Stress accelerates Alzheimer's progression
.
Alzheimer's Donation
Donate Online Now
.

A new research by scienctists at the University of California, Irvine has found that stress hormones appear to rapidly exacerbate the formation of brain lesions that are the hallmarks of Alzheimer’s disease.
The findings suggest that managing stress and reducing certain medications prescribed for the elderly could slow down the progression of Alzheimer’s.
The study, which was conducted on genetically modified mice, was carried out by a team of researchers led by Frank LaFerla, professor of neurobiology and behaviour.
The boffins found that when young animals were injected for just seven days with dexamethasone, a steroid hormone with anti-inflammatory properties that controls the metabolism of carbohydrates, proteins, and fats similar to the body’s stress hormones, the levels of the protein beta-amyloid in the brain increased by 60 percent. When beta-amyloid production increases and these protein fragments aggregate, they form plaques, one of the two hallmark brain lesions of Alzheimer’s disease.
The scientists also found that the levels of another protein, tau, also increased. Tau accumulation eventually leads to the formation of tangles, the other signature lesion of Alzheimer’s.
“It is remarkable that these stress hormones can have such a significant effect in such a short period of time. Although we have known for some time that higher levels of stress hormones are seen in individuals in the early stages of Alzheimer’s, this is the first time we have seen how these hormones play such a direct role in exacerbating the underlying pathology of the disease,” Frank LaFerla said.
The increased accumulation of beta-amyloid and tau appears to work in a “feedback loop” to hasten the progression of Alzheimer’s.
“This study suggests that not only is stress management an important factor in treating Alzheimer’s disease, but that physicians should pay close attention to the pharmaceutical products they prescribe for their elderly patients,” said Kim Green, a postdoctoral researcher in neurobiology and behavior and first author of the paper.
“Some medications prescribed for the elderly for various conditions contain glucocorticoids. These drugs may be leading to accelerated cognitive decline in patients in the early stages of Alzheimer’s,” Green added.

In search of Alzheimer’s
.
Alzheimer's Donation
Donate Online Now
.

Does the diagnosis of dementia come years too late? There’s plenty of evidence that the processes leading to Alzheimer’s disease (AD) and other dementing illnesses begin as early as age 30 or 40. Dementia, according to the Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), is a syndrome that may be caused or characterised by multiple cognitive deficits, which include memory impairment and at least one of the following: aphasia, apraxia, agnosia or disturbance in executive functioning. Social or occupational function is also impaired. Moderate dementia, according to the standard Clinical Dementia Rating Scale, implies difficulty in performing acts like dressing, bathing, and toileting. Yet it is estimated that more than two-thirds of people with Alzheimer’s disease are already moderately demented by the time they receive a diagnosis, and more than half of those now suffering from dementia have never been diagnosed by a physician.Some may wonder whether early diagnosis matters, since as yet there is no way to cure or prevent the most common type of dementia. However, research is producing both more potential ways to recognise the symptoms at an early stage and more reasons for needing to.Early diagnosis of AD allows time to initiate appropriate treatments that may delay cognitive deterioration and to consider such nonpharmacologic interventions as behaviour therapy. Additionally, early diagnosis provides the patient and family with time to plan for caregiving and management decisions, proper referrals and legal and financial decisions. More importantly for research purposes, earlier detection of the signs of dementia would make clinical trials easier to conduct, and the development of drugs and other treatments would become quicker, safer, and more effective. Here, the two lines of research converge and reinforce each other. The earlier we can detect Alzheimer’s disease, the better chance we have of finding ways to treat or prevent it; and the more we learn about risk factors and potential treatments, the more important early detection will become.However, given the lack of an effective treatment, early detection could have some drawbacks. Surveys show that most people don’t want to take a test for future Alzheimer’s disease unless it is more than 90% accurate — a level that is still unreachable. A study found that children of Alzheimer’s patients did not become depressed or anxious when they were told that they carried the APO E4 genetic variant. But they were six times more likely to buy long-term care insurance, which is both good and bad news. Certainly in the US, federal law restricts the use of genetic information to deny health insurance, but the law does not apply to long-term care insurance. If the number of people carrying this insurance who develop Alzheimer’s increases, the cost will rise for everyone.That problem requires a political solution, but otherwise knowing the risk has obvious advantages. Patients can decide whether to participate in clinical research. People who learn they are not going to develop Alzheimer’s will be able to rest easier. Early diagnosis would also allow patients with other, reversible causes of dementia to receive proper treatment.

A New Tool Against Brain Disease
.
Alzheimer's Donation
Donate Online Now
.

Snail toxin may spur new meds for Alzheimer's, Parkinson's, depression
University of Utah researchers isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases.
"We discovered a new toxin from a venomous cone snail that may enable scientists to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh.
Discovery of the new cone snail toxin will be published Friday, Aug. 25 in The Journal of Biological Chemistry by a team led by McIntosh, a University of Utah research professor of biology, professor and research director of psychiatry, member of the Center for Peptide Neuropharmacology and member of The Brain Institute.
McIntosh is the same University of Utah researcher who – as an incoming freshman student in 1979 – discovered another "conotoxin" that was developed into Prialt, a drug injected into fluid surrounding the spinal cord to treat severe pain due to cancer, AIDS, injury, failed back surgery and certain nervous system disorders. Prialt was approved in late 2004 in the United States and was introduced in Europe last month.
Prialt, sold by Ireland's Elan Pharmaceuticals, took roughly 25 years to reach market after its discovery in venom from the fish-eating cone snail Conus magus or magician's cone. McIntosh says he expects it will take 10 to 20 years to develop new medications based on what is learned from the new toxin – named alpha conotoxin OmIA (oh-em-one-ay) – isolated from a cone snail species named Conus omaria, which lives in the Pacific and Indian oceans and eats other snails. It ranges from 1¾ to 3½ inches long.
McIntosh discovered and analyzed the new toxin with help from University of Utah cone snail research pioneer Baldomero "Toto" Olivera, who is a distinguished professor of biology, and lab technicians Sean B. Christensen and Cheryl Dowell.
Other coauthors of the study are Palmer Taylor, professor and dean of pharmacology at the University of California, San Diego, and his associates – Todd Talley, Igor Tsigelny and Kwok-Yiu Ho – as well as Kyou-Hoon Han at the Korea Research Institute of Bioscience and Biotechnology.

Alzheimer's reversed in mice
.
Alzheimer's Donation
Donate Online Now
.

Giving mice with Alzheimer's disease a certain enzyme seems to restore memory, U.S. researchers said Thursday.
The enzyme is called ubiquitin C-terminal hydrolase L1 (Uch-L1), said the team at Columbia University Medical Center in New York.
The research was led by Ottavio Arancio and Michael Shelanski, who noted that, when the mice were given supplemental Uch-L1, their ability to form new memories returned.
"What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins," Arancio said.
Because amyloid beta proteins play important roles in the rest of the body in both mice and humans, the researchers said it was not possible to eliminate them to slow Alzheimer's.
Shelanski added that, although their discovery was promising, it was currently useful only in animals and it would take some time before it could lead to therapies in humans. "We continue to work towards that crucial goal," he said.
Uch-L1 is part of a biochemical network that controls the CREB molecule, which is necessary for normal memory in mice. CREB is inhibited by the amyloid beta proteins that are produced in the brains of mice and humans with Alzheimer's disease and cause the memory impairment and brain damage typical of the disorder.

Scyllo-inositol appears promising for Alzheimer's disease
.
Alzheimer's Donation
Donate Online Now
.

Scyllo-inositol " is an exciting experimental therapy, but until it has actually been tested in humans, it should not be considered the cure for Alzheimer's disease," St George-Hyslop said. " There are many things that are very promising when done in animal models that turn out to either not work in humans or to have unexpected toxicity." St George-Hyslop and his colleagues are optimistic that scyllo-inositol will be less toxic to humans than some previous drug candidates for Alzheimer's disease. A vaccine designed to destroy beta-amyloid, for example, was first tested successfully in the same type of mice used in the scyllo-inositol studies, but the vaccine turned out to be toxic in some humans. It caused an autoimmune reaction in about 10 percent of patients who were immunized, St George-Hyslop said.Autoimmune responses shouldn't be a problem with scyllo-inositol. " This compound works by a different mechanism and doesn't involve immunizing a patient with his own protein, which was probably the origin of the allergic reaction to the vaccine, " the researcher said.Another complication with previous attempts to treat Alzheimer's disease has been that some compounds, such as beta secretase inhibitors, cannot enter the brain easily, St George-Hyslop explained. Scyllo-inositol, on the other hand, readily passes through the blood-brain barrier where it is made available to the central nervous system.Even if scyllo-inositol does prove safe and effective in humans, patients will likely still need drugs designed to attack other aspects of Alzheimer's pathology, such as tau neurofibrillary tangles, St George-Hyslop said.

Diabetes research could aid in Alzheimer's fight
.
Alzheimer's Donation
Donate Online Now
.

A growing body of scientific evidence showing strong links between diabetes and Alzheimer's disease could have major health implications for a Canadian population that is getting older and fatter.
Several recent studies suggest Type 2 diabetes, a mounting concern in Canada and around the world that is usually associated with obesity, increases the risk of Alzheimer's disease by up to 70 per cent and adds dementia to the arsenal of plagues already threatening diabetics, including heart disease, stroke, kidney failure, blindness and amputations. Experts say the global explosion of diabetes could substantially increase the burden of Alzheimer's disease, which is already set to become bigger as baby boomers turn 60 this year and fast approach the age of highest risk for developing the deadly form of dementia. The link between the two common maladies -- buildup of a sticky, gunky plaque called beta-amyloid that clogs up brain cells in those with Alzheimer's, and was also recently discovered in the pancreases of people with Type 2 diabetes -- is leading researchers around the world to seriously ponder whether both are actually different forms of the same disease.

Several studies also found that people with poor blood-sugar control have a higher risk of Alzheimer's. These discoveries, Dr. Diamond said, "are opening up an entirely new thinking about Alzheimer's disease. . . . The particular risk factor for Alzheimer's that seems to be genuinely increasing most is diabetes, and that will mean an increase in Alzheimer's disease numbers."

Enzyme May Help Memory in Alzheimer's
.
Alzheimer's Donation
Donate Online Now
.

Scientists have discovered an enzyme that could thwart some Alzheimer's memory problems.
Columbia University's Bing Gong, MD, and colleagues describe the enzyme, called Uch-L1, in the journal Cell.
Alzheimer's diseaseAlzheimer's disease erodes memory. Brains affected by Alzheimer's tend to be low in Uch-L1, according to Gong's team.
They used Uch-L1 to help mice with Alzheimer's brain plaque make new memories.
The enzyme "could be an attractive target for the development of new therapeutic approaches to Alzheimer's disease," write the researchers.
First, the scientists studied healthy mice without brain plaques. They gave some of the mice a shot that blocked Uch-L1. Gong's team then put the mice in a special cage, one by one, and tried to train them, using a mild foot shock, to stay still. The mice that had gotten the enzyme-blocking shot were less likely to stay still in the cage.
Next, the researchers made a protein that includes Uch-L1. They injected that protein into mice that had brain plaque. The mice that got the Uch-L1 shot were more likely to learn to stay still in the test cage, just like healthy mice, starting three weeks after the Uch-L1 injection.
The enzyme didn't destroy brain plaque's building blocks, which are called amyloid beta proteins. That might be a good thing, according to Columbia University's Ottavio Arancio, MD, PhD.
"Because the amyloid beta proteins that cause Alzheimer's may play a normal, important physiological role in the body, we can't destroy them as a therapy," says Arancio, who worked on the study, in a Columbia University news release. "What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins," Arancio adds. The enzyme needs much more study before it's ready for human tests, the researchers note.

During the recent International Conference on Alzheimer's Disease and Related Disorders (ICAD), IOS Press was honored to present Queen Sofia of Spain with a commemorative edition of Alzheimer's Disease: A Century of Scientific and Clinical Research. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=50446&nfid=al

Treatment for Alzheimer's Disease
.
Alzheimer's Donation
Donate Online Now
.

Treatment of high blood sugar may have a scientific connection to memory loss that could, one day, benefit millions of people with Alzheimer's Disease, which affects up to 4.5 million older Americans, bringing with it impaired thinking and memory.
New research at the University of Virginia Health System and Case Western Reserve University shows that a drug approved by the Food and Drug Administration to treat type 2 diabetes may hold promise in treating Alzheimer's as well, without serious side effects. "We believe that the drug may reduce the body's inflammatory reaction to one of the toxic components that builds up in Alzheimer's, called amyloid plaque," said Dr. David Geldmacher, an associate professor of neurology at UVa.
The drug, called pioglitazone HCl, was tested in a placebo-controlled trial involving 25 people with mild to moderate Alzheimer's. The study assessed the safety of the drug and, although the treatment appeared to reduce Alzheimer's progression, the study was too small for investigators to be sure of the effects on memory and everyday abilities. However, the findings are promising enough, researchers say, to carry out larger studies of pioglitazone.
The research was presented July 16 to the world's largest Alzheimer's conference, ICAD 2006, in Madrid, Spain. It was selected by ICAD organizers to be highlighted because of a growing sense of the relationship between diabetes and Alzheimer's.
"We don't know exactly how pioglitazone works in Alzheimer's, but there are two possibilities," Geldmacher said. "It could be that the drug reduces the body's response to the amyloid protein found in Alzheimer's. Or, it could be that this drug helps brain cells function. The real advantage is that it's a completely novel approach to treating the disease."
In the next few years, Geldmacher and his colleagues hope to study the effectiveness of pioglitazone in a group of 200 to 300 Alzheimer's patients nationwide. "If it works, this treatment might allow people to better hold on to memory and brain function over a period of time, despite having Alzheimer's," Geldmacher said. "It could also complement other treatments and become part of a multi-pronged approach to Alzheimer's treatment." Right now, there are 5 drugs approved by the FDA to treat Alzheimer's, Geldmacher said, but pioglitazone is unrelated to any of the others. The trial of pioglitazone at UVa and Case Western Reserve was supported by the National Institutes of Health and Takeda Pharmaceuticals North America, Inc., which manufactures the drug.

Closer To Early Alzheimer's Diagnosis
.
Alzheimer's Donation
Donate Online Now
.

A painless skin test for Alzheimer's disease? It may seem unlikely, but scientists at the Blanchette Rockefeller Neurosciences Institute (BRNI) have isolated a substance in skin cells that may provide doctors with a quick and accurate yes-or-no answer when they suspect a patient is showing early signs of the disease. The test could be performed easily by a nurse or medical technician in a doctor's office or outpatient clinic.

Many scientists have concluded in recent years that Alzheimer's effects are found throughout the body, not just in the brain. By testing for signs of Alzheimer's-related inflammation in skin cells called fibroblasts, the BRNI team has located a biomarker for the disease that can be tested without the invasive tests previously required, such as a lumbar tap.

Alzheimer's disease stimulates a change in the enzyme, MAP Kinase Erk 1/2. When fibroblasts are tested by exposing them to Bradykinin, a common inflammatory signal, the Erk 1/2 response in skin cells of Alzheimer's patients was sharply distinguished from the results in cells from age-matched controls. It was also differentiated from the skin cells from patients with non-Alzheimer's dementias, such as Parkinson's disease, multiple infarct dementia and Huntington's chorea.

Scientists have created an Alzheimer's Index that may contribute greatly to physicians' evaluations of patients with dementia. The index is a mathematical formula that allows the scientists to convert the test results for each patient to a single number. The results demonstrate that when the Alzheimer's Index agrees with the clinical diagnosis of the presence of Alzheimer's, there is a high probability of accurate diagnosis.

Overweight and Alzheimer’s linked
.
Alzheimer's Donation
Donate Online Now
.

The link between obesity and Alzheimer's has been known for some time, says Professor Ralph Martins. What hasn't been found is the exact mechanism, he says. Prof Martins holds the inaugural chair in Aging and Alzheimer's Disease at Edith Cowan University in Perth, Western Australia. In collaboration with researchers in Melbourne, Prof Martins has been studying a protein - beta amyloid - which builds up in the brain. "What we are finding is that people who are obese have a high level of this particular protein in their blood." Beta amyloid acts as a neurotoxin, killing brain cells. It does that by promoting oxidative stress resulting in increased radical formation, Prof Martins explains. Melbourne research recently showed that it acts as an enzyme, "so it generates hydrogen peroxide", he says. "Basically, it bleaches your brain when there's too much of it."
Beta amyloid, we think, is going to be a key candidate to check out
The Perth researchers feel that as people become more overweight, the risk creeps up and are now studying a group of 200 people to establish that correlation. The study is in the early days, says Prof Martins. "But what we are clearly showing is that if you have low levels of HDL (good cholesterol), levels of beta amyloid are high."HDL can be raised by exercise and moderating alcohol consumption, says Prof Martin. Studies with mice have shown that animals with high deposits of beta amyloid benefit when put on the treadmill for six to eight weeks. "You see a very marked lowering of amyloid in the brain." Physical activity is important in preventing Alzheimer's, stresses Prof Martins. The health message for preventing Alzheimer's, it seems, is the same as it is for staying healthy in general. Eat a good diet with plenty of antioxidants, cut back on alcohol, watch your cholesterol and exercise.

Clinical diagnosis of Alzheimer's is still difficult, agrees Prof Martins. What's needed is "a good blood test", he says. But in order to be definitive, a larger study needs to be done and that is the next step for Prof Martins and his colleagues in Melbourne.The need is strong. Two hundred thousand Australians suffer from dementia: 70 per cent with Alzheimer's Disease. By 2050, the projections are for 700,000 people to have a form of dementia. The earlier the onset of the Alzheimer's, the faster the progression, says Dr Martins. People who have a genetic defect can begin to manifest symptoms in their thirties, he says. Within six years their cognitive functioning can cease and they would need full time care.What drugs are available treat only the symptoms, he says and have a very short term effect. "That is why is it's so essential to get drugs which tackle the cause of the disease."Yet, the professor is optimistic. There are many groups worldwide researching the condition, he says. "I anticipate within three to four years, the first of these drugs will come on the market."

Protect Against Protein Aggregation
.
Alzheimer's Donation
Donate Online Now
.

Alzheimer's disease now strikes more than one in 30 Americans, and about half the population that lives past 85 acquires Alzheimer's. Approximately one million Americans have Parkinson's disease, including three out of every 100 people over age 60. Aging is the most important risk factor for both of these diseases.
The new study-conducted in a C. elegans model, a roundworm that expresses a protein whose aggregation appears to cause Alzheimer's disease-showed that toxicity from protein aggregation is "drastically reduced" when aging is slowed by modulating the insulin growth factor (IGF) signaling pathway.
Moreover, the researchers found two novel independent activities promoting this cellular survival. The first protective mechanism disassembles and cuts up protein aggregates. Surprisingly, the second protective mechanism enables the formation of larger aggregates from smaller ones that appear to be more toxic.

"Now, we want to use this mechanistic information to discover the macromolecular basis for these activities and to discover small molecules that will delay the aging program and thus delay the onset of proteotoxicity associated with these diseases by modulating aggregation and disaggregation activities," Kelly states. "The hope is that, by manipulating the protective mechanism inherent in cells, we can find a single entity-a single drug-that would be useful for a variety of neurodegenerative diseases where protein aggregation leads to neurodegeneration."

Points toward mechanism of age-onset toxicity of Alzheimer's protein
.
Alzheimer's Donation
Donate Online Now
.

Like most neurodegenerative diseases, Alzheimer's disease usually appears late in life, raising the question of whether it is a disastrous consequence of aging or if the toxic protein aggregates that cause the disease simply take a long time to form.
Now, a collaboration between researchers at the Salk Institute for Biological Studies and the Scripps Research Institute shows that aging is what's critical. Harmful beta amyloid aggregates accumulate when aging impedes two molecular clean-up crews from getting rid of these toxic species.

New model for neurodegenerative diseases

Half of all people who reach age 85 will likely be affected by Alzheimer's disease, and the onset age – usually around 75 – is almost the same for all sporadic neurodegenerative aggregation diseases. Thus, Salk researchers have developed a model that explains why these disorders diseases occur late in life.Throughout life, brain cells produce aggregation-prone beta-amyloid fragments that must be cleared. "This process is very efficient when we are young but as we get older it gets progressively less efficient," says Cohen. As the affected individual reaches the seventh decade of life the clearance machineries fail to degrade the continually forming toxic aggregates and the disease emerges. In individuals who carry early onset Alzheimer's-linked mutation, an increased "aggregation challenge" leads to clearance failure and the emergence of Alzheimer's much earlier – usually during their fifth decade."It was very satisfying when the biochemical data from Jeffery's lab and genetic results from our lab came together," recalls Dillin. Both scientists are continuing the collaboration by searching for small molecules that delay the aging program and boost protective mechanisms.Other contributing authors were co-lead author Jan Bieschke, Ph.D., formerly at Scripps and now at Max Delbrueck Center in Berlin, and research assistant Rhonda M. Perciavalle.

A “Leaky” Blood-Brain Barrier And Alzheimer's
.
Alzheimer's Donation
Donate Online Now
.

Alzheimer's disease (AD) affects 4.5 million Americans according to the National Institutes of Aging; the direct and indirect costs of the disease exceed $100 billion each year. As the wave of baby boomers continues to age it is apparent that the number of people with AD will increase, along with the costs for care. While no one knows the precise underlying cause leading to the characteristic pathology of the disease, a new study finds that a “leaky” blood-brain barrier (BBB) - and levels of water-soluble antioxidants - may offer clues to unlocking this haunting disease.--

As expected, the concentration of AA was higher in the CSF compared to the plasma reflected by a CSF-to-plasma ratio of AA greater than 1.0 in all cases, with an average of 4.0. In contrast, the concentration of UA in the CSF was lower than plasma reflected by a CSF-to-plasma ratio of UA was less than 0.25 in all subjects. -- The mean CSF-albumin index was 7.2. However, in 22% of the study participants, the CSF-albumin index was greater than 9.0, indicating blood-brain barrier disruption. -- There were no correlations appreciated between plasma AA and age, gender, APOE status, MMSE at baseline or rates of clinical decline at 12 months. However, a positive correlation did exist between plasma AA and hippocampus volume at baseline and at 12 months. Study participants in the upper 25% of plasma AA at baseline showed the least temporal-lobe volume rate of decline at 12 months. -- CSF-to-plasma AA ratio inversely correlated with hippocampus volume rate of decline and temporal-lobe volume rate of decline at 12 months. An inverse correlation between CSF-to-plasma AA ratio and CSF-albumin index, and a positive correlation between the CSF-to-plasma UA ratio and the CSF albumin index was significant.

Current And Future Approaches To Dementia Diagnosis
.
Alzheimer's Donation
Donate Online Now
.

Given that Alzheimer's disease and most of the other dementias have specific biologic findings at autopsy, one would think that the clinical diagnoses would be very straightforward. Not so! In fact, clinical diagnoses are often difficult, causing confusion in research settings and delays in treatment. The September issue of SAGE Publications' Journal of Geriatric Psychiatry and Neurology brings together some of the world's experts to review the current and future approaches to dementia diagnosis as the American Psychiatric Association prepares for the fifth update of its Diagnostic and Statistical Manual (DSM-V). Many different issues in dementia and its diagnosis are discussed in the journal, including such topics as: # The frequencies of different types of dementia (about 80% of cases are Alzheimer's) # The differences between normal memory impairment in an aging brain and dementia # The agreement on the definition of dementia between the American Psychiatric Association and the World Health Organization# Improved assessment tools such as brain imaging and the testing of blood and spinal fluid # Diagnosing non-cognitive symptoms, such as psychosis, depression, sleep disturbance, and agitation Genetic research and how it relates to dementias "As new and better medications become available for the treatment of Alzheimer's disease, an early and accurate diagnosis becomes increasingly important for researchers, physicians, patients and their families. This collection of articles summarizes the state-of-the-art in dementia diagnosis and points the way to a future where we might diagnose and even treat Alzheimer's disease and other dementias before classic memory symptoms are evident. This would represent a major medical advance for all of us," states guest editor, Trey Sunderland MD, from the National Institute of Mental Health, about the special issue of Journal of Geriatric Psychiatry and Neurology. The issue is available to read at no charge for a limited time at http://jgpn.sagepub.com/ .

Purified water
.
Alzheimer's Donation
Donate Online Now
.

Trace amounts of metals such as copper and lead can be present in tap water and, depending on their levels, could affect your health. The risks of lead are well-documented - if you live in a house built before 1930, you should check that any old lead plumbing has been replaced with copper.
Could copper itself cause problems? Research in the US on animals suggested that trace copper ions present in drinking water can stop amyloid beta protein from being cleared from the brain (Alzheimer's disease is characterised by a built-up of this protein).
Follow-up studies concluded that drinking purified tap water could cut the risk of Alzheimer's-like memory problems - at least in experimental animals. Trials on people have yet to be carried out.

Too much ‘bad’ fat plus copper may lead to mental decline

‘Breakthrough’ news presented at Alzheimer’s meet

Alzheimer’s Disease: New Doors Opened
.
Alzheimer's Donation
Donate Online Now
.

In a recent research, US scientists have been able to pinpoint to the exact causes of Alzheimer’s disease. The research has found that Alzheimer’s disease is caused due to aging. It is caused by the brain’s inability to clean house as it gets older.
Scientists have discovered molecular janitors that clear away a gummy muck, but in the later stages of life, the janitors are not able to clean and this causes Alzheimer’s disease.
The finding helps explain why Alzheimer's is a disease of aging. The experiment was performed on a roundworm at California's Salk Institute for Biological Studies and Dr. Dillin and his team said that roundworms were used because they are commonly used in age related genetic research. It has been pointed out for the first time that a genetic link is present between aging and the onset of one of the world's most scourging brain diseases.
The accumulation of toxic protein, called beta-amyloid is the cause for Alzheimer’s. Dillin found two genes that are responsible for preventing these toxic proteins from multiplying. One gene, called HSF-1, destroys toxic protein inside cells. Another called DAF-16, herd’s toxic proteins cluttering the environment outside cells into less harmful clumps.
The study found that these genes become dormant with age. The disease makes a person lose his memory in the initial stages and later causes death. Less than 5 percent of cases are believed to be caused by a genetic defect, and the rest mysteriously appear with age.
Scientists say that the findings have opened doors for the development of drugs that will prevent build up of the toxic protein. Preliminary drug tests have started and show some effect in preventing the build up of the toxic protein. They provide some of the first steps toward new drugs that might someday boost the HSF-1 gene in humans and stop Alzheimer's in its tracks.

New Research Points Toward Mechanism Of Age-Onset Toxicity Of Alzheimer's Protein

New Biomarkers Could Help Doctors Spot Alzheimer's And Other Neurodegenerative Diseases

A Cure For Alzheimer’s?
.
Alzheimer's Donation
Donate Online Now
.

Even though it afflicts more than 4.5 million Americans, Alzheimer’s became more of a high-profile disease after it became known that former President Ronald Reagan suffered from it.
The toll of the disease is expected to triple by 2050 as the nation’s population becomes older.
So it’s remarkably good medical news that scientists may have isolated the reason for Alzheimer’s. The lead suspect is a gooey protein called beta-amyloid. All brains contain it, although healthy brains somehow get rid of excess amounts. Scientists now believe that the molecular janitors that clean away the protein break down in some older patients, causing Alzheimer’s. They also suspect the "toxic aging" plays a role in other neurodegenerative diseases.
Scientists are now trying to create drugs that will rid the brain of the excess amyloid. There is no projected cure date but the identification of the beta-amyloid buildup – and the proteins that clear it away in healthy brains – is a giant step forward in research.
Alzheimer’s is a particularly horrific disease, causing suffering and anguish not only to the patient, but to his or her relatives also. Watching a relative mentally degenerate is a wrenching experience.
Sadly, scientists will not find a cure within the next week, or the next year, but there is more hope today than there was last week.
The research shows again that it might be better for a culture to be acquainted with the names of scientists who improve the quality of life, rather than brainless celebrities, who tend to degrade it.

Alzheimer’s Disease Treatment May Involve Molecular Janitors

Genetic link is identified for aging, Alzheimer's

Alzheimer's study results reported

.
Alzheimer's Donation
Donate Online Now
.

U.S. scientists say they've determined Alzheimer's disease is caused by aging and not the aggregates of a toxic protein.
Like most neurodegenerative diseases, Alzheimer's disease usually appears late in life. And that raised the question of whether it is a disastrous consequence of aging or if the toxic protein aggregates that cause the disease simply take a long time to form.
In a collaboration of researchers at the Salk Institute for Biological Studies and the Scripps Research Institute, scientists have shown aging is critical to its cause. Harmful beta amyloid aggregates accumulate when aging impedes two molecular clean-up crews from getting rid of those toxic species.
The finding, say the scientists, opens the door for development of drugs preventing build-up of toxic protein aggregates in the brain.
The study appears in the Aug. 10 issue of Science Express, the advanced online edition of the journal Science.

Aging is the Critical Factor Allowing Alzheimer's to Develop

Toward Mechanism of Age-Onset Toxicity of Alzheimer's Protein

Copper May Play a Role in Alzheimer’s
.
Alzheimer's Donation
Donate Online Now
.

How much copper you take in could worsen your risk of the brain-destroying disease Alzheimer’s, U.S. researchers said.
Their studies have only been done in rabbits so far but may raise important questions about how much copper is allowed into the water supply.
Rabbits that drank distilled water did not develop an animal version of Alzheimer’s disease, but when ordinary tap water containing copper was given to them, they did, said Dr. Larry Sparks of Sun Health Research Institute in Sun City, Arizona, who led the study.
"Copper is an essential nutrient but has also been implicated as an important factor in Alzheimer’s disease," Sparks and Bernard Schreurs of West Virginia University wrote in their study, published in the Proceedings of the National Academy of Sciences.
"This is something we need to investigate," Sparks said in a telephone interview.
The U.S. Environmental Protection Agency has a maximum contaminant level goal for copper in drinking water of 1.3 parts per million.
Levels in the rabbits’ drinking water were well below that. "We are working at one-tenth that," Sparks said.
Sparks said his work was done in a rabbit model of Alzheimer’s. The rabbits develop symptoms and physical signs of Alzheimer’s when fed a high-cholesterol diet.
But he believes that copper somehow interferes with the body’s ability to clear out the amyloid-beta protein that is an important component of the senile plaques that clog up the brain of an Alzheimer’s patient.
"If there is no copper in the water then the amyloid beta is shuttled to the blood for clearance," he said.
It turns out the rabbits there were given distilled water, while all the other research animals Sparks had worked with got tap water.
He analyzed the tap water from previous labs and found it contained copper. When the rabbits at Sun Health were fed tap water, they also developed Alzheimer’s symptoms.
When Sparks added copper to the distilled water and gave the rabbits cholesterol, they also developed Alzheimer’s-like symptoms and brain lesions.
This does not mean that copper pipes are bad, Sparks said.
"Metal pipes are inert. I could throw a penny in a gallon of water and get no copper into the water," he said.
But acid in the water can cause copper to leach out.
Sparks checked for zinc, aluminum, iron and other metals and did not find them consistently in the drinking water his experimental rabbits were given.

Scientists Make Advancements With Alzheimer's Disease

Exercise May Have Neuroprotective Effect

Calories and Alzheimer’s
.
Alzheimer's Donation
Donate Online Now
.

Scientists are finding that reducing calories might be a way to slow the progression of Alzheimer's disease. This ScienCentral News video explains how a study in mice is offering new clues in fighting the disease.
Alzheimer's brake?
Calorie-restriction -- consuming 30-percent fewer calories than normal -- is the only scientifically proven way to slow the process of aging in organisms ranging from yeast to mammals. Now a new study in mice shows that through a similar mechanism, calorie restriction may also slow or prevent Alzheimer's disease.
"A decrease in amount of calorie intake might have a causal effect in prevention of Alzheimer's disease," says Giulio Pasinetti, professor of psychiatry and neuroscience at Mount Sinai School of Medicine. He and his team conducted the study in a strain of transgenic mice destined to develop Alzheimer's-like symptoms. The mice that were fed a calorie-restricted diet, mainly by a reduction in their carbohydrate intake, over a period of six months, had fewer disease symptoms than their normal-diet counterparts.

"With this kind of calorie restriction we were able to improve memory function – I would say five-fold times more efficient," says Pasinetti. The amount of beta-amyloid peptides, molecules that cause the build-up of characteristic Alzheimer's plaques, was also much lower in the brains of the mice on the low-calorie diet.

The calorie restriction was initiated between four and five months of age, when the mice were in the first stages of developing Alzheimer-type symptoms. Pasinetti says that this corresponds roughly to the stage of Mild Cognitive Impairment in people, which isn't Alzheimer's yet, but is a high-risk condition for developing it. Since drug intervention at a late stage of the disease is unlikely to ever be successful because of the intensity of damage done, prevention is the main goal.

Although he says it's too soon to know whether calorie restriction can prevent Alzheimer's in people, the results of his studies have already convinced Pasinetti to change his own behavior.
"I decided personally and my family, definitely to have a major reduction in the total amount of food that actually we eat," he says.
While the weight of the evidence is building that drastically cutting calories might just be worth it, eventually it might not prove necessary. Pasinetti says that the ultimate goal is to design a pill that imitates calorie restriction without actually requiring us to eat less – leaving us both with healthy minds and healthy appetites.

Aging adds to toxicity of Alzheimer's
.
Alzheimer's Donation

Donate Online Now
.
Alzheimer's is a disease of aging because part of the brain's cleanup crew that clears away the toxic buildup becomes less efficient, scientists have found.
Alzheimer's disease is the most common form of dementia. About 290,000 Canadians over 65 have the disease, approximately one in 20 in that age group. The number rises to one in four in those over 85. It slowly robs people of their memories and leads to behavioural changes.
"Our study revealed that the age onset of these diseases is not simply a matter of time but that the aging process plays an active role in controlling the onset of toxicity," said senior author Andrew Dillin, a biologist at the Salk Institute for Biological Studies in La Jolla, Calif.
The brain accumulates a sticky protein called beta-amyloid. Healthy people are able to clear out excess protein, but it builds up in people with Alzheimer's, forming a plaque-like clump in their brain cells.
Researchers haven't been able to figure out if Alzheimer's is a consequence of aging itself or if beta-amyloid simply takes a long time to form.
To find out, Dillin's team turned to roundworms, a common model for geneticists. The experiments are described in Friday's issue of the journal Science.
They found aging erodes the body's detoxification ability, a finding that opens the door to developing drugs to prevent the toxic buildup.
"Every pathway we can discover that modifies amyloid provides us with new drug targets," said Dr. Sam Gandy, a neuroscientist at Philadelphia's Thomas Jefferson University and a spokesman for the Alzheimer's Association.
Toxic cleanup
The researchers experimentally slowed aging in the worms by changing genes in a key pathway for controlling lifespan.
Slowing down aging also slowed the buildup of toxic amyloid in a two-step process, the team found.
In the first step, a cleanup protein called HSF-1 breaks amyloid apart. Then a second protein called DAF-16 clumps together the extra amyloid, reducing its toxicity.
"For a long time large protein aggregates were considered the toxic species," said the study's co-lead author Ehud Cohen, a postdoctoral researcher at the institute.
"The fact that cells protect themselves by temporarily storing small fibrils as [heavier] aggregates marks a clear paradigm shift."
The researchers hope to apply what they've learned to boost the cleanup process and prevent amyloid from accumulating. With files from the Associated Press

Alzheimer's Medication Shows Promise In Treating Nerve Agent And Pesticide Poisoning http://www.medicalnewstoday.com/medicalnews.php?newsid=49108&nfid=al

PET Finding May Precede Clinical Onset of Alzheimer's Disease
.
Alzheimer's Donation
Donate Online Now

.
NEW YORK (Reuters Health) Aug 09 - Binding of a PET imaging tracer called [11-C]PIB to various brain regions may be able to identify people destined to develop Alzheimer's disease, according to a report in the August 8th issue of Neurology.
Previous reports have shown that [11-C]PIB (for carbon-11 labeled Pittsburgh Compound B) binds to beta-amyloid plaques and that patients with Alzheimer's dementia display increased binding compared with nondemented controls. However, it was unclear if elevated [11-C]PIB binding was also seen in clinically normal patients who would later develop Alzheimer's disease.
To investigate, Dr. Mark A. Mintun, from Washington University in St. Louis, and colleagues performed PET brain imaging with [11-C]PIB in 41 nondemented subjects and in 10 patients with Alzheimer's dementia. The nondemented subjects ranged in age from 10 to 86 years, while the Alzheimer's patients were between 66 and 86 years old.
Consistent with previous reports, increased [11-C]PIB binding was seen in the Alzheimer's patients compared with nondemented subjects. However, four of the nondemented subjects displayed binding that, as a group, was not significantly different from that of their Alzheimer's counterparts. In fact, two of these subjects had binding that was indistinguishable from that of Alzheimer's patients.
Now, time will tell. "Longitudinal studies will be required to determine the association of elevated [11-C]PIB binding and risk of developing dementia of the Alzheimer type," the authors point out.

Brain's 'Gambling Circuitry' Identified

Animal fats increase risk of Alzheimer's disease
.
Alzheimer's Donation
Donate Online Now
.

A fresh study conducted at the University of Kuopio shows a connection between a substantial consumption of animal fat and an increased risk of Alzheimer's disease. From saturated or so-called hard fat, deposits of beta-amyloid protein will accumulate in the brain. This protein causes nerve cells of the brain to die, thus bringing on the disease. According to docent Miia Kivipelto, the intake of hard fat, for example from butter and milk, should be cut down in middle age at the latest. Kivipelto urges people to replace butter with light margarines and to introduce olive and rape-seed oils to their diets. Fish is also recommended as part of the diet. In the study, which is an offshoot of the North Karelia Project, the nutritional habits of about 1,500 residents of Northern Savo and Northern Karelia were followed for a couple of decades. Alzheimer's disease is the most common cause of dementia. In Finland there are an estimated 70,000 Alzheimer's patients.

A structural model for Alzheimer's beta -amyloid fibrils based on ...

New Insights Into Brain Organisation
.
Alzheimer's Donation
Donate Online Now
.

Scientists have provided new insights into how the brain is organised - knowledge which could eventually inform diagnosis of and treatments for conditions like Alzheimer’s Disease and autism.
Instead the study, which carried out a sophisticated computer analysis of public databases containing detailed information of worldwide anatomical studies on primate and worm brains, found that long nerve fibre connections were just as vital to overall brain function as short ones.
Much of what we know about the human brain derives from neuroscience research on primates, which are used because they have have experienced similar evolutionary stages to humans.
Brain scans of Alzheimer’s patients and people with autism have shown that they are lacking certain long-distance neural interactions, although experts have yet to discover their specific purpose.
The new study, published in the academic journal PLoS Computational Biology, found that long fibres are important because they can send messages quickly over a longer distance compared with if the same message was sent over the same distance via lots of short fibres. It also found that long fibres are more reliable for transmission of messages over longer distances.
“You can draw parallels with a train journey from Newcastle to London,” said lead researcher, Dr Marcus Kaiser (pictured), of Newcastle University’s School of Computing Science and the University’s Institute of Neuroscience.
“For example, you would get to London much more quickly and easily if you took a direct train there. However, if you had to make the journey via Durham, Leeds and Stevenage, changing trains each time, then it will take you longer to get there, and there is the possibility you would miss a connection at some point. It’s the same in the human brain.”
The computer programme, run over several days, took information about the length of nerve fibres in the primate brain and neuronal connections called axons in the brain of a species of worm known as Caenorhabditis elegans. It then tested if the total length of fibres could be reduced, by testing billions of different position arrangements. Indeed, wiring lengths could be reduced by up to 50% owing to the fact that neural systems have surprisingly many long-distance connections.

Art boosts Alzheimer's patients' spirits
.
Alzheimer's Donation
Donate Online Now
.

"One of the things that emerged was that even with the loss of memory the capacity for imagination still has it place," said Dr. Gene Cohen, the director of the Center on Aging, Health & Humanities at George Washington University who has studied the effect of art on people with Alzheimer's.
"Art is a wonderful activity that taps into imagination," Cohen said. "That is one reason there has been increasing attention to art for people with Alzheimer's. Even as memory fades the imagination has the capacity to be robust."
The illness affects parts of the brain that control thought, memory and language. Its cause remains unknown and there is no cure, though some drugs can slow the illness in its early and middle stages.
There is research that suggests artwork helps Alzheimer's patients. A small study last year of 12 people, ages 65 to 85, found that weekly sessions helped Alzheimer's patients focus their attention for 30 to 45 minutes and that completing artwork brought them "pleasure and satisfaction."
"This was particularly encouraging, given that most individuals with dementia have difficulty with attention and concentration and are unable to initiate, maintain, or complete a task without assistance and cueing," according to the study led by Clarissa Rentz, program director for the Cincinnati chapter of the Alzheimer's Association, and Jennifer Kinney, a gerontology expert at Miami University of Ohio.
The only activity that comes close to helping Alzheimer's patients the same way is music, the researchers said.
There is no indication the good feelings last, but few dispute the benefits of the art therapy.
"It is an opportunity to express themselves even after some of their standard human communications abilities of expression have gone," said Peter Reed, director of care services for the Alzheimer's Association.
Just being around people brings a smile to Lash, who can remember the day he went to work as a paper hanger — the same day Wendell Wilkie was nominated for president by the Republican Party in 1940.
"It's annoying that I can't remember the names of people I met six hours ago," said Lash, who produced two small watercolors of lions.
"It's better than sitting home and just doing nothing," he said.
For those who have problems carrying out movements, facilitators will use a hand-over-hand technique, which guides the artist so he or she can do it on their own. Volunteer aides can help artists identify objects and provide the words to help them express their feelings.
For retired Army officer Alex Zenz, 78, artwork is "an escape."
"I can do what I want to do," Zenz said as he drew a copy of Robert Campaign's "Master of Females" from a book.
Zenz's wife, Dolores, said art is "a way for him to let out steam. He had a number of tough years in the military, in Korea and Vietnam."
The paintings and drawings of Alzheimer's patients like Cohen and Lash sell at Memories in the Making-led auctions throughout the country, helping fund efforts to fight the disease.
"I really like what I am doing," Lash said. "I always say that if I can see anything I can draw it."

Researchers Develop Risk Predictor For Dementia
.
Alzheimer's Donation
Donate Online Now
.

A team of researchers have developed a new method to predict dementia risk that could help to identify individuals who might benefit from intensive lifestyle consultations and drug interventions. They published their findings online in The Lancet Neurology. Risk scores have already been developed to predict the risk of cardiovascular events, diabetes, and mortality. They enable preventive measures to be targeted to those most at risk of the disease and can be used to distribute easily understandable information about risk factors to the general population. Miia Kivipelto and colleagues aimed to develop a simple technique to predict the late risk of dementia on the basis of risk factors present in middle age. The researchers used data reported in the population-based CAIDE study, which assessed 1409 individuals in midlife and again 20 years later for signs of dementia. Kivipelto's team studied several midlife risk factors to develop the dementia risk score, such as systolic blood pressure, body-mass index, cholesterol levels, smoking, and physical activity. Kivipelto's team found that their risk score predicted dementia well. Future dementia was associated with high age, low education, high blood pressure, high cholesterol levels, and obesity. Since there is no cure for dementia-related diseases, primary prevention is important. If doctors can predict future risk of dementia then they can initiate preventive measures early for risk factors such as high blood pressure and cholesterol levels and obesity.

Fatty acids commonly found in dairy products have successfully treated diabetes in mice, according to a researcher at Penn State. The compounds, known as conjugated linoleic acids (CLA), have also shown promising results in human trials, signaling a new way of potentially treating the disease without synthetic drugs. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=48845&nfid=al

New Frontotemporal Dementia Gene
.
Alzheimer's Donation
Donate Online Now
.

Scientists have discovered genetic mutations that cause a form of familial frontotemporal dementia (FTD), a finding that provides clues to the underlying mechanism of this devastating disease and that may provide insight for future approaches to developing therapies. The mutations are contained in a single gene that scientists can now identify as responsible for a large portion of inherited FTD. A rare brain disorder, FTD usually affects people between ages 40 and 64 with symptoms that include personality changes and inappropriate social behavior. Published online July 16, 2006, in Nature, the research was funded by the National Institute on Aging (NIA), part of the National Institutes of Health (NIH).
The discovery builds on a 1998 finding of mutations in another gene that is responsible for a smaller proportion of inherited FTD cases. Amazingly, both the gene found in 1998 and the newly found gene were found on the same region of chromosome 17. Today’s discovery appears to explain all the remaining inherited FTD cases linked to genes on chromosome 17 and may provide new insights into the causes of the overall disease process. Geneticist Michael Hutton, Ph.D., of the Mayo Clinic College of Medicine, Jacksonville, Fla., led an international scientific team to discover the new gene.
“This new finding is an important advance in our understanding of frontotemporal dementia,” says NIA director Richard J. Hodes. “It identifies a mutation in the gene producing a growth factor that helps neurons survive, and it suggests that lack of this growth factor may be involved in this form of frontotemporal dementia.”
FTD encompasses a set of rare brain disorders. While most cases are sporadic, an estimated 20 to 50 percent has a family history of dementia, according to the Association for Frontotemporal Dementias. FTD affects the frontal and temporal lobes of the brain. People with FTD may exhibit uninhibited and socially inappropriate behavior, changes in personality and, in late stages, loss of memory, motor skills and speech. There is no treatment.
Hutton and colleagues began looking for genetic causes of FTD after a 1996 NIA–funded conference on the disorder. The conference, he recalls, encouraged researchers to cooperate, rather than compete, to find the FTD gene. At the start, they knew only that the inherited changes were linked to chromosome 17. Two years later, Hutton along with other researchers discovered that mutations in a particular gene on chromosome 17 were responsible for a subset of inherited FTD cases. That gene, called MAPT, contains instructions for a protein known as tau.
But, the researchers also knew there were many other families where FTD was inherited but without mutations in the tau gene. Further searching of chromosome 17 in the families without tau mutations finally turned up what is reported today -- another set of mutations in another gene, this one containing instructions for the assembly of a protein known as progranulin. The progranulin, or PGRN, gene, makes a growth factor protein that stimulates cell division and motility during multiple processes including embryonic development, wound repair and inflammation. Scientists say it is unclear what role progranulin plays in the normal brain. In the FTD families, they explain, the progranulin mutations appear to cut short the assembly process for the protein in brain nerve cells (neurons), and the lack of progranulin eventually causes neurons to die.
Understanding how the mutations of the two different genes on chromosome 17 cause neuronal death might help scientists better understand the different pathways that cause dementia. The findings also suggest that PGRN may play a role in other neurodegenerative diseases, such as ALS (Amyotrophic Lateral Sclerosis) or Lou Gehrig’s disease, the researchers noted.

Aricept
.
Alzheimer's Donation
Donate Online Now
.

Does caring for your loved one at home mean everything to you? If your loved one has Alzheimer's, Aricept® (donepezil HCl) may help. Aricept is one treatment option for mild to moderate Alzheimer's disease.
Aricept:
May help maintain overall function, which includes effects on memory and behavior
Has been approved by the FDA since 1996
Is the #1 prescribed Alzheimer’s drug—worldwide, more than 3.8 million people have been treated with Aricept
Is in a class of medicines known as cholinesterase inhibitors
Is a once-a-day treatment for mild to moderate dementia of the Alzheimer's type
Has been shown to be effective in both 5-mg and 10-mg daily doses
Is well tolerated

http://www.aricept.com/about/index.aspx

Benefits Of Apple Juice On Neurotransmitter Affecting Memory
.
Alzheimer's Donation
Donate Online Now
.

For those who think that apple juice is a kid's drink, think again. Apples and apple juice may be among the best foods that baby boomers and senior citizens could add to their diet, according to new research that demonstrates how apple products can help boost brain function similar to medication.
Animal research from the University of Massachusetts Lowell (UML) indicates that apple juice consumption may actually increase the production in the brain of the essential neurotransmitter acetylcholine, resulting in improved memory. Neurotransmitters such as acetylcholine are chemicals released from nerve cells that transmit messages to other nerve cells. Such communication between nerve cells is vital for good health, not just in the brain, but throughout the body.
"We anticipate that the day may come when foods like apples, apple juice and other apple products are recommended along with the most popular Alzheimer's medications," says Thomas Shea, Ph.D., director of the UML Center for Cellular Neurobiology and Neurodegeneration Research.
The study will be published in the August issue of the international Journal of Alzheimer's Disease. The abstract is now available online at http://www.j-alz.com/issues/9/vol9-3.html

FDA OK's trial of Transition's AZD-103
.
Alzheimer's Donation
Donate Online Now
.
TORONTO

Transition Therapeutics said Tuesday the U.S. Food and Drug Administration cleared a phase 1 trial of AZD-103 for Alzheimer's.
Transition said it anticipates beginning the trial in September. Healthy volunteers will receive placebo or an escalating dose of AZD-103.
The company said a previous phase 1 trial of AZD-103 announced in April has completed enrollment. The company said in a statement that it plans to release data from the study in "the near future."
A study in a transgenic mouse model of Alzheimer's disease indicated AZD-103 reduced the accumulation of amyloid beta and amyloid beta plaques in the brain. The compound also reduced learning deficits in the mice.

Structure Of Protein Involved In Preventing Alzheimer’s
.
Alzheimer's Donation
Donate Online Now
.

Dr. John Cavanagh, professor of molecular and structural biochemistry, teamed with colleagues from the Mayo Clinic and Duke University to describe the shape of the protein, calbindin-D28K. Understanding a protein’s structure allows researchers to learn more about how it functions and interacts with other proteins, which, in this case, may provide clues to developing drugs to halt the diseases.
The research appears in the July 2006 edition of Nature Structural and Molecular Biology.
Calbindin-D28K is a protein that either grabs calcium from areas that have too much or serves as an on/off switch for further chemical reactions. It is known for its flexibility; it is found in the kidneys, pancreas, ocular nerve and in abundant quantities in the brain. Recent studies show, Cavanagh says, that it acts as a bodyguard in the brain, binding to and inhibiting caspase-3, a protein that stimulates plaque formation and tangle formation, which are hallmark characteristics of neurodegenerative disease. Until now, however, the structure of calbindin-D28K remained a mystery.
“If you don’t know the shape of the protein, you can’t figure out how it works,” Cavanagh says. “It took a long time – about five years – but we’ve characterized the structure of this protein and found where it binds caspase-3. Insight into how it binds to caspase-3 might lead to a way of exploiting those interactions to develop therapeutics.”
It took a long time to characterize calbindin-D28K, Cavanagh says, because it was initially a challenge to force cells to make enough protein in order to do the requisite studies. Additionally, many parts of the protein are very similar and so are extremely difficult to distinguish from each other.
The research team used nuclear magnetic resonance to get a high-resolution picture of what the protein looks like. In this painstaking technique – occurring inside machines that have magnetic fields several hundred times greater than the Earth’s magnetic pull – radio waves are bounced off the approximately 5,000 nuclei in the protein.
“When you hit a nucleus with a radiofrequency pulse, it resonates, sort of making its own little noise, like a tuning fork,” Cavanagh says. “The frequency at which the nuclei resonate after being hit with a pulse is very specific to their specific position in the protein. So after we hit all of them with a pulse, it’s like hitting all the keys of a piano at the same time and it’s just an awful mess. And remember, we’re doing this for 5,000 separate keys. Yet, we’re able to untangle this mess to find the specific frequency of each nucleus and relate that to where it lies in the protein.”
Cavanagh isn’t satisfied with this knowledge, however. He says the shape-shifting protein sometimes contains no calcium. When it grabs calcium, it changes its shape.
“This could be why the protein plays so many different roles,” Cavanagh says. “Proteins that change shape usually serve as on/off switches, but this protein also grabs calcium and takes it elsewhere. Now we’re working to determine the structure of this protein when it has no calcium.”

Scientists Work On Anti-Alzheimer's Pill

http://www.medicalnewstoday.com/healthnews.php?newsid=48389&nfid=al