DNA Vaccine Protects Against Alzheimer's Disease

Doses of DNA-gene-coated gold particles protect mice against a protein implicated in Alzheimer's disease, researchers at UT Southwestern Medical Center have found.
By pressure-injecting the gene responsible for producing the specific protein – called amyloid-beta 42 – the researchers caused the mice to make antibodies and greatly reduce the protein's build-up in the brain. Accumulation of amyloid-beta 42 in humans is a hallmark of Alzheimer's disease.
"The whole point of the study is to determine whether the antibody is therapeutically effective as a means to inhibit the formation of amyloid-beta storage in the brain, and it is," said Dr. Roger Rosenberg, the study's senior author and director of the Alzheimer's Disease Center at UT Southwestern. more...

The Information Rx program, successfully piloted in Southwest Florida, will officially kick off on March 31, 2006, with a community-based mental health fair in Naples, FL at St. Johns the Evangelist Church, at 10:30am. The event will be highlighted by a press conference attended by local and national government officials. This event is a cooperative venture between the Fisher Center for Alzheimers Research, the National Library of Medicine, Senior and Law Enforcement Together of Southwest Florida, the Collier County Council on Aging, Alzheimers Support Network, and Fifth Third Bank.Read more...

Humanetics Corporation and Mount Sinai School of Medicine to Begin ...Genetic Engineering News - Larchmont,NY,USA... found to be effective in preventing the formation or slowing the progression of beta amyloid plaques, which are believed to be a cause of Alzheimer's disease. ...

Asleep Or Awake We Retain Memorymore...
Discovery About Protein Sorting In Pigment Cells Sheds Light On Melanoma, Alzheimer’s Diseasemore...

Vaccine may protect against Alzheimer's

University of Texas scientists say they've found doses of DNA-gene-coated gold particles protect mice against a protein involved in Alzheimer's disease.
The researchers at UT's Southwestern Medical Center say by pressure-injecting the gene responsible for producing the specific protein -- amyloid-beta 42 -- they caused the mice to make antibodies and greatly reduced the protein's build-up in the brain.
Accumulation of amyloid-beta 42 in humans is a hallmark of Alzheimer's disease.
"The whole point of the study (was) to determine whether the antibody is therapeutically effective as a means to inhibit the formation of amyloid-beta storage in the brain, and it is," said Dr. Roger Rosenberg, the study's senior author and director of the Alzheimer's Disease Center at UT Southwestern.
The gene injection avoids a serious side-effect that caused the cancellation of a previous multi-center human trial with amyloid-beta 42, researchers said. In that earlier study, people received injections of the protein itself and some developed dangerous brain inflammation.
The new study is available online and will appear in an upcoming issue of the Journal of the Neurological Sciences.

Discovery About Protein Sorting In Pigment Cells Sheds Light On Melanoma, Alzheimer’s Disease

Source: University of Pennsylvania School of Medicine
Researchers at the University of Pennsylvania School of Medicine have discovered how a protein called Pmel17 is sorted by pigment cells in the skin and eye to make a fiber matrix that eventually sequesters melanin, the dark pigment found in skin, hair, and eyes. Understanding the molecular steps prior to fiber formation – and when this process goes awry – may lead to a better understanding of melanoma and Alzheimer’s disease. Pmel17 is a major target within the immune system in current anti-melanoma immunotherapies. Michael S. Marks, PhD, Associate Professor of Pathology and Laboratory Medicine, and colleagues published their findings in the March issue of Developmental Cell. more...

Alzheimer's-protein link foundIndianapolis Star - United States... School of Health Sciences researchers discovered, this tissue called choroid plexus, acts like a fishnet, capturing the protein beta-amyloid and preventing it ...
Enzyme prevents Alzheimer'smyDNA.com - Austin,TX,USA... authors hypothesized that Pin1 might be acting in a similar fashion to regulate APP (amyloid precursor protein) cleavage and amyloid beta production, thereby ...

"Bad" Enzymes May Wear White Hats After Stroke

Enzymes that can harm the brain immediately after a stroke may actually be beneficial days later, according to new research. Insights from the study could change the way stroke is treated, extending the window for effective treatment from a couple of hours to a couple of weeks. The results may suggest new ideas for drug development.
Working with rats, a team from the Harvard Medical School Departments of Radiology and Neurology found that the enzyme matrix metalloproteinase-9 (MMP-9) may help remodel brain tissue seven to 14 days after a stroke. Their findings are published in the April 2006 issue of Nature Medicine, and were made available in an advance online publication on March 26, 2006.

Novel Nasal Vaccine is Effective in Treating Mouse Model ...eMaxHealth.com - Hickory,NC,USA... memory and cognition. A major goal in Alzheimer's research is to develop ways to remove this beta-amyloid build-up. One of the strategies ...

Discovery About Protein Sorting In Pigment Cells Sheds Light On Melanoma, Alzheimer’s Disease

Donepezil can help individuals with severe forms of the brain disease

Donepezil, a drug prescribed for people with mild to moderate Alzheimer's, can help individuals with severe forms of the brain disease, a study published on Thursday says.
Donepezil was tested for six months among 95 Swedish nursing-home patients with severe dementia, and compared against 99 similar patients who were given a placebo, a harmless lookalike tablet. The patients were assessed, both before and after the test, on a range of cognitive skills and basic coping skills. Those on the donepezil showed good improvements in memory, orientation, language and spatial awareness, and their decline in coping skills such as bathing, grooming, bowel and bladder function either slowed or stabilised. The drug was well tolerated. The study, published online by The Lancet, is led by Bengt Winblad, a professor of geriatrics at Sweden's Karolinska Institutet. Several theories compete as to the cause of Alzheimer's. One of them suggests the disease is caused by a deficiency in chemicals called neurotransmitters that are used by brain cells to communicate with each other. Donepezil and other drugs in its class inhibit acetylcholinesterase, an enzyme responsible for the destruction of an important neurotransmitter, acetylcholine. As a result, levels of acetylcholine in the brain are increased, which apparently causes the improvement in symptoms. These drugs improve symptoms but do not halt them, nor do they stop the underlying progression to dementia and eventually death. The two other hypothesis say the cause lies with tangles of protein called tau or with deposits of a plaque protein called beta amyloid that also are the hallmarks of Alzheimer's. Global population growth, greater longevity and changing lifestyles in developing countries point to an explosion in incidence of Alzheimer's in the coming decades, according to a paper published last December. Twenty-four million people today have Alzheimer's and the figure will rise to 42 million by 2020 and 81 million by 2040, it said. Donepezil is manufactured by Pfizer Pharmaceuticals under the brand Aricept.

Researchers link insulin, Alzheimer'sUnited Press International - USA... Their work showed that Alzheimer's is a distinct neuroendocrine disorder, or Type 3 ... of rats with a chemical that, when metabolized, destroys the beta cells in ...
Loss of Insulin in Brain Triggers Alzheimer's, Says Pioneering ...SeniorJournal.com - San Antonio,TX,USAMarch 21, 2006 – Beta-amyloid fragments that lump in the brain to form plaque has long been associated with Alzheimer's disease. ...

Reduced Insulin In The Brain Triggers Alzheimer's Degeneration

26 Mar 2006
Providence, RI - By depleting insulin and its related proteins in the brain, researchers at Rhode Island Hospital and Brown Medical School have replicated the progression of Alzheimer's disease - including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration - in an experimental animal model. The study demonstrates that Alzheimer's is a brain-specific neuroendocrine disorder, distinct from other types of diabetes. In the study, brain deterioration was not related to the pancreas, which regulates insulin for the body. When pancreatic insulin is deficient or the body fails to respond to it, the result is Type 1 or Type 2 diabetes. Previous work by the researchers with postmortem brain tissue of Alzheimer's patients showed a strong link between insulin depletion in the brain and Alzheimer's disease, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a Type 3 diabetes. "We have demonstrated that a loss of insulin in the brain triggers the onset of Alzheimer's, probably because as the brain loses insulin, the cells that require insulin to function and survive also eventually die. The consequences are increased oxidative stress, brain deterioration, loss of cognitive function, and a buildup of plaques and tangles in the brain - all hallmarks of Alzheimer's, says senior author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI. "We now know that if you specifically target insulin and its actions in the brain, you could develop new treatments for this disease," de la Monte says. The study is published in the current issue (Volume 9, Issue 1) of the Journal of Alzheimer's Disease (http://www.j-alz.com/).

Drug Effective For Severe Alzheimer's Disease

25 Mar 2006

The drug donepezil can reverse some aspects of cognitive and functional deterioration seen in patients with severe Alzheimer's disease, according to a randomised trial published online (March, 2006) by The Lancet. About 20% of Alzheimer's patients have severe dementia. As their health deteriorates they become less able to communicate, less mobile, and increasingly reliant on nursing care. Donepezil is used to treat mild-to-moderate Alzheimer's disease but its effectiveness in severe dementia has not been assessed until now. In their trial Bengt Winblad (Karolinska Institutet, Huddinge, Sweden) and colleagues recruited Alzheimer's patients over 50 years of age from 50 nursing homes in Sweden. They assigned 95 patients to donepezil and 99 to a placebo for 6 months. The investigators found that those on donepezil had improved cognition and ability to carry out daily activities when compared with those on placebo. More patients on the active drug had side effects than those in the placebo group but these were usually transient and mild to moderate in severity. Professor Winblad states: "Donepezil slows, and can reverse some aspects of deterioration of cognition and function in individuals with severe Alzheimer's who live in nursing homes."

Alzheimer's Study Finds Natural 'Fishnet' Captures Damaging Beta ...SeniorJournal.com - San Antonio,TX,USAMarch 21, 2006 – Beta-amyloid fragments that lump in the brain to form plaque has long been associated with Alzheimer's disease. ...

New Research Shows Pin1 Enzyme Is Key In Preventing Onset Of ...Medical News Today (press release) - UK... may be a key culprit in the onset of Alzheimer's disease.". ... fashion to regulate APP (amyloid precursor protein) cleavage and amyloid beta production, thereby ...
Alzheimer's May Be Diabetes-Like IllnessForbes - USA... in the rodent's brains, the researchers say they have been able to replicate the progression of Alzheimer's disease. This included amyloid plaque deposits ...

A simple and efficient method that facilitates Parkinson's disease treatment has been developed by researchers of the Institute of Human Brain, Russian Academy of Sciences. Influence of feeble electric current on the brain via electrodes laid on the head skin - the so-called transcranial electric polarization (TCEP) - reduces muscle tone and partially restores patients' movements. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=40260

Samaritan Pharmaceuticals: "We LIV....to Save Lives."

Samaritan Pharmaceuticals Inc. a developer of innovative drugs, announced today, its Alzheimer's drug SP233, recently registered as Caprospinol, showed no toxic effects in standard preclinical assays used to evaluate its safety. This is an important finding for SP233's future as a possible life-saving, memory-saving, Alzheimer's drug. Samaritan has concluded a number of preclinical studies of SP233, in preparation to file an investigational new drug (IND) application, with the FDA.
While the jury is still out as to the exact cause of Alzheimer's, most researchers think a buildup of the protein beta-amyloid in the brain is what causes the disease. So far, each preclinical study has given Samaritan hope that SP233 holds promise to exert neuroprotective properties against beta-amyloid toxicity.
Dr. Greeson, CEO of Samaritan stated, "We are wrapping up the last preclinical study to file an IND with the FDA, it's been a complex process but we are almost there, it's exciting. We are cautiously optimistic the FDA will grant us an IND and if so, SP233 would be one of the few drugs to be tested in humans that could actually treat Alzheimer's, not just alleviate its symptoms."

Samaritan is the Little Biotech That Could Be Remembered for ...Genetic Engineering News - Larchmont,NY,USAWhile the jury is still out as to the exact cause of Alzheimer's, most researchers think a buildup of the protein beta-amyloid in the brain is what causes the ...
Reduced insulin in the brain triggers Alzheimer's degenerationEurekAlert (press release) - Washington,DC,USA... They found that amyloid beta deposits in vessels and plaques did build up in the brain, and they suggest that these abnormalities occurred due to increased ...
Alzheimer's Pathology Linked To Single EnzymeMedPage Today - Little Falls,NJ,USA... combined with its effects on APP processing and A-beta production in culture and in animals, suggest a novel understanding of the way amyloid plaques form. ...

The choroid plexus prevents build up of plaque related to ...News-Medical.net - Sydney,Australia... Researchers had already known that the cerebrospinal fluid in the brains of Alzheimer's patients contains abnormally high quantities of beta-amyloid fragments. ...

Possible Alzheimer's Link To Brain Organ

23 Mar 2006
Researchers have discovered that an organ in the brain called the choroid plexus apparently plays a critical role in preventing the accumulation of a protein associated with Alzheimer's disease. The researchers found that the choroid plexus acts as a sort of "fishnet" that captures the protein, called beta-amyloid, and prevents it from building up in the cerebrospinal fluid, which surrounds and bathes the brain and spinal cord. Moreover, tissue in the organ is able to soak up large amounts of the protein and may contain enzymes capable of digesting beta-amyloid. Click link to read more. http://www.medicalnewstoday.com/medicalnews.php?newsid=40091

Karen Duff Receives Prestigious Prize for Alzheimer’s ResearchNYU Medical Center (press release) - New York,NY,USA... She also bred transgenic mice carrying the presenilin mutation and the human gene for the plaque-forming protein amyloid beta, which litters the brains of ...

Tarry no more; let's find a cure for Alzheimer'sPhiladelphia Inquirer - Philadelphia,PA,USA... resources toward finding a prevention, treatment and cure for Alzheimer's. ... Another promising approach is an antibody directed against beta-amyloid, the protein ...

4 million people

Alzheimer's is an illness that makes it hard for people to remember, think, and use language. It can make them act strange or seem moody. After a while, people with Alzheimer's have a hard time with things like using the phone, cooking or handling money.Sadly, many people think the early symptoms of Alzheimer's are signs of normal aging. So Alzheimer's is often not diagnosed and treated early.The disease is more common in older adults. And it affects all races. About 1 in 10 people over the age of 65 have Alzheimer's. As many as 5 in 10 people over the age of 85 have Alzheimer's.Through research, we are learning more about how the brain is affected in Alzheimer's. We do not yet know how to prevent or cure it. But we do know how to treat its symptoms. Aricept® can help treat the symptoms of mild to moderate Alzheimer's.People with Alzheimer's often do better if they start treatment early. Aricept can slow down the symptoms of Alzheimer's. People who start treatment with Aricept early may keep higher memory and thinking skills longer. Also, treatment may help people keep doing their daily tasks longer. Taking Aricept may help people stay in the community longer.

New Drug Target for Alzheimer'seMaxHealth.com - Hickory,NC,USAWorking with cell cultures, the scientists investigated how amyloid beta proteins, which build up in the brain tissue of people with Alzheimer's disease, kill ...
Findings Reveal Possible Alzheimer's Link to Brain OrganNewswise (press release) - USAThe researchers found that the choroid plexus acts as a sort of "fishnet" that captures the protein, called beta-amyloid, and prevents it from building up in ...

Announced That Gregory Spear Highlights the Following Stocks: Myriad Genetics

CHICAGO--(BUSINESS WIRE)--March 20, 2006--Gregory Spear explains that the market is once again celebrating the end of the Federal Reserve rate hike scenario. Learn about Myriad Genetics (Nasdaq:MYGN), Dynamic Materials (Nasdaq:BOOM), Flextronic International (Nasdaq:FLEX), Marathon Oil Corporation (NYSE:MRO) and Cummins Inc. (NYSE:CMI). Gregory Spear is the editor of The Spear Report newsletter. Click here for the full story exclusively on Zacks.com: http://at.zacks.com/?id=84
Highlights from the March 17 Featured Expert column by Gregory Spear include:
A sampling of profiled stocks:
Myriad Genetics (Nasdaq:MYGN) is a biotech company that is developing Flurizan, a therapeutic drug for the treatment of Alzheimer's disease. Flurizan is the first in a new class of drug candidates known as Selective Amyloid beta-42 Lowering Agents (SALAs). Abbreviated "Abeta42," this compound is the primary constituent of senile plaque that accumulates in the brain of patients with Alzheimer's disease. Most genetic mutations that cause early-onset Alzheimer's disease appear to do so by increasing production of Abeta42, which then causes neuronal damage. MYGN grew revenues 65% in 2005 to $80 million, posting a net loss of about $40 million. Cash on hand totals over $200 million, which is plenty to survive. Technically, a monthly chart of the stock shows a solid basing pattern and a new uptrend in progress.
Dynamic Materials (Nasdaq:BOOM) began over 30 years ago as an explosive metal forming business for the aerospace industry. Subsequently, the company licensed metal cladding technology from Dupont and eventually acquired Dupont's metal cladding business, as well as several other competitors in the U.S. and eventually in Europe. Explosion-welded clad metal is primarily used in the construction of large industrial equipment involving high pressures and temperatures, along with a requirement for corrosion-resistance. The company has operations in Pennsylvania, France and Sweden, and is 55% owned by SNPE, a French government-owned defense contractor. BOOM showed up on the radar of stock traders and investors in early 2005. Sales for that year grew 46% to $79 million and the company's EPS spiked 120% to $0.86 per share with improved margins, as well.

'Memory robber' Alzheimer's sign

Clusters of "memory-robbing" proteins could be one of the earliest signs of degenerative brain disorder Alzheimer's, scientists have suggested.
People at high risk of the disease show subtle signs years before the onset of more serious clinical symptoms.
This US study suggests that an early form of the plaque-forming protein seen in Alzheimer's affects memory.
Experts said the finding, published in Nature, could lead to a test to detect early signs of the disease. 'Memory robber' Alzheimer's sign

Discovery of substance in the brain that is proven to cause memory ...News-Medical.net - Sydney,Australia... Alzheimer's disease was caused by plaques and tangles, unnatural accumulations of two naturally occurring proteins in the brain: amyloid-beta, which builds ...

Scientists pinpoint cause of memory lossInTheNews.co.uk - London,UK... School and the University of Minnesota led a study published in the Nature periodical today, which claims that a new kind of the amyloid-beta protein triggers ...

Research Holds Promise for Early Memory Loss TreatmentIvanhoe - Winter Park,FL,USA... The authors explain scientists have traditionally believed Alzheimer's disease was caused ... different form of the plaque-causing protein, known as amyloid-beta. ...

OHSU study aims to halt Alzheimer’s by blocking enzyme

Inhibiting gamma secretase may prevent amyloid plaque build-up thought to trigger disease, but trials continue Oregon Health & Science University is participating in a national study of a drug that may prevent Alzheimer’s disease by blocking an enzyme that produces plaques believed to trigger the disorder. OHSU is one of six sites around the country taking part in a double-blind, placebo-controlled study of the agent known as LY450139, a gamma secretase inhibitor manufactured by Indianapolis-based Eli Lilly and Co. Other study sites are in Indianapolis, St. Louis, Philadelphia, Seattle, and La Jolla, Calif. Lilly is funding the study. Gamma secretase is an enzyme that produces beta-amyloid by snipping a fragment of the protein from a larger protein that extends across the plasma membrane of the cell. The beta-amyloid fragments clump together to form dense, insoluble plaques inside the hippocampus, a curved, elongated ridge deep in the brain that controls learning and memory, and the cerebral cortex, the surface layer of gray matter of the cerebrum where sensory and motor information is coordinated. The gamma secretase enzyme is made up of a complex of four proteins, and LY450139 is thought to de-activate it by binding within the complex, although the exact location is still being studied. "There is a theory that beta-amyloid produces Alzheimer’s disease, so if you stop the amyloid, you stop the disease," said Joseph Quinn, M.D., associate professor of neurology, and cell and developmental biology, OHSU School of Medicine and the Portland Veterans Affairs Medical Center. He also is an investigator at OHSU’s Layton Aging & Alzheimer’s Disease Center.

Alzheimer's Study To Explain Death Of Brain Cells

Researchers at Children's Hospital & Research Center at Oakland (CHRCO) have published a new study that is the first to explain how brain cells die in patients with Alzheimer's Disease. This discovery is an important first step to helping researchers devise ways to slow, prevent and eventually cure a disease that affects an estimated 4. Click link to read more. http://www.medicalnewstoday.com/medicalnews.php?newsid=39603

Blood Pressure Lowering Drugs Linked To Reduced Risk of ...SeniorJournal.com - San Antonio,TX,USABeta blockers and anti-hypertensives also were linked to a slightly ... They have demonstrated that bone marrow-derived microglia infiltrate amyloid plaques that ...
Early Detection of Alzheimer's Disease May Involve Protein - A ...Best Syndication - Pinon Hills,CA,USAThe identifying characteristic for AD is numerous insoluble clumps, or plaques, composed of a specific protein called amyloid-beta (A beta). ...

Experts Call for Expanded Alzheimer's Research

A recent report from government experts at the National Institutes of Health (NIH) calls for expanded research aimed at finding strategies to preserve brain health and ward off Alzheimer's disease as people grow older. In addition to research on the underlying causes of Alzheimer's disease and the need for effective new treatments, the report cites education, heart health, physical activity, psychosocial factors, and genetics as important avenues for prevention research.Read more...

Protein complex in brain may be key to Alzheimer'sNews-Medical.net - Sydney,Australia... that Alzheimer's disease was caused by plaques and tangles, unnatural accumulations of two naturally occurring proteins in the brain: amyloid-beta, which ...See all stories on this topic
Axonyx Reports Fourth Quarter and Full Year 2005 Financial ResultsGenetic Engineering News - Larchmont,NY,USA... significant reduction in the plasma levels of beta-amyloid 1-42 (A beta-42) in healthy ... Geneva/Springfield Symposium on Advances in Alzheimer Therapy in ...

PORTLAND, Ore. - Oregon Health & Science University is participating in a national study of a drug that may prevent Alzheimer's disease by blocking an enzyme that produces plaques believed to trigger the disorder. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=39601

How Our Brains Recognize Other Individuals

Source: Cornell University News Service
Imagine seeing a former high school classmate you always wanted to know better. Then imagine seeing that kid who used to push you in the hallways. Do you react differently? What happens in your brain during these encounters? more...
Protein complex in brain found to cause memory lossReuters - USA... They found a form of the amyloid beta protein in the transgenic mice that displayed early signs of memory loss but which had no plaques or nerve cell loss. ...See all stories on this topic

Single Amyloid Protein Compound May Start Memory DeclineMedPage Today - Little Falls,NJ,USA... The compound -- a derivative of the amyloid-beta precursor protein (APP) that is linked to the characteristic plaques and fibrillary tangles of Alzheimer's ...

Taking medications to lower blood pressure, particularly those known as diuretics, may be associated with a lower incidence of Alzheimer's disease, according to a study posted online today that will appear in the May 2006 print issue of Archives of Neurology, one of the JAMA/Archives journals. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=39485

Myriad Alzheimer's drug produces long-term benefit in trial

14th March 2006
By Staff Writer
A phase II follow-on study has shown that Myriad Genetics' Alzheimer's treatment Flurizan, when taken in an 800mg dosage, continued to demonstrate increasing benefit in cognition and memory loss 21 months after treatment began.
The data suggest that study participants on 800mg of Flurizan maintained more of their global function and activities of daily living than those on 400mg of Flurizan or than the projected placebo.
The data suggest that during the follow-on period from months 12 to 21, the benefit of Flurizan on the measures of Alzheimer's disease increases, in terms of both effect size and significance, the longer patients remain on Flurizan.
"The 21 months of data give us further confidence in the power of our phase III trial to demonstrate a benefit from Flurizan for Alzheimer's patients," said Dr Adrian Hobden, president of Myriad Pharmaceuticals. "The results are additional evidence that Flurizan appears to be modifying the course of the underlying disease process."
Flurizan is the first in a new class of drug candidates known as selective amyloid beta-42 lowering agents (SALAs).

Studies: Embryonic Stem Cells As a Cure for Alzheimer's DiseaseGNIF Brain Blogger - Los Angeles,CA,USA... The peptide Glenner and Wong first found was later named "A-beta" for amyloid beta. A-beta is a fragment that escapes from the amyloid ...

Excessive peroxidase of amyloid-beta- understanding AlzheimersRxPG NEWS - Westchester,CA,USA... Ph.D., found that alterations in the production of heme (a molecule that contains iron) may be the key to understanding why excessive amyloid-beta is toxic to ...

Alzheimer's study first to explain death of brain cellsEurekAlert (press release) - Washington,DC,USA... drugs that directly and selectively target the excessive peroxidase of amyloid-beta, which could lead to the first significant therapy for Alzheimer's disease ...
Study Aims To Halt Alzheimer's By Blocking EnzymeScience Daily (press release) - USA... "There is a theory that beta-amyloid produces Alzheimer's disease, so if you stop the amyloid, you stop the disease," said Joseph Quinn, MD, associate ...

Growing Research Finds Physical and Mental 'Workouts' Can Keep You Sharp in Later Life

The March 1-3 conference, "Does Mental and Physical Activity Promote Cognitive Vitality in Late Life?" was organized by the American Geriatrics Society (AGS) and made possible by a grant from the National Institute on Aging (NIA).

Numerous animal and human studies have found that physical exercise and intellectually stimulating activities can promote lifelong "cognitive vitality" in a variety of ways. Among the findings experts discussed during the conference:
* Regular physical exercise appears to help preserve cognitive function via several mechanisms -- by spurring the creation of new blood vessels in the brain and new connections among brain cells (or "neurons"), and by encouraging the creation of neurons. Though prevailing wisdom had been that neurogenesis, or the creation of new brain cells, ended after adolescence, more recent studies have shown that certain regions of the brain create new neurons even in adulthood.
* Both physical exercise and activities that are intellectually simulating may help the brain "stay young" by prompting the production of certain hormones and neurochemicals, including brain-derived neurotrophic factor (BDNF), a neurochemical that plays a key role in learning and memory.
* In mice that are genetically engineered to develop a disease similar to Alzheimer's, living in a stimulating environment and running regularly have been shown to both improve learning and decrease the build-up of beta-amyloid, a protein that appears to contribute to the creation of
brain lesions characteristic of the disease.
* In the watershed Nurses' Health Study, women 70 and older who exercised regularly -- for instance, by walking at a leisurely pace for 90 minutes per week -- ran a lower risk of cognitive impairment than those who were inactive.
* Several large studies have found that older persons who often engage in intellectually stimulating activities -- including social activities, which involve intellectual effort -- are less likely to develop Alzheimer's than those who do so less frequently.
* Cognitive stimulation in childhood and middle age may also lessen the odds of developing late-life dementia.
* "Mental exercise programs" developed to provide cognitive stimulation appear to enhance cognitive function in older adults.

Gladstone Presents Public Lecture on Alzheimers Disease on March ...UCSF Today - San Francisco,CA,USA... including amyloid beta and apolipoprotein E4, whose aggregation, fragmentation and/or malfunctioning are thought to play key roles in causing Alzheimer’s ...
Transition Therapeutics Completes Acquisition of Alzheimer's ...Canada NewsWire (press release) - Canada... positioned to be an effective therapy for preventing or reversing Alzheimer's disease by inhibiting the aggregation and accumulation of amyloid beta in the ...

Flurizan Shows Continued Benefit In Alzheimer's Disease

Myriad Genetics, Inc. (MYGN charts news Powerrating) said Sunday that data from its Phase 2 follow-on study of Flurizan in patients with mild Alzheimer's disease suggest that the participants on 800 mg BID of Flurizan continued to demonstrate increasing benefit through month 21 in the area of cognition and memory loss. The data is being presented at the 19th annual meeting of the AAGP.
The data suggest that the benefit of Flurizan on the measures of Alzheimer's disease increases in terms of both effect size and significance, the longer patients remain on Flurizan.
Flurizan is the first in a new class of drug candidates known as Selective of Amyloid beta-42 - the primary constituent of senile plaque that accumulates in the brain of patients with Alzheimer's disease. Based on the positive Phase 2 results, Myriad is enrolling patients with mild Alzheimer's disease for a Phase 3 trial.

Stolen memoriesBrisbane Courier Mail - Queensland, Australia... is big business - the drug company that backs research which leads to a big dent in Alzheimer's will become a powerful beast. The beta-amyloid hypothesis is in ...

Biotech company launches largest-ever Alzheimer's drug trial

By Paul Elias, AP Biotechnology Writer

SAN FRANCISCO --It's tragedy enough that Pat Williams' mother has Alzheimer's disease. But Williams is also terrified because her chances of inheriting the disease are much better than average.
So Williams, who lives in Boston, eagerly enrolled her 90-year-old mother last year in a massive, 1,600-patient, 18-month clinical trial testing an experimental drug made by the biotechnology company Myriad Genetics Inc. The drug, called Flurizan, slowed the mind-robbing disease in some of the 128 patients with mild Alzheimer's participating in a smaller test.
Based on those results, the company has gambled millions of research dollars on the largest-ever Alzheimer's drug trial. It aims to win an intense, international race among several biotech companies to find the first effective treatment to at least slow the disease's progression in the 4.5 million Americans who suffer from it.
Analysts predict the market for such a drug could reach $4 billion annually by 2013 and success for Myriad would lift the company's fortunes considerably. The Salt Lake City company is now best known for drilling deep into the Mormon community's detailed genetic history to develop a popular breast cancer test.
Myriad's Alzheimer's drug wasn't effective for patients with moderate forms of the disease, so the company is targeting patients who have just been diagnosed. Scientists are also using the latest in brain imaging and genetic technology to develop tests to find people like Williams who have above-average chances of coming down the disease.
"I'm hoping they will have a miracle pill so that I won't contract it," said Williams, who lives in Boston.
At least two other companies are hot on Myriad's tail.
Neurochem Inc., a Quebec company, has enrolled about 1,000 patients in its late-stage human test in Canada and the United States. It's also recruiting a similar number for a European trial. Neurochem hopes to complete the trial by January 2007, perhaps a few months ahead of Myriad.
"If everything goes well, we could have approval in 2008," said Neurochem spokeswoman Lise Hebert. Myriad hopes to have approval in 2008 as well.
Further behind is the Ireland-based Elan Pharmaceuticals, which is testing its drug in about 180 patients.
The three drugs now approved in the United States for the disease temporarily alleviate Alzheimer's symptoms, rather than treating them.
Doctors are hopeful that experimental drugs like Flurizan can slow the march of Alzheimer's, which is expected to claim a staggering 14 million in the United States by 2050 if no advances are made, according to Thies.
Myriad hustled Flurizan, which is a modified arthritis drug that is more than 20 years old, into final testing last year after the positive results of the smaller test.
If it succeeds, it will most likely spark interest in other anti-inflammatory drugs, including controversial painkillers like Merck's Vioxx, which was pulled from the market in 2004 after it appeared likely to increase the risk of heart disease.
"These drugs are interesting and are real harbingers of a new class of Alzheimer's medication," said Dr. Robert C. Green, associate director of Boston University School of Medicine's Alzheimer's Disease Center.
Because of the typical design of such drug trials, Williams, and her mother Rose Turner, don't know whether they're receiving Myriad's Flurizan or a dummy pill. Williams said it would be nice if her mother was receiving the drug, but they're still proud to be in the study even if they're receiving the placebo. That's because Williams and millions of others are desperate for even a modicum of relief.
"If it's going to help people with Alzheimer's, then we've accomplished something special," Williams, 53, said. "My mom right now is my new child."

'Shuttling' Protein

LAFAYETTE, Ind.
Researchers at Purdue University have discovered a molecular mechanism that may play a crucial role in cancer's ability to resist chemotherapy and radiation treatment and that also may be involved in Alzheimer's and heart disease. The scientists, using an innovative imaging technique invented at Purdue, have learned that a protein previously believed to be confined to the nucleus of healthy cells actually shuttles between the nucleus and cytoplasm, the region of the cell surrounding the nucleus. Moreover, the protein's shuttling is controlled by the presence of another protein in the nucleus and its attachment to that second protein. "Our findings may provide a new avenue for the development of innovative treatments for certain cancers and other conditions," said an assistant professor in Purdue's Department of Medicinal Chemistry and Molecular Pharmacology and an investigator at the Walther Cancer Institute in Indianapolis.

Red cabbage could cut Alzehimer’s riskNutraIngredients.com - Montpellier,France... from dietary sources for neurodegeneration diseases, like Alzheimer's, is only ... on the oxidative stress on cell cultures by the amyloid protein A-beta. ...
Firm gambles on Alzheimer's drugTracy Press - Tracy,CA,USA... All three are attempting to block production of the plaque-causing protein beta-amyloid. While the exact cause of Alzheimer’s remains a mystery, most ...
AC Immune selects Alzheimer's drug candidatesPharmaceutical Business Review - USA... to the soluble form of the plaque-forming beta amyloid protein. ... "The highly significant functional improvement of memory function in Alzheimer's disease animal ...

Alzheimer's Foundation of America

Care for individuals with Alzheimer's disease and related illnesses
Care for family members and others caring for those with brain disorders
Care for healthcare professionals in the dementia field
Care for Alzheimer's-related community organizations

MGI_3.43: Alzheimer's disease amyloid beta protein Protein ...Classification. Term: Alzheimer's disease amyloid beta protein ID: SF002381.MGI mouse protein superfamily detail pages represent the protein classification ...
Major Biomarker Candidates For Alzheimer's Disease Explored: Holds ...Medical News Today (press release) - UK... of the current candidates for AD biomarkers, such as amyloid-beta, tau, and ... In “The search for antecedent biomarkers of Alzheimer's disease,” Anne M. Fagan ...
AC Immune Identifies Clinical Lead Compounds for Alzheimer's ...PR Newswire (press release) - New York,NY,USA... monoclonal antibody which was highly active in animal models for Alzheimer's Disease ... the insoluble to the soluble form of the plaque forming beta amyloid protein ...

Three stages of Alzheimer's disease

Alzheimer's disease is a progressive disease. This means that patients will increasingly show the symptoms of the disease. As this progression tends to be accompanied by distinct symptoms, the disease is typically divided into three stages:
The first stage of the disease is called the mild stage or early-stage Alzheimer. This stage is characterised by impaired mental ability as well as mood swings.
The second stage is called the moderate stage or mid-stage Alzheimer. During this stage behavioural disturbances usually increasingly develop.
In the advanced stage or late-stage Alzheimer physical problems are dominant.

Graphic Shows 3-D Structure of Alzheimer's Brain as It Zips Up ...SeniorJournal.com - San Antonio,TX,USA... In Alzheimer’s disease, amyloid plaque form when enzymes cleave the amyloid precursor protein (APP), thereby releasing the toxic beta amyloid fragments. ...
AC Immune Identifies Clinical Lead Compounds for Alzheimer's ...PR Newswire (press release) - New York,NY,USA... to the soluble form of the plaque forming beta amyloid protein. ... "The highly significant functional improvement of memory function in Alzheimer's Disease animal ...See all stories on this topic
JAX®Mice Database - 004462 B6C3-Tg(APPswe,PSEN1dE9)85Dbo/JThe DeltaE9 mutation of the human presenilin 1 gene is a deletion of exon 9 andcorresponds to a form of early-onset Alzheimer's disease. The amyloid beta ...

Major biomarker candidates for Alzheimer's disease

Holds promise for improving the diagnosis and management of dementiaAlzheimer's disease--specific biomarkers clearly are needed for the differential diagnosis of cognitive impairment in the elderly. What sets age-related disorders like hypertension, hypercholesterolemia and diabetes mellitus apart from Alzheimer's disease is that each has biomarkers that can be followed easily and repeatedly, not simply to diagnose, but also to monitor response and optimize treatment. In contrast, the current role of clinical laboratory evaluation for dementia is exclusionary. The development of such biomarkers is critical to translating efficiently the new therapeutic approaches for AD under development by many research groups into treatments for the millions who suffer from AD. Read more: Major biomarker candidates for Alzheimer's disease explored

Garlic health effects and Alzheimer's disease

The epidemiological, clinical and laboratory data have shown that garlic contains many biologically active compounds which are beneficial to human health in general. Among all, one garlic-preparation called aged garlic extract, is proven to be safer. Although additional studies are warranted in humans, compelling evidence supports the health effects attributed to aged garlic extract and its implications in preventing or reducing the risk of cardiovascular ailments, stroke and cancer. Recently, the beneficial effects of garlic and its constituents on neuronal physiology and brain functions are beginning to emerge. However, this field is still in infancy and not yet fully explored. This review encompasses multiple health effects of garlic and its constituents with reference to neuroprotection. Possible potential of dietary garlic as an alternative herbal pharmacotherapy for Alzheimer's disease is discussed.Read on
Brain estrogen deficiency accelerates Abeta plaque formation in an Alzheimer's disease animal model.Read on

First Compound To Block Progression Of Alzheimer's Disease
Researchers at UC Irvine have found that a new compound not only relieves the cognitive symptoms of Alzheimer's disease, but also reduces the two types of brain lesions that are hallmarks of this devastating disease, thereby blocking its progression.
In a study with genetically modified mice, a team of UCI researchers led by Frank LaFerla, professor of neurobiology and behavior, found that a compound known as AF267B, developed by paper co-author Abraham Fisher of the Israel Institute for Biological Research, reduced both plaque lesions and tangles in brain regions associated with learning and memory. Although drugs exist on the market today to treat the symptoms of Alzheimer's, AF267B represents the first disease-modifying compound, meaning it appears to affect the underlying cause and reduces the two signature lesions, plaques and tangles. The original news release can be found here.


Medication May Slow Progression Of Alzheimer Disease A medication used to treat the symptoms of mild-to-moderate Alzheimer disease may actually do more - it may be able to delay progression of the disorder, according to a study conducted at the Indiana ...
Cholesterol Treatment May Slow Alzheimer's Disease Progression Cholesterol lowering drugs, including statins, may slow the progression of Alzheimer's disease, concludes a study in the Journal of Neurology Neurosurgery and Psychiatry. The research team assessed ...

Latest Discoveries In Alzheimer's Disease Therapy To Be Presented

05 Mar 2006

The world's leading physicians and scientists in the fields of Alzheimer's disease treatment and dementia research will participate in the 9th International Geneva/Springfield Symposium on the Advances in Alzheimer Therapy. The conference will be held April 19-22 at the International Conference Center in Geneva, Switzerland. They will highlight the latest discoveries in the treatment of dementia and results of the most recent clinical trials using drug, cellular and gene therapies. More than 100 sessions will be presented by 125 speakers during the four-day symposium. Nearly 800 specialists are expected to attend the international gathering. Included in those presentations will be historical data reflecting the progress of the treatment of Alzheimer's disease with cholinesterase inhibitors over the past 20 years; the results of three large clinical trials utilizing cholinesterase inhibitors in at-risk patients; and recommendations for usage of vaccination against beta-amyloid aggregation, the accumulation of toxins in the brain that destroys nerves which can lead to Alzheimer's disease. Dr. Paul Coleman, neuroscientist at the Center for Aging and Developmental Biology in Rochester, New York, will give the keynote address entitled The Impact of Science on Future Alzheimer Disease Diagnosis. The symposium was established by Dr. Ezio Giacobini, Ph.D., professor of rehabilitation and geriatrics at the University of Geneva Medical School in Switzerland and professor emeritus of the Southern Illinois University School of Medicine in Springfield, Ill., USA. Giacobini organized this year's conference with Dr. Jean-Pierre Michel, professor and chair of rehabilitation and geriatrics at the University of Geneva Medical School in Switzerland.

Alzheimer's and Brain Health

Alzheimer’s disease is an irreversible brain disorder that leads to memory loss, personality changes, and a general decline in cognitive function. The disease progresses from mild forgetfulness to a severe loss of mental function leading to death and is most prevalent in people over the age of 65. However, Alzheimer’s is not a normal part of aging. Instead, it is caused by the breakdown of connections between damaged brain cells and eventual brain-cell death. It is estimated that more than 4.5 million people in this country suffer from Alzheimer’s disease and that by 2050, 14 million Americans will have the disease.
The scariest thing about this disease is that it seems to be brand new! There is absolutely no mention of anything that could be considered Alzheimer’s disease in any medical, religious, or secular literature before the turn of the last century. That means that in the last 100 years, Alzheimer’s disease has gone from non-existence to a disease that kills nearly 54,000 people every year in the United States alone and affects millions more.
What is the cause of this deadly and frightening epidemic? Could it be linked to the exponential rise in meat consumption, as well as to the unnatural ways that animals are fed? The evidence points in that direction. Recent research suggests that Alzheimer’s disease, like heart disease and strokes, is linked to the saturated fat, cholesterol, and toxins found in meat and dairy products. Studies have shown that people who eat meat and dairy products have a greater risk of developing Alzheimer’s disease. In contrast, the protective properties of plants, including antioxidants, vitamins, and minerals, are not only essential to good health, but help substantially lower the risk of developing Alzheimer’s disease. Read more.

Fat and the Baby Boomer BrainCommunity Dispatch (press release) - USA... with more weight, there was an increase in blood levels of proteins that form beta-amyloid plaques -- substances thought to play a big role in Alzheimer's. ...

A new drug that enhances the activity of a key brain cell receptor involved in Alzheimer's disease (AD) reverses learning and memory deficits in mice engineered to have pathological hallmarks of the disease. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=38724

Berries May Be Good for the Brain

Add black currants, popular in the U.K., and their American cousins boysenberries to the list of colorful fruits and vegetables that may help to ward off Alzheimer's disease. Researchers at the Horticulture and Food Research Institute in New Zealand found that natural compounds found in the flavorful fruits helped protect rat brain cells from the kind of damage that occurs in human brains afflicted by dementia.Read more...

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Scientists Gain New Understanding Of Age-Related Depression And Dementiamore...

Drug Found to Reverse the Ravages of Alzheimer's

Researchers have identified a compound that could significantly improve treatment of Alzheimer's disease. When administered to mice engineered to develop hallmarks of the disease, the drug reversed cognitive decline and reduced the two types of brain lesions--plaques and tangles--that occur in Alzheimer's patients. Drug Found to Reverse the Ravages of Alzheimer's in Mice

Alzheimer's progress 'halted by new drug'Telegraph.co.uk - United Kingdom... In the brain of an elderly Alzheimer's patient, protein molecules clump together to ... on blocking the formation of plaques from a molecule called beta amyloid. ...
New drug shows promise in the treatment of Alzheimer's diseaseArs Technica - Boston,MA,USAAnother Alzheimer's disease (AD) post today, and one that we might remember fondly in ... These come in two forms, neurofibrillary tangles and beta-amyloid plaques ...
Amyloid beta - Wikipedia, the free encyclopediaAmyloid beta (Aβ or Abeta) is a protein fragment of 39-42 amino acids that is... in various neurological disorders, most prominently Alzheimer's disease. ...

The effect of planned walking on communication in Alzheimer's disease.

Friedman R, Tappen RM
One of the effects of Alzheimer's disease is a diminution in the ability to communicate. A randomized, non-blinded two-group experimental study was undertaken to determine if planned walking has the capacity to improve the communication performance of patients with moderate to severe Alzheimer's disease. Thirty subjects meeting NINCDS-ADRDA diagnostic criteria for probable Alzheimer's disease, selected from two nursing homes, participated in the study. Intervention and comparison groups were each made up of subjects from both nursing homes. Subjects in one group were walked individually for 30 minutes three times a week for 10 weeks. Subjects in the comparison group were engaged in conversation for the same amount of time for 10 weeks. A multivariate analysis of variance (MANOVA) was performed on the communication data. Analysis of the data at post-testing indicated that communication performance improved significantly in the planned walking group over the conversation-only group (f = 4.29; df = 2.28; P = 0.024). The results suggest that a planned walking program has the capacity to improve the communication performance of patients with Alzheimer's disease.

Exercise helps slow down mental deteriorationSun.Star - Philippines... A recent study reinforces what is known of amyloid-beta in bringing out mental deterioration in patients with Alzheimer's disease, a common age-related ...
Transition reports positive preclinical Alzheimer's dataPharmaceutical Business Review - USATransition Therapeutics has presented data showing that its lead Alzheimer's disease product, AZD-103, neutralized and rescued amyloid beta inhibition of ...
Samaritan's Alzheimer's Drug Registered as CAPROSPINOL; SP-233 ...Genetic Engineering News - Larchmont,NY,USA... AMEX:LIV), a developer of innovative drugs, announced today it has received its unique CAS Registry Number for the chemical substance in its Alzheimer's drug SP ...