzheimer's disease.

Among several hundred drugs that were identified in Dr. Pasinetti's laboratory as having promise in preventing beta-amyloid build-up, seven of the drugs are commonly prescribed to treat hypertension. This recent, promising evidence indicates that cardiovascular anti-hypertensive agents may decrease the incidence or slow the progression of Alzheimer's disease.

During the course of the research, one drug in particular was identified as effective in blocking the accumulation of beta-amyloid in the brain and preventing the deterioration of cognitive performance. The drug, Propranololo-HCL (Inderal) for example, is widely prescribed in elderly patients to treat high blood pressure. Further research is necessary to determine if these patients may also be benefiting from the potential cognitive effects of the drug.

Pasinetti noted that it might also be possible to identify a concentration of this compound that confers the beta-amyloid blocking benefit without affecting blood pressure.

"If we can give this drug at concentrations that do not affect blood pressure, this drug could be made available for all members of the geriatric population identified as being at high risk for developing Alzheimer's disease," said Pasinetti.

Pasinetti was quick to point out the limitations of the research, noting that studies must be conducted in human subjects that examine the effects of the drug independent of its role as an anti-hypertensive agent.

"The use of these drugs for their potential anti-amyloidogenic role is still highly experimental, and at this stage we have no clinical data beyond phenomenological observation," said Pasinetti. "We need to complete clinical trials in the future if we are to identify preventive drugs, which will need to be prescribed at dosages that do not interfere with hypertension."

Deal for a New Drug

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Biotechnology giant Genentech has signed a licensing deal worth up to $300 million for a potential Alzheimer's disease treatment being developed by AC Immune of Switzerland, the companies announced Thursday. The deal involves AC Immune's early-stage research into fighting Alzheimer's by coaxing the patient's immune system to create antibodies against the beta amyloid protein, which causes a sticky plaque believed to inhibit brain functions.

South San Francisco-based Genentech already has a variety of treatments for everything from cancer and psoriasis to arthritis and asthma. Even so, "we're always open to pursuing research in other areas," said Genentech spokeswoman Caroline Pecquet. "This is just part of our business development strategy."

In October, Genentech announced it would pay CGI Pharmaceuticals of Branford, Conn., up to $500 million for treatments CGI is developing for cancer and autoimmune ailments. And in July, Genentech announced a similar deal worth up to $405 million with Inotek Pharmaceuticals of Beverly, Mass., for a cancer treatment Inotek is working on.

Under the licensing deal with AC Immune, Genentech will make payments potentially totaling $300 million if AC Immune meets milestones in developing the Alzheimer's treatment. The companies didn't explain what those milestones were. They also did not disclose how much money South San Francisco-based Genentech would pay initially or the length of the licensing arrangement. Genentech has a manufacturing facility in Vacaville.

The signing of the contract yesterday signalled the start of the active phase of the EU MimoVax project. The project is part of the sixth EU Framework Programme and is seeking to develop an Alzheimer's vaccine that targets specific types of beta-amyloid, the causative agent of Alzheimer's disease. MimoVax is now pursuing an additional strategy. The project aims to investigate whether an immune reaction can also be induced against other, rarer, forms of beta-amyloid. Indeed, not all peptides in the plaques consist of 40 or 42 amino acids. Mechanical stress or enzymes can cause some amino acids to break down or can alter their chemical composition. Although these modified peptides are also a suitable point of attack for novel treatment strategies, no relevant development programme has been started to date. MimoVax is now changing this.

It was a technology from Affiris GmbH that proved decisive in securing approval for the project. This technology enables scientists to get round a key problem posed by vaccines against degenerated human proteins such as beta-amyloid – the development of autoimmune reaction. By carefully selecting the correct peptides for the vaccine, Affiris GmbH's mimotope technology enables a precise immune reaction to be implemented against only the degenerated form of the protein, and for this to be done without attacking the natural form. This principle has already been proven in the first vaccine developed by Affiris.

Alzheimer’s Disease and Water

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Alzheimer’s disease is a progressive illness which affects the areas of the brain that involve memory, intelligence, judgment and behavior. That said, the disease is more than just the memory loss often most associated with it. Daily tasks may even begin to be impossible. As the disease progressives, the symptoms get worse. There is not an exact known cause yet, but in most cases it is due to deterioration of tissue in the brain. The deterioration may be caused by the loss of chemical messengers that in essence tell the brain what to do.
Is heavy metal really bad for you? Okay. Heavy metals, like aluminum, are thought to be a cause of a sad and debilitating memory-loss disease affecting 4.5 million people around the world. While age is the major risk factor, what we drink and eat as we age could also play a vital role.

An eight-year French study concluded that people exposed to water with high aluminum concentrates were more likely to suffer from Alzheimer’s or dementia. It was noted that aluminum could damage nerve cells and their connectors. The major symptoms of this disease are progressive decline of memory and other higher mental functions. These changes are associated with the loss of brain cells and the development of two kinds of microscopic damage in the brain, which doctors dub the plaques and tangles. The plaques consist of abnormal deposits of a protein, beta amyloid, between the brain cells. The tangles occur within the cells. These are formed from abnormal thread-like deposits of the protein tau, normally part of the cell's 'skeleton'.

There is much evidence that aluminum is associated with the disease. Studies note that there is a higher concentration of Alzheimer’s where there is also a higher concentration of aluminum in the water. In animal tests, aluminum was shown to have negative effects on the nervous system. Also, drugs that remove aluminum from the body are said to decrease the effects of Alzheimer’s. Much of this evidence is argued and great research efforts are still being put into the cause of this disease. Although there is controversy surrounding aluminum, or any other metal, causing Alzheimer’s, it doesn’t hurt to play it safe by investing in a reverse osmosis water filter or other means to get safe drinking water. In fact, some doctors will state that it is just plain unhealthy for the brain. Also, certain foods contain this metal. In addition, doctors say the mercury is also bad for the brain- a metal found in the flu shot.

A side effect of Alzheimer’s, and rightfully so, is depression. When the body is dehydrated, it is more likely to go into depression mode (see related article). So, staying healthy and hydrated can keep an Alzheimer’s patient in good spirits.

The development of anti-beta-amyloid antibodies

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AC Immune, Ltd., a Swiss Biotech Company developing innovative therapies against Alzheimer's Disease, today announced that it has entered into an exclusive global license agreement and research collaboration with Genentech, Inc. for the development of anti-beta-amyloid antibodies for the potential treatment of Alzheimer's Disease and other human diseases. Beta-amyloid constitutes an important target for disease-modification of Alzheimer's disease and AC Immune has developed conformation-specific antibodies against this protein generated by its SupraAntigenTM Technology.

Under the terms of this agreement, Genentech will make an upfront payment to AC Immune, with the potential for a total of over $300 million in payments upon successful completion of clinical and regulatory milestones for Alzheimer's and additional applications. Upon commercialization of a product, Genentech will pay AC Immune royalties on net sales of AC Immune's antibodies in the field of Alzheimer's or other human applications. Genentech will also provide funding for a multi-year collaborative research program and will cover all development and clinical costs of the lead antibody and subsequent antibody candidates.

"Out-licensing one of our lead programs to Genentech achieves a major business objective for the company and represents a significant milestone in the 3-year history of AC Immune", said Prof. Andrea Pfeifer, CEO of AC Immune Ltd. "Genentech is an excellent, and our preferred, collaborator for the antibody program due to its expertise in development and commercialization of antibodies".

"The terms of the deal will provide AC Immune with a solid financial basis beyond the next three years to develop other programs at full speed", said Dr. Armin Mader, CFO of AC Immune.

AC Immune's proprietary SupraAntigenTM Technology resulted in the development of an anti-beta-amyloid antibody program with a selected lead antibody, which has been shown to be highly active in animal disease models for Alzheimer's disease. The lead antibody is conformation-specific and induced the proposed transition from an insoluble to the soluble form of the plaque forming beta-amyloid protein. This event directly correlated with memory improvement.

"AC Immune's technology has proven very effective for the generation of conformation-specific antibodies that have potential for the treatment of conformational diseases", said Dr. Andreas Muhs, CSO of AC Immune.

"We are thrilled that Genentech has taken such an interest in our Alzheimer's antibody program", said Martin Velasco, Chairman of the Board of AC Immune. "We are hopeful that in collaboration with Genentech we may develop a potential treatment for Alzheimer's disease for the benefit of millions of patients worldwide".

The effect of Huperzine A on cognitive performance

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Neuro-Hitech, Inc. (OTCBB: NHPI), a biopharmaceutical company focused on the development and commercialization of next-generation compounds against proven targets for neurodegenerative diseases, today announced that it has decided to expand the enrollment level for its Phase II clinical trial on the efficacy of Huperzine A, a highly promising second-generation acetylcholinesterase inhibitor, for people with mild to moderate Alzheimer's. The trial will be expanded by 30 to 60 participants, an increase of up to 40% from the number originally planned. The company also has earmarked an additional $2 million in funding for the study.

"The primary reason for increasing enrollment is to boost the predictive power of the study in demonstrating the effect of Huperzine A on cognitive performance," said Dr. Paul Aisen, the principal investigator of the study and professor of neurology at Georgetown University Medical Center. In addition to the inhibition of acetylcholinesterase, the mode of action of the most widely available Alzheimer's disease drugs, Neuro-Hitech's Huperzine A has other modes of action directed against other disease targets. "Another key benefit of expanded enrollment is to improve the power of secondary analyses assessing, for example, the impact of Huperzine A on behavior and function," Dr. Aisen added.

In collaboration with leading organizations in this field -- the Alzheimer's Disease Cooperative Study, the National Institutes of Health and Georgetown University Medical Center -- Neuro-Hitech has already completed two U.S. Phase I studies and reached the original enrollment goal of 150 patients in the Phase II trials of Huperzine A. The participants are being evaluated at more than 33 locations nationwide in a double-blind, placebo-controlled efficacy trial. Patients are randomly assigned to three groups, allowing comparison of Huperzine A 200ug bid, Huperzine A 400ug bid and a placebo.

The targeted increase in enrollment builds on the momentum currently enjoyed by Neuro-Hitech, which just merged with Q-RNA, Inc., a New York-based biotechnology company focused on diseases such as Alzheimer's, epilepsy and Parkinson's. The merger enables the company to benefit from a unique mix of expertise and experience that complements its existing strengths and resources.

"By expanding the trial, which has a projected completion date of late 2007, we believe the increased enrollment will enable us to enhance the power of this study, allow for an in-depth analysis of secondary measures, and position us to move forward with clinical development," said Reuben Seltzer, Neuro-Hitech's President and CEO. "We are very confident in the potential of this clinical trial and we look forward to the results, as well as the impact that a markedly improved drug in this class could have on the treatment of patients with Alzheimer's."

Alzheimer's drug

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U.S. firm Samaritan said Thursday it is cleared to begin testing its novel plaque-clearing Alzheimer's drug. The company added that the Food and Drug Administration has requested some additional information of the safety of the drug, Caprospinol, before it can launch its proposed phase 1 study. Samaritan said its potential treatment has the potential to clear beta-amyloid plaques from the brain, the condition believed to be the cause of Alzheimer's. "The filing of this IND speaks to the scientific merit of Caprospinol and the research collaboration we have with Georgetown University," said Samaritan CEO Janet Greeson. "This is the first IND as a result of our collaboration with Georgetown University and we have high hopes Caprospinol will make a significant contribution to the treatment of suffering Alzheimer patients."

AC Immune Ltd. said it entered into a $300 million licensing agreement with Genentech Inc. for the development of antibodies for the treatment of Alzheimer's disease and other illnesses. The Swiss biotech firm will give an exclusive global license to Genentech for the development of antibodies that target a plaque-forming protein known as beta-amyloid, which is believed to be an important target for Alzheimer's disease drugs. The company did not disclose specific details of the financial arrangements, but said Genentech will make an upfront and milestone payments that could total $300 million. Genentech (NYSE: DNA), which is based in South San Fancisco and has a production facility in Vacville, will also provide funding for a multiyear collaborative research program and will cover all development and clinical costs of the lead antibody and subsequent antibody candidates. Upon commercialization of a product, Genentech will pay AC Immune royalties on net sales of AC Immune's antibodies in the field of Alzheimer's or other human applications.

Alzheimer's Disease Slowed by Anti-Hypertension Drugs

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A broad screening of existing drugs has found "promising evidence" that cardiovascular anti-hypertensive agents may decrease the incidence or slow the progression of Alzheimer’s disease and one, in particular, Propranololo-HCL (Inderal), is targeted for further study.
Among several hundred drugs that were identified in Dr. Pasinetti’s laboratory as having promise in preventing beta-amyloid build-up, seven of the drugs are commonly prescribed to treat hypertension. These findings suggest that a large number of geriatric patients currently under pharmacological treatment for high-blood pressure with certain anti-hypertensive drugs may also reap the benefits of the drug’s cognitive effects.

Over the past two years, researchers have begun screening drugs that are already commercially available for treatment of other disorders to determine their potential value in treating Alzheimer’s disease and cognitive impairment.

Commonly prescribed drugs were administered in vitro (in artificial environment, such as a test tube) to brain cells derived from animal models genetically predisposed to develop Alzheimer’s disease amyloid neuropathology. The drug, Propranololo-HCL (Inderal), is widely prescribed in elderly patients to treat high blood pressure. Further research is necessary to determine if these patients may also be benefiting from the potential cognitive effects of the drug.

The brain cells in vitro were then monitored to systematically assess the potential beneficial effect of novel drugs, especially in respect to generation of abnormally processed beta-amyloid.
This recent, promising evidence indicates that cardiovascular anti-hypertensive agents may decrease the incidence or slow the progression of Alzheimer’s disease. During the course of the research, one drug in particular was identified as effective in blocking the accumulation of beta-amyloid in the brain and preventing the deterioration of cognitive performance.

A way to reduce amyloid beta deposition

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he pathological embrace between two proteins, apolipoprotein E (apo E) and amyloid, plays a key role in the development of Alzheimer's disease by triggering the formation of neuron-killing plaques of amyloid beta protein.
The NYU scientists have now devised a way to reduce amyloid beta deposition by interfering with the deadly embrace of these proteins thereby reducing or preventing the aggregation of amyloid beta.
Amyloid beta deposits are one of the defining characteristics of Alzheimer's disease. Although scientists still aren't sure whether plaques are the initial trigger for the disease or are a consequence of it, the clumps can appear years before the onset of clinical symptoms. By the time dementia emerges, the plaques litter the brain.

Apo E acts as a sort of biological chaperone, ferrying cholesterol and fats around the brain. Deprived of its biochemical chaperone, amyloid won't form deadly plaques. The researchers reported a nearly 50 percent reduction in the aggregation of toxic amyloid protein in the brains of mice. In a series of experiments that followed, the researchers noted that the peptide reduced the amount of plaque in the brain and the amount of amyloid in the brain's blood vessels. It also did not cause any apparent inflammation or leaks in blood vessels in the animals' brains.

Finally, another set of experiments showed that the treated mice did not exhibit any memory decline when they were put into a radial arm maze, which evaluates working memory based on the animals' behavior.

The NYU researchers said they were encouraged that their synthetic peptide did not appear to cause inflammation or bleeding in the brains of the animals tested, and that the next step was transforming it into an agent that could be used clinically. "In order for a peptide like this to be used in humans it would have to be taken for many years, much like statin medications for cholesterol. Our ongoing research is now focusing on transforming the peptide used in the study into an agent that could be used clinically. It would have to be taken for a very long period of time without causing toxicity," Dr. Sadowski.

The study is published in the December 5, 2006, issue of the PNAS.

Beta-carotene may protect against Alzheimer’s

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Cognitive performance declines naturally with age, but genetics does play a part in the complex progression of Alzheimers. Indeed, in 1993 scientists reported that people with a gene that codes for the blood lipoprotein, apolipoprotein E4 (apoE4) have a higher risk of developing Alzheimer's disease at an earlier age than people with apoE2 or apoE3.

The new study, by researchers at UCLA School of Medicine, the University of Southern California, and the National Institute on Aging, used data from a seven-year cohort study of older people to investigate if serum beta-carotene levels had an effect on cognitive decline in people with differing ApoE 4 genotypes (homo- or heterozygous).

Out of the sample population of 455 people, the researchers report that nine people were ApoE4 homozygous, and 97 were ApoE4 heterozygous. Serum beta-carotene levels were measured at baseline, and cognitive function assessed using a 9-item Short Portable Mental Status Questionnaire (SPMSQ).

During the seven years of follow-up, cognitive decline (as measured by falling SPMSQ scores) was documented in 249 people. Hu and co-workers reported that the presence of at least one ApoE 4 allele was linked to a higher risk and larger decline in SPMSQ scores.

The researchers report that high serum beta-carotene levels was associated with a 89 per cent reduction in the risk of cognitive decline in people with at least one APOE 4 allele. For those with no ApoE4 alleles, high serum beta-carotene levels were associated with only a modest 11 per cent reduction in the risk of cognitive decline.

Although the mechanism of Alzheimer's is not clear, more support is gathering for the build-up of plaque from beta-amyloid deposits. The deposits are associated with an increase in brain cell damage and death from oxidative stress.

It is against the oxidative stress that beta-carotene may offer protection.

Oxidative stress during aging

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Your brain is your greatest asset but it is also your body's most vulnerable organ. It requires constant support from other major organs and is your most susceptible organ to oxidative stress during aging.

Here are some brain facts:

1. Your brain makes up only 2% of your total body weight but requires 20% of your heart�s output of blood to sustain the amount of oxygen that it needs.
2. Your brain is the most oxygen-demanding organ in your body.
3. Your brain uses chemicals (neurotransmitters) to relay important messages to other parts of your body. These same chemicals are also involved in chemical reactions that produce damaging free radicals.
4. If your brain cells become weak or die they cannot repair themselves. Their functions then can be permanently lost if cell death or damage occurs.

Given these susceptibilities, your brain is especially vulnerable to conditions that threaten oxygen supply, such as in head injury, stroke, lung diseases and heart failure. Under these conditions, brain activity will continue even without enough oxygen. This can cause problems that lead to extreme levels of oxidative stress and the over-production of damaging free radicals.

In diseases like Alzheimer's and Parkinson's, other damaging factors are at work. In Alzheimer's disease, a toxic protein called beta-amyloid, forms in your brain tissue. This protein acts as an irritant and causes inflammation in your brain. This inflammation then causes the production of free radicals that can destroy any membranes and cells in their path.

Even in a healthy brain, oxygen radicals are produced every moment during normal high-oxygen demand of neuronal activity. In a healthy brain, enzymes and nutritional antioxidants neutralize these radicals.

Bio-marker for Alzheimer's disease

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The amyloid precursor protein (APP) in brain is processed either by an amyloidogenic pathway by beta-secretase and gamma-secretase to yield Abeta (beta-amyloid 4 kDa) peptide or by alpha-secretase within the beta-amyloid domain to yield non-amyloidogenic products. The blood platelet levels of a 22-kDa fragment containing the Abeta (beta-amyloid 4 kDa) peptide, beta-secretase (BACE1), alpha-secretase (ADAM10), and APP isoform ratios of the 120-130 kDa to 110 kDa peptides from 31 Alzheimer's disease (AD) patients and 10 age-matched healthy control subjectshave been studied. Increased levels of Abeta4, increased activation of beta-secretase (BACE1), decreased activation of alpha-secretase (ADAM10) and decreased APP ratios in AD patients compared to normal control subjects. These observations indicate that the blood platelet APP is processed by the same amyloidogenic and non-amyloidogenic pathways as utilized in brain and that APP processing in AD patients is altered compared to control subjects and may be a useful bio-marker for the diagnosis of AD, the progression of disease and for monitoring drug responses in clinical trials.

Statins can affect Alzheimer’s disease
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A newly published editorial in Expert Opinion on Investigational Drugs has concluded that statins, the widely used cholesterol drugs, “probably strike at the heart of the sporadic Alzheimer’s disease-inducing mechanism” (Expert Opin. Investig. Drugs (Dec. 2006) 15(12):1479-1485). The editorial, “Can statins put the brakes on Alzheimer’s disease?”, reviews current research into the potential benefits that statins may offer for the prevention or treatment of Alzheimer’s disease and concludes that statins can affect Alzheimer’s disease (AD) in at least two ways: by reducing cerebrovascular damage and by inhibiting some of the biochemical pathways believed to be implicated in the disease process.
This may become welcome good news for AD patients and their families. Statins are well-known, widely available cholesterol-lowering drugs with a well-established track record of safety and may offer a relatively straightforward regulatory path to a new treatment for Alzheimer’s disease. Statins are the biggest-selling prescription pills in pharmaceutical history with estimated 2004 global sales of $26 billion. Further trials are needed to advance these findings according to the editorial.