Alzheimer's Cognitive Decline by New Treatment
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Unprecedented results using a new way to treat Alzheimer's Disease(AD) were published this week in the neurology section of the peer-reviewed journal, Medscape General Medicine. The article presents the results of a six-month, open-label, uncontrolled pilot study in which 15 patients with Alzheimer's ranging in severity from mild to severe received weekly perispinal injections of etanercept, a medication designed to reduce excess levels of tumor necrosis factor (TNF). TNF is a molecule which initiates and amplifies the inflammatory response in the brain and other organ systems. "There is an enormous unmet medical need in Alzheimer's disease, an incurable, terminal and devastating affliction for the patient, as well as for families and society in general," stated Dr. Cohen. "We should take these findings very seriously and confirm them in broader trials initiated immediately." The full-study is available at www.medscape.com

U of T find could lead to treatment for Alzheimer'sNews@UofT - Toronto,Ontario,Canada... newly found protein blocks the creation of nerve toxins in Alzheimer's, a disease ... an increase in levels of the neurotoxin, called Abeta or beta-amyloid peptide ...
Korean scientists find new trigger for Alzheimer'sKorea Herald (subscription) - Seoul,South Korea... which reside at the tip of the amyloid precursor-like ... indirubin-3, an inhibitor against GSK3-beta, will help ... the number of dying neurons in Alzheimer's patients ...

Researchers from Georgetown University Medical Center's Memory Disorders Program are directing the first U.S. study to determine whether huperzine A, derived from the Chinese club moss plant Huperzia serrata, improves cognitive function in people with Alzheimer's disease (AD). http://www.medicalnewstoday.com/medicalnews.php?newsid=42330

Blood Clots Present In 40% Of Alzheimer's Disease Patients
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According to a report published in the British Medical Journal (BMJ), spontaneous blood clots are significantly associated with both Alzheimer's Disease and Vascular Dementia. The researchers, from the University of Manchester, UK, say this finding may hold the key to preventing and/or treating dementia. Alzheimer's Disease and Vascular Dementia represent four fifths of all dementias. To date, nobody has known why. In this study, researchers monitored the occurrence of spontaneous cerebral emboli in 170 patients, half had Alzheimer's Disease and the other half had Vascular Dementia. They also monitored a control group of 150 healthy people of the same age and sex ratio. Another name for spontaneous blood clots or debris from arterial disease in the brain is ‘spontaneous cerebral emboli'. In just one hour of monitoring, cerebral emboli was present in 40% of the Alzheimer's Disease patients and 37% of the Vascular Dementia patients, compared with just 15% in the control group. The researchers concluded that spontaneous cerebral emboli are closely linked to Alzheimer's Disease and Vascular Dementia. They also added that further research is needed as this study is the first of this type.

Cayman Chemical New ProductsAn affinity probe for arachidonic acid binding proteins. Arachidonic acid-biotinimidewas designed to allow arachidonic acid to be detected in complexes ...
Prostaglandin endoperoxide synthetase-dependent cooxidation of ...Binding was dependent upon the presence of PES and arachidonic acid and wasinhibited by indomethacin. Experiments were then carried out by using microsomes ...

CORRECTING and REPLACING Reversal of Alzheimer's Cognitive Decline ...Genetic Engineering News - Larchmont,NY,USAUnprecedented results using a new way to treat Alzheimer's Disease(AD) were published this week in the neurology section of the peer-reviewed journal, Medscape ...

Posiphen May Support Stem Cell Transplantation in Alzheimer's Disease
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Axonyx Inc. (NASDAQ: AXYX) today announced the results of an independent study showing that Posiphen increased the ability of transplanted human neuronal stem cells (HNSC) to differentiate into neurons in APP transgenic mice, a model of Alzheimer's disease (AD) in humans. The research was reported by Kiminobu Sugaya, Ph.D., Professor of Molecular Biology, Biomolecular Sciences Center, University of Central Florida, Orlando, Florida at the 9th International Geneva/Springfield Symposium on Advances in Alzheimer's Disease held April 19 - 22, 2006 in Geneva, Switzerland.
Dr. Sugaya's research showed that when APP transgenic mice had been pre-treated with Posiphen, transplanted HNSC start to differentiate into neurons in the brain area where they are needed. When HNSC were transplanted into the brains of APP transgenic mice in the absence of Posiphen, HNSC did not differentiate into neurons. Dr. Sugaya attributed this effect to Posiphen's ability to decrease the synthesis of amyloid precursor protein (APP). Posiphen may support and augment production of the new neurons through the suppression of APP production in the brain. The differentiation of stem cells into functioning neurons is critical to the success of stem cell therapy of AD.
"Although a better understanding of the mechanisms of APP function HNSC biology may be needed", stated Dr. Kiminobu Sugaya, "regulation of APP levels by a combination of Posiphen and stem cell treatments could be a promising strategy to treat AD."

Block Alzheimer's disease?myDNA.com - Austin,TX,USA... memory re-arranging), Buck scientists believe the symptoms of Alzheimer's develop when ... and 635th amino acids release the so-called beta-amyloid peptides, which ...

Signet Laboratories Announces the Release of an sAPPbeta Antibody ...Yahoo! News (press release) - USA... Alzheimer's disease (AD) presently affects over 4 million people, a number ... These plaques are predominantly composed of beta amyloid protein, which is derived ...

For years, doctors have encouraged people to consume foods such as fish that are rich in omega-3 fatty acids because they appear to improve memory and other brain functions. http://www.medicalnewstoday.com/medicalnews.php?newsid=42365

Protein Found that Prevents Key Alzheimer's Pathology
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A better understanding of the insidious forces that culminate in Alzheimer's disease was revealed here today.
The process of protein slicing that leads to the development and accumulation of beta-amyloid plaques in the brains of Alzheimer's patients appears to cut both ways, reported Peter St. George-Hyslop, M.D., D.Sc., director of the Center for Research in Neurodegenerative Disease at the University of Toronto, and colleagues, in the April 27 issue of Nature.
A lowly "cargo transporter" protein called TMP21 seems to play a key role in preventing the abnormal cleavage of amyloid precursor protein (APP) into beta-amyloid fragments, they found. At the same time, TMP21 does not interfere with a different form of protein cleavage essential for normal cell signaling processes, they said.
The discovery could lead the way to new therapies for preventing or treating Alzheimer's, perhaps an analog of TMP21 that targets the abnormal cleavage while leaving other protein slicing functions intact.

Leuprolide Acetate Stabilises Cognitive Decline in Women With ...DG News - USA... Recent preclinical studies have shown that leuprolide acetate reduces brain levels of beta-amyloid 42 (A-beta 42 ) and beta-amyloid 40 (A-beta 40 ) by about 40 ...

Buck researchers find Alzheimer's 'switch'Marin Independent-Journal - San Rafael,CA,USA... No one knows what causes Alzheimer's. ... Perhaps the most distinctive of these is the formation of beta-amyloid plaques, sticky clumps of protein fragments that ...

New Weapon Against Alzheimer’s FoundPakTribune.com - PakistanBuildup of beta-amyloid protein plaques in the brain is a hallmark of Alzheimer’s and toxicity related to this buildup is thought to be a major cause of the ...

The Republic of Belarus
20 years after

The Chernobyl disaster had an enormous impact on Belarus, a small country in Eastern Europe with a population of 10.4 million. 70 percent of the total radioactive fallout from the accident descended on nearly one-fourth of the country. The fallout affected more than 2.2 million people, including 500,000 children. Immediately after the accident, UN system organizations sought ways to provide emergency assistance to those exposed to massive amounts of radiation. Also, the UN system remained actively involved in dealing with the long-term effects of the disaster in Belarus. However, despite the assistance the international community has provided, the region still suffers from the consequences of Chernobyl today. According to the data we have received, UN system organizations, leading NGOs, and international foundations have implemented nearly 92 projects, providing $58.1 million in assistance to the Chernobyl region since 1986. (This information does not include Chernobyl projects implemented by the European Community and UNESCO). In 1988, UN system organizations became involved in the region’s recovery. In the period following the disaster, UN system organizations focused on projects that provided immediate relief, targeting health, environmental and agricultural issues. Close to $10 million was allocated to these types of projects. Nuclear safety and economic rehabilitation projects were found to be less of a priority at that time, and received only $620,000. NGOs and Foundations initiated projects in the Chernobyl around 1991. Eventually, these types of organizations would account for close to 80 percent of total project expenditures, and many of these NGO’s focused on supporting overwhelmed local health care systems. For example, the Chernobyl Children’s Project, a non-governmental organization, implemented projects estimated at $29.9 million, which largely focused on the mental and physical health of those exposed to radiation. NGOs also worked with local government to build the capacity of the Belarus health care system to respond effectively to the crisis. NGO and UN Projects also focused on the study and treatment of diseases and other conditions that resulted from the disaster. Assistance went to the diagnosis and treatment of thyroid cancers, the treatment of leukemia, the study of the genetic implications of the disaster, as well as collecting health data. The government of Belarus estimated that thyroid cancer rates in children under 15 years rose dramatically from 2,000 cases in 1990 to 8,000-10,000 in 2001. Hundred of thousands Chernobyl liquidators, who were involved in the clean-up operations and received high doses of radiation, developed a number of diseases and required medical treatment. Already facing severe economic problems, dealing with the Chernobyl disaster further taxed the economy of Belarus and government spending. As a result, government assistance to study and treat the health consequences of Chernobyl was limited. In Belarus 20 percent of agricultural lands and 23 percent of forests were contaminated by radionuclides. UN system organizations invested in the use of Caesium Binders to reduce Caesium-137 found in the soil. Rapeseed cultivation in contaminated areas helped to support agricultural recovery. Fertilizers, which were used to combat the effects of radionuclides, were estimated to cost nearly $77 million per year. As a result, only large enterprises could afford to use fertilizers and the majority (80 percent) of small households in the affected areas continued to consume foods contaminated by radionuclides. Organizations focused on subsidizing the cost of fertilizers and making them available throughout agricultural areas. After 17 years of international assistance, it is clear that millions of people in Belarus still suffer from radioactive contamination. A great deal of work still needs to be done. Contributions for Chernobyl projects represent only a small amount of what is required to help Belarus recover and develop. When projected over 30- year recovery period, the total damage to the economy of Belarus can be estimated at $235 billion.The United Nations recently announced a new focus on sustainable development for the countries affected by Chernobyl. Efforts to address the health effects of Chernobyl, for example, need to be undertaken in the context of broader reform of the health care system in Belarus. The hope is that new approaches to development in the three countries affected by Chernobyl can empower individuals and communities, and mobilize additional resources for recovery.

Shutting Down Alzheimer's
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New research reveals strategies for blocking the molecular processes that lead to this memory-destroying disease. By Michael S. Wolfe

The human brain is a remarkably complex organic computer, taking in a wide variety of sensory experiences, processing and storing this information, and recalling and integrating selected bits at the right moments. The destruction caused by Alzheimer's disease has been likened to the erasure of a hard drive, beginning with the most recent files and working backward. An initial sign of the disease is often the failure to recall events of the past few days--a phone conversation with a friend, a repairman's visit to the house--while recollections from long ago remain intact. As the illness progresses, however, the old as well as the new memories gradually disappear until even loved ones are no longer recognized. The fear of Alzheimer's stems not so much from anticipated physical pain and suffering but rather from the inexorable loss of a lifetime of memories that make up a person's very identity.
Unfortunately, the computer analogy breaks down: one cannot simply reboot the human brain and reload the files and programs. The problem is that Alzheimer's does not only erase information; it destroys the very hardware of the brain, which is composed of more than 100 billion nerve cells (neurons), with 100 trillion connections among them. Most current medications for Alzheimer's take advantage of the fact that many of the neurons lost to the disease release a type of chemical communicator (or neurotransmitter) called acetylcholine. Because these medicines block an enzyme responsible for the normal decomposition of acetylcholine, they increase the levels of this otherwise depleted neurotransmitter. The result is stimulation of neurons and clearer thinking, but these drugs typically become ineffective within six months to a year because they cannot stop the relentless devastation of neurons. Another medication, called memantine, appears to slow the cognitive decline in patients with moderate to severe Alzheimer's by blocking excessive activity of a different neurotransmitter (glutamate), but investigators have not yet determined whether the drug's effects last more than a year.

More than a decade ago few people were optimistic about the prospects for defeating Alzheimer's. Scientists knew so little about the biology of the disease, and its origins and course were thought to be hopelessly complex. Recently, however, researchers have made tremendous progress toward understanding the molecular events that appear to trigger the illness, and they are now exploring a variety of strategies for slowing or halting these destructive processes. Perhaps one of these treatments, or a combination of them, could impede the degeneration of neurons enough to stop Alzheimer's disease in its tracks. Several candidate therapies are undergoing clinical trials and have yielded some promising preliminary results. More and more researchers are feeling hope--a word not usually associated with Alzheimer's.

Although cholesterol has a bad rap as the sticky, fatty substance responsible for clogging arteries, Vanderbilt University Medical Center researchers recently found that the attachment of cholesterol to an important developmental protein controls the development of fingers and toes in mice. http://www.medicalnewstoday.com/medicalnews.php?newsid=42112

According to the World Health Organization (WHO), more than 75% of women over the age of 30 are now overweight in countries as diverse as Egypt, Mexico, South Africa and Turkey. Estimates are similar for men, with over 75% now overweight in Argentina, India, China, Kuwait and Greece. http://www.medicalnewstoday.com/medicalnews.php?newsid=42137

LDPOST.com

Latest Issue Of Alzheimer's & Dementia
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Though publishing only its fourth issue, Alzheimer's & Dementia: The Journal of the Alzheimer's Association continues to feature valuable new data, and stimulate thought and discussion with provocative perspectives on key issues, such as alternative theories for the cause of Alzheimer's. Included in the journal's April 2006 issue are: Screening - A call for consideration of dementia risk factors in individuals at age 50, with routine yearly screening after age 75. Cause - A new theory for the cause of Alzheimer's based on research with a well-known diabetes drug.

A large-scale observational study in twins, some tracked for as long as 45 years, suggests education, physical exercise and inflammatory load (as shown by tooth loss) as risk factors for Alzheimer's disease and vascular dementia. "Should older adults be screened for dementia?" J. Wesson Ashford, et. al. Read more: http://www.medicalnewstoday.com/medicalnews.php?newsid=41976

Alzheimer's Fears Over Camelford Water Fiasco International News Service - Sydney,Australia... 2004. Examination of her brain revealed a rare form of Alzheimer's, known as sporadic early onset beta amyloid angiopathy. Aluminium ...

Social Contact Protects Senior Citizens from Alzheimer's Damaging Effects
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Social network offers protection despite the tangles and plaques of Alzheimer's
April 21, 2006 - Having close friends and staying in contact with family members offers a protective effect against the damaging effects of Alzheimer’s disease according to research by physicians at Rush University Medical Center in Chicago. The study, which is currently posted online in The Lancet Neurology, will be published in the May print edition of the journal.
While other studies have shown people with more extensive social networks were at reduced risk of cognitive impairment, the study by Dr. David A. Bennett, and his colleagues from the Rush Alzheimer's Disease Center, is the first to examine the relations between social networks and Alzheimer’s disease pathology.
Researchers studied elderly people without known dementia who are participating in the Rush Memory and Aging Project, an epidemiological and clinicopathological study of aging and Alzheimer's disease that involves over 1,100 volunteers across northeastern Illinois. Brain autopsy was done at the time of death and post mortem data was available for analysis from the first 89 people.

Camelford Resident Died of Rare Form of an Aluminium-Associated ...innovations report - Bad Homburg,Germany... normally associated with early-onset forms of Alzheimer’s Disease. The neuropathology was characterised by severe deposition of beta-amyloid in cortical and ...See all stories on this topic
Axonyx Reports Data on Effects of Phenserine on the Brains of ...Finanzen.net - Germany... to cognition andthe regulation of beta-APP and/or amyloid beta will be ... theirrespective clinical indication or slow the progression of Alzheimer'sdisease; any ...
Alzheimer's fear grips poisoned water townTelegraph.co.uk - United Kingdom... Mrs Cross's post mortem examination revealed a rare form of Alzheimer's disease, known as sporadic early onset beta amyloid angiopathy. ...
Rare Form Of Alzheimer's Disease Found In Camelford Resident, UKMedical News Today (press release) - UK... ordinary. But her brain revealed a rare form of Alzheimer's disease, known as sporadic early onset beta amyloid angiopathy. Other ...

Mediterranean Diet Lowers Alzheimer's Risk In American Cohort
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The "Mediterranean diet" may reduce the risk for developing Alzheimer's disease. Researchers in New York examined over 2000 subjects, interviewing them about dietary habits and testing their cognitive ability over time. Those who ate a Mediterranean diet--high in vegetables, grain, and unsaturated fats, and low in meat and dairy--were less likely to develop Alzheimer's disease. Obesity in midlife may increase the risk of Alzheimer's disease, according to researchers in California. Health records from 1964 and the present were examined for almost 9,000 middle-aged individuals, correlating past obesity to the risk for a current diagnosis of Alzheimer's disease. Individuals in the top 20 percent of obesity measures in 1964 were two to three times as likely to develop Alzheimer's disease as those in the bottom 20 percent. Cognitive decline is also increased with lower blood levels of the hormone leptin, which affects both appetite and brain development. In a study of almost 3,000 healthy elderly followed over five years, those with the lowest leptin levels had a greater decline in their cognitive ability than those with the highest levels. Sex hormones may also play a role in the risk for cognitive decline. In a study of almost 800 men and women, those women with the lowest levels of estradiol (a type of estrogen) declined fastest, compared to those women with the highest levels. This correlation was seen in both black and white women. No effect of estradiol was seen in men, and no effect was seen for the hormone testosterone in either sex.
These findings are published in the April issue of Annals of Neurology, a journal published by John Wiley & Sons. Experts theorize that diet may play a role in the development of Alzheimer's disease but epidemiological data on diet and Alzheimer's is conflicting and while individual foods and nutrients have been previously studied, general dietary patterns have not. To address this paucity of data, researchers led by Nikolaos Scarmeas of Columbia University Medical Center, designed a prospective community-based study of 2,258 non-demented people in New York City. The study was funded by the NIH/NIA. The article is also available online via Wiley Interscience (http://www.interscience.wiley.com/).

Having close friends and staying in contact with family members offers a protective effect against the damaging effects of Alzheimer's disease according to research by physicians at Rush University Medical Center in Chicago. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=42075

Being Overweight May Be Bad for the Brain
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Men and women who are overweight or obese in their forties have a greater risk of developing Alzheimer's disease later in life, according to a large new study from California. The findings, presented at the American Academy of Neurology's 58th Annual Meeting in San Diego earlier this month, add to a growing body of medical evidence about the perils of excess pounds. Read more...

Cornell Undergrads Show Off Research Cornell University The Cornell Daily Sun - Ithaca,NY,USA... polymers that bind to a beta-amyloid peptide were structurally and functionally similar. This peptide is known to be responsible for Alzheimer's disease and ...
Trial vaccine shows promise Palm Beach Post - FL, United States... attack beta-amyloid plaque — an abnormal protein that builds up in the brain's memory circuits and is a key factor in the development of Alzheimer's disease. ...
Axonyx Reports Data on Effects of Phenserine on the Brains of ... Genetic Engineering News - Larchmont,NY,USA... cognition and the regulation of beta-APP and/or amyloid beta will be ... their respective clinical indication or slow the progression of Alzheimer's disease; any ... Researchers Discover A New Genetic Cause Of Alzheimer's Disease more...

Axonyx Reports Data on Stabilized Brain Volumes in Alzheimer's
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Axonyx Inc. (NASDAQ: AXYX) today reported an analysis of results suggesting stabilization of total brain volume and brain parenchymal fraction of mild-to-moderate Alzheimer's disease (AD) patients treated with Phenserine 10mg or 15mg twice daily (BID) for 26-weeks.

Following Phenserine treatment, patients' mean total brain volume and parenchymal fraction remained stable from baseline but decreased in the one placebo patient. Mean changes in brain volume were +0.99% (Phenserine 15mg BID), +2.68% (Phenserine 10mg BID) and -5.15% (placebo) and mean parenchymal fraction changed from baseline by +0.21%, +0.46% and -2.97% respectively. Although not statistically significant, the mean percentage changes of brain volumes seen in the treated groups suggests a preservation of volume compared with the brain atrophy (loss of brain volume) seen in the placebo patient. There was no notable effect in the hippocampal area of the brain; however this may have been due to the difficulty associated with measurements of this small brain structure.
It is well known that Alzheimer's disease is associated with an acceleration of brain atrophy that is generally greater than expected for non-demented persons of similar age. Brain atrophy as measured by MRI has emerged as a potential outcome measure of AD treatments and marker of disease severity and progression. The possible neuro-protection seen in this sub-study may potentially reflect the effects of Phenserine on amyloid beta (A beta) - a protein thought to be a potential cause of Alzheimer's disease and its progression. Phenserine's effects are associated with reductions of A beta levels in pre-clinical studies, as well as a correlation seen between Phenserine levels and a reduction of plasma A beta in Phenserine-treated human volunteers. While the signal from this sub-study of a potential effect of Phenserine on the brains of AD patients is encouraging, the Company notes that MRI brain studies are generally of longer duration and include more patients, particularly in the placebo group. Nevertheless, the absence of brain atrophy in Phenserine treated AD patients in this sub-study is contrary to what would be expected to occur and may justify a definitive MRI evaluation of the effects of Phenserine on brain atrophy in patients with Alzheimer's disease.

Researchers from the Flanders Interuniversity Institute for Biotechnology (VIB) connected to the University of Antwerp are the first to show that the quantity of amyloid protein in brain cells is a major risk factor for Alzheimer's disease. http://www.medicalnewstoday.com/medicalnews.php?newsid=41922

US drug breakthrough
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The first disease-modifying drug for the treatment of Alzheimer's could soon be developed, thanks to a research group at the University of California Irvine.
The researchers found that AF267B, an analogue of the neurotransmitter acetylcholine, decreased plaque and tangle formations in the brains of mice engineered to display the symptoms of Alzheimer's, thus improving memory and learning. The brains of Alzheimer's patients show a large loss of the neurons that produce acetylcholine.
This is the first time a drug has demonstrated the ability to tackle the beta-amyloid protein lesions that are thought by some to cause Alzheimer's disease.

A Mediterranean diet involves eating more fruit, vegetables, olive oil and cereals and less meat and dairy than the Northern European or North American diet. Click link to read more.
http://www.medicalnewstoday.com/healthnews.php?newsid=41797

Interactive Feature: Wines of The Times A tasting of premier cru Chablis from 2004 finds that this wine of distinction has returned to form, where subtlety, balance and keen precision hold sway. Related Article

Vitamins E And C Plus Ibuprofen May Protect Against Alzheimer's
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For patients at high risk of Alzheimer's disease, taking a combination of vitamins E and C plus ibuprofen significantly reduces their risk, results of a longitudinal study suggest. "We found that for people at low risk, taking vitamin C and E alone is sufficient to further reduce their risk. But for those with apolipoprotein epsilon-4 (APOE-epsilon-4) alleles, the combination exerts a synergistic benefit," Dr. Majid Fotuhi told Reuters Health. Full Story

Cancerous Vs. Healthy Cells: Researchers Identify The Road To Success more...

Carnosine Therapy in Alzheimer's Disease
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The main reason for brain cell destruction is probably the inhibition of the proteasome, a protein which removes damaged and denaturated proteins from the brain cells. The causes of proteasome inhibition are explained in a separate review.
Carnosine protects the proteasome and hence fights Alzheimer´s disease. Carnosine is a dipeptide, also called a neuropeptide and neurotransmitter. Patients with Alzheimer´s disease develop extracellular deposits of amyloid protein and microscopic tangles of fibrils inside nerve cells. In experiments, treatment with carnosine was found to reduce or completely prevent cell damage caused by ß-amyloid. Carnosine blocks and inactivates ß-amyloid, so it protects neural tissues against dementia.
Moreover, carnosine protects the brain cells by fighting the highly toxic alpha, beta-unsaturated aldehyde acrolein which is formed during the peroxidation of polyunsaturated lipids, raising the possibility that it functions as a 'toxicological second messenger' during oxidative cell injury.
Recent research also confirms that the toxic unsaturated aldehyde crotonaldehyde (CA) contributes to carbonylation resulting in protein damage during lipid peroxidation. As carnosine combats all aldehydes, it offers another explanation for its benefits in prevention of Alzheimer´s disease and other conditions with oxidative stress. Moreover, Carnosine protects proteasomes, protein molecules which detoxify the brain cells, and Carnosine removes toxic heavy metals from the brain cells in a biochemical process called chelation.

A team led by a Canadian researcher has discovered a process by which a small protein acts directly within muscles to increase the body's metabolism to burn fat while simultaneously suppressing appetite. http://www.medicalnewstoday.com/medicalnews.php?newsid=41666

Older Americans Act Supportive Services and Other Services for Seniors
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Title I-IV of the Older Americans Act provides authorization for a variety of programs that support seniors. This includes everything from health services, social opportunities, transportation, and nutrition services. Easter Seals actively works with Congress to increase supports for seniors through the Older Americans Act and other legislation affecting seniors. Jennifer Dexter Assistant Vice President, Government Relations
What’s Happening in Washington
For fiscal 2006, Congress allocated $354 million for the Supportive Services and Senior Center Program and $157 million for the National Family Caregivers Support Program. This is essentially level funding for programs that serve older adults, and is insufficient to meet the rapidly increasing need for services. Easter Seals will continue to advocate for increased resources to serve older adults.
In early 2006, the Ronald Reagan Alzheimer's Relief Act was introduced. The bill would double funding for the National Family Caregivers Support Program, implement the Lifespan Respite Care Act, increase funding for Alzheimer's research, and provide tax credits to those caring for someone with Alzheimer's. Easter Seals supports this legislation and will be working to ensure final passage. http://www.easterseals.com/site/PageServer?pagename=homepage

The Juvenile Diabetes Research Foundation (JDRF) said today that the federal government's approval of an insulin pump that also provides real-time, continuous glucose monitoring is a significant step on the path to the development of an artificial pancreas, with the potential to significantly improve diabetes care and lower the risk of complications. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=41679

The Senior Research Officer and his team at UQ's Centre for Immunology and Cancer Research (CICR) are developing a drug that targets liver cells to prevent their inflammation in obesity -- a common precursor to diabetes. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=41575

Doctors May Fail to Recognize Anxiety in Alzheimer's Sufferers
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Physicians who treat people with Alzheimer's disease often fail to recognize symptoms of anxiety, researchers report. In many cases, anxiety may be mistaken for other psychological or medical problems, and the confusion may lead to inappropriate treatment. “Anxiety in Alzheimer's disease right now is not being picked up, and current assessment tools may be mistaking anxiety for agitation,” said Dr. Maria S. Almeida of the University of Nebraska Medical Center in Omaha. She presented her findings at the 26th Annual Conference of the Anxiety Disorders Association of America.Agitation is common in people with Alzheimer's and may share many of the symptoms of anxiety. But agitation is treated with psychosis-fighting medicines and other drugs that may not be appropriate for managing anxiety.Anxiety is a natural reaction to stress that everyone experiences from time to time. Anxiety can be a beneficial human response for recognizing danger, but an excessive and persistent state of anxiety can interfere with daily functioning and compound emotional distress. Symptoms are varied and can include:

• Intense worry and feelings of dread.
• Poor concentration and restlessness.
• Irritability and poor sleep.• Muscle tension and trembling.
• Palpitations or chest pains.
• Profuse sweating and hot flashes.

Alzheimer's is a distressing illness, and it is not surprising that anxiety would arise in someone with the disease. As memory and thinking skills fade, someone with Alzheimer's disease can be easily challenged by everyday situations or demands. Changes in the patient's surroundings, lack of social contact with others, and lack of structure can all compound anxiety in the person with Alzheimer's disease.Fortunately, anxiety is among the most treatable of all mental disturbances. Antidepressant drugs, such as Paxil, Prozac, and Celexa, may be very effective in alleviating anxieity. Tranquilizers, such as Ativan and amytriptyline, can also reduce anxiety, but in an Alzheimer's patient such drugs often increase confusion, and are usually avoided. Behavioral counseling might also help. If someone with Alzheimer's disease is experiencing distress and symptoms of anxiety, the best course would be to check with your doctor. There may be effective medicines or therapy tools to help calm the nerves and ease distress. By alzinfo.org

IOS Press is pleased to announce the forthcoming publication of a landmark work commemorating the centennial of Alois Alzheimer's discovery of what would be known as Alzheimer's disease (AD). Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=41422

Mayo Clinic researchers are sounding an alert about side effects of shock wave lithotripsy: in a research study, they found this common treatment for kidney stones to significantly increase the risk for diabetes and hypertension later in life. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=41413

Results of a new study support the hypothesis that periodontal therapy may improve metabolic control (lower HbA1c) in diabetic patients. This study appears in April's issue of the Journal of Periodontology. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=41496

Moderate Drinking Associated With Better Cognition In Women
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Source: American Heart Association
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A drink or two a day may be associated with better cognitive function in women, according to a report from an ongoing study of New York City residents. The report was published in the rapid access issue of Stroke: Journal of the American Heart Association.
"Women who had up to two drinks a day scored about 20 percent higher on the Mini Mental State Exam (MMSE) than women who didn't drink at all or who consumed less than one drink a week," said Clinton Wright, M.D., M.S., lead author of the study and assistant professor of neurology at the College of Physicians and Surgeons of Columbia University in New York. "The difference remained after adjusting for risk factors such as income, marital status, race or ethnicity and other vascular risk factors such as high blood pressure and cardiac disease."
The researchers said they were surprised by the lack of association between carotid plaque and alcohol consumption. Other research had suggested that alcohol consumption might slow the progression of plaque, the fatty material that builds up in arteries and increases the risk of heart attack and stroke.
"This study suggests that the relationship between alcohol and cognition was not mediated by large vessel atherosclerosis," Wright said. "Future studies with brain imaging are planned to examine the importance of small vessel disease in this relationship." more...

King Tut Mixed His Drinks more...

Stroke Patients May Be More Likely To Experience Memory Decline more...

Vitamins E And C Plus Ibuprofen May Protect Against Alzheimer's

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Source: Reuters Health
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For patients at high risk of Alzheimer's disease, taking a combination of vitamins E and C plus ibuprofen significantly reduces their risk, results of a longitudinal study suggest. "We found that for people at low risk, taking vitamin C and E alone is sufficient to further reduce their risk. But for those with apolipoprotein epsilon-4 (APOE-epsilon-4) alleles, the combination exerts a synergistic benefit," Dr. Majid Fotuhi told Reuters Health. Full Story

Antioxidant in green tea may improve memory Channel News Asia - Singapore... of the Neuroimmunology Laboratory at the University of South Florida, was quoted as saying that if the nature of beta-amyloid in the Alzheimer's mouse model is ...

Fish Oil May Help Protect Against Retinal Degenerative Diseases

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Source: Louisiana State University Health Science Center
A invited paper published in Trends in Neuroscience this week by Nicolas G. Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health Sciences Center in New Orleans, reports on the role that the omega-3 fatty acids in fish oil play in protecting cells in the retina from degenerative diseases like retinitis pigmentosa and age-related macular degeneration, the leading cause of loss of vision in those older than 65. The paper is titled, Cell survival matters: docosahexaenoic acid signaling, neuroprotection and photoreceptors.

The Alzheimer's BrainThis damage results in a buildup of Amyloid beta 42 peptide leading to neuronedysfunction and death. The role of neurofibrillary tangles in Alzheimer's ...
Impaired clearance of amyloid-beta causes vascular damage in ...Impaired clearance of amyloid-beta causes vascular damage in Alzheimer's disease... Amyloid-É¿ (AÉ¿) deposition is a hallmark of Alzheimer's disease and ...
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Miracle cures: expensive pills of the future

Alzheimer's Donation

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We are on the edge of a new era of drug discovery and decades of research into the basic science of biological systems is starting to bear fruit. Within the next 10 years new drugs tailored to individuals that will be both safer and more effective are set to appear on the market. New additions to the bathroom cabinet will include powerful statins to cut cholesterol, enzymes to promote digestive health and new classes of painkillers geared to personal pain receptors. Patients will have access to stem cells from which new tissue can be grown, and DNA profiling setting out their risks of developing or passing on inherited disease, and tests for predicting individual drug response.Gene therapy for certain childhood blood conditions such as severe combined immunodeficiency disorder has already proved effective, heralding a revolution in treatments for inherited disease.

The Alzheimer's BrainThis damage results in a buildup of Amyloid beta 42 peptide leading to neuronedysfunction and death. The role of neurofibrillary tangles in Alzheimer's ...
Impaired clearance of amyloid-beta causes vascular damage in ...Impaired clearance of amyloid-beta causes vascular damage in Alzheimer's disease... Amyloid deposition is a hallmark of Alzheimer's disease and ...

Liver Signal Critical For Insulin's Brain Action

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New research in the April, 2006 Cell Metabolism identifies a key player in the body's ability to respond to insulin action in the brain by ratcheting down the export of blood sugar from the liver. The findings point to a potential new drug target for the treatment of type 2 diabetes, according to the researchers. The group found evidence in mice that the gene STAT3 in liver mediates the effects of brain insulin. The STAT3 response depends upon interleukin-6, a chemical involved in the body's reaction to stresses, they reported. Earlier evidence by the researchers showed that the gene STAT3 controls glucose balance by limiting the activity of genes that manufacture glucose in the liver. However, the mechanism by which nutritional and hormonal status controls hepatic STAT3 had remained unknown, said study author Masato Kasuga of Kobe University Graduate School of Medicine in Japan. Insulin secreted by the pancreas after a meal normally allows body tissues, such as muscle and fat, to take up the blood sugar glucose. "In liver, which is responsible for minute-by-minute regulation of blood glucose levels and can export glucose as well as store it, insulin not only promotes the storage of glucose but also inhibits the production of sugar for export," explained Martin Myers, Jr., in a preview. The brain participates in the regulation of glucose production and insulin response by sensing and responding to nutrient levels and hormonal signals of energy intake and storage. In those with diabetes due to a lack of normal insulin or insulin resistance, blood sugar rises, a condition that can lead to tissue damage. An increase in glucose issued from the liver is largely responsible, Kasuga said. Now, the researchers have found in mice that an increase in blood insulin levels, achieved by administering glucose or insulin, leads to the activation of STAT3 in liver. The response depends upon the hormone's effects in the brain and an increase in interleukin-6. Animals lacking STAT3 only in the liver and those deficient for interleukin-6 lost the ability to respond normally to brain insulin by lowering the production of glucose, they reported. The current findings provide a "first glimpse" into the mechanisms that operate within the liver to decrease glucose output in response to insulin action in the brain, Myers said. "Given that disregulation of glucose production in the liver is an important pathophysiological feature of type 2 diabetes, the mechanism uncovered in this study may serve as a therapeutic target for this increasingly prevalent condition," the research team wrote.

Alzheimer's Drug Aricept May Have Benefit in Severe Alzheimer's Disease

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Aricept, currently approved for those with mild to moderate Alzheimer's disease, may offer modest benefits to those in the more advanced stages of the illness, researchers report. The drug appeared to reverse some of the memory loss and day-to-day deterioration seen in men and women with severe Alzheimer's disease, though the effects were not dramatic.About one in five people with Alzheimer's have severe disease. These later, more advanced stages of the illness are a particularly stressful time for families and patients, as patients become increasingly unable to wash, bathe, communicate, and care for themselves. Many must leave the home and enter a nursing home. The Food and Drug Administration (FDA) has approved only one medication, Namenda (medical name memantine) for the advanced stages of Alzheimer's. Aricept (donepezil) is currently approved only for the mild to moderate stages of Alzheimer's, though it is sometimes given along with Namenda for those with advanced disease. Aricept belongs to a class of drugs called “cholinesterase inhibitors,” which work differently than Namenda. Other drugs in the group include Exelon (also called rivastigmine) and Reminyl (galantamine). While these drugs may cause modest delays in deterioration of memory and thinking skills in early stages of the illness, they do nothing to stop the relentless progression of the disease.The current trial, published in the medical journal The Lancet, assessed the role of Aricept alone in severe disease. In the study, researchers at the Karolinska Institute in Sweden recruited men and women age 50 and older with severe Alzheimer's who were being cared for in Swedish nursing homes. Ninety-five were given Aricept, while ninety-nine were given a placebo (dummy pill). After six months, those taking Aricept did better on tests designed to measure thinking skills. They could also better carry out some daily activities compared to those taking the dummy pill. Side effects were similar in both groups. “Our findings indicate that donzepezil [Aricept] can improve cognition and preserves function in patients with severe Alzheimer's disease,” the authors write. “Overall, our data suggest that donepezil is an effective and well tolerated treatment, even when initiated in patients with severe Alzheimer's disease.” It remains uncertain whether costly medications such as Aricept are worth giving to people in the advanced stages of Alzheimer's disease. Indeed, studies suggest these drugs may have limited benefit even in those in the early stages of disease. Further study is needed. At the Fisher Center for Alzheimer's Research Foundation, the search for more effective treatments, and a cure, continues.

Breeding Better Animal ModelsDrug Discovery & Development (subscription) - Rockaway,NJ,USA... implicated in Alzheimer's such as tau or amyloid precursor protein ... have been implicated in early onset Alzheimer's, with over-expression of tau and beta. ...
Pfizer to Buy Rinat, a Biotechnology Drug MakerNew York Times - United States... Pfizer, however, appears to be more interested in Rinat's Alzheimer's drug, RN1219. It is a monoclonal antibody that blocks the amyloid beta peptide, which is ...See all stories on this topic

Ovary Removal Surgery Elevates Risk For Dementia

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Mayo Clinic researchers have found that ovariectomy, surgical removal of a woman's ovaries, raises her risk of developing dementia or cognitive impairment. Risk is especially increased if a woman has her ovaries removed at a young age.
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The findings will be presented Wednesday at the American Academy of Neurology meeting in San Diego.
The researchers studied 1,209 women who had surgical removal of both ovaries and 1,302 women who had only one removed from 1950 to 1987 in Olmsted County, Minn., home of Mayo Clinic. They compared each of the women who had undergone ovary removal with women who had no ovaries removed and followed them over time to see whether they developed dementia or cognitive impairment. Dementia or cognitive impairment was determined by interviewing a family member who reported a diagnosis of dementia, or by a low score on a telephone cognitive test given to the affected individual.


New guidelines developed by the American Academy of Neurology aim to educate physicians on the diagnosis and treatment of Parkinson disease and provide people with Parkinson disease an improved quality of life. Click link to read more. http://www.medicalnewstoday.com/medicalnews.php?newsid=40941

Alzheimer's rises with fat in certain spots, study saysMilwaukee Journal Sentinel (subscription) - Milwaukee,WI,USA... researchers reported finding a link between overweight middle-aged men and amyloid beta, the protein that accumulates in the brains of people with Alzheimer's. ...
New findings in the area of Alzheimer disease detailedTherapeutics Daily (subscription) (press release) - Newtown,PA,USA... in microglia perturbs genes relevant to Alzheimer disease (AD). "Key pathological processes in AD include the accumulation of amyloid beta peptide (Abeta) which ...

According to researchers at the Birmingham Veterans Affairs Medical Center, Alabama, USA, exposure to second hand smoking (passive smoking) is linked to higher incidences of glucose intolerance, which can lead to diabetes. Click link to read more.
http://www.medicalnewstoday.com/healthnews.php?newsid=41229

Higher Self-awareness Of Memory Complaints Predict Brain Function Decline

In one of the first studies of its kind, a UCLA team found that a higher self awareness of memory difficulties may be associated with brain function decline over time, particularly in older adults with a genetic risk for Alzheimer's disease. Published in the April issue of the Archives of General Psychiatry, the study offers a greater understanding of how different types and varying degrees of memory complaints may relate to brain function decline, a finding that may lead to early treatment interventions for people who could develop Alzheimer's disease.
"These findings may eventually help us identify which patients may benefit from clinical monitoring and early interventions to prevent or delay the onset of Alzheimer's disease," said Dr. Gary Small, principal investigator, professor at the Semel Institute and Parlow-Solomon Professor on Aging.
http://www.medicalnewstoday.com/medicalnews.php?newsid=40906
The Seven Major Markets for Alzheimer's Disease is Expected to Be ...Genetic Engineering News - Larchmont,NY,USA... Alzheimer's disease remains a challenge in management. ... inhibitors but they do not correct the basic pathology of the disease, beta amyloid deposits and ...

Two New Drugs for the Treatment of Alzheimer's Enter the Market by 2008

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Research and Markets (http://www.researchandmarkets.com/reports/c31730) has announced the addition of Emerging Diagnostic Markers in Alzheimers Disease to their offering.
- Currently, the most promising diagnostic agent for Alzheimer's disease (AD) is Pittsburgh Compound B, an A(beta)-amyloid imaging agent in development by GE Healthcare. We expect this agent to reach the market by 2011 and to increase the number of diagnosed and drug-treated patients by 2013.
- Several drugs are in development for treatment of AD; we expect two of these to reach the market by 2008. To be most effective, these treatments must be initiated in patients as soon as possible.
- Besides elucidating the progression of AD, a biomarker for AD would increase drug-treatment rates and therefore increase revenues for drug companies with marketed AD therapies. The increase in drug-treatment rates would result from earlier diagnosis of more patients and, consequently, longer durations of disease treatment. However, if no biomarker becomes available during our study period, we estimate that AD drugs will not attain their full market potential.
- The potential for sales of an AD diagnostic agent could be significant, due to the increasing prevalence of the disease and the potential for a diagnostic agent to command better pricing than a traditional diagnostic, given the large unmet need.
- A diagnostic agent approved by the FDA as an efficacy end point could dramatically grow the market potential for a disease-modifying drug by increasing diagnosis rates, drug-treatment rates, and duration of therapy. A therapeutic agent that demonstrated disease modification based on a biomarker could command a significant premium.
- An AD biomarker will greatly reduce costs associated with drug development by enabling selection of a more homogeneous patient population for smaller, more cost-effective clinical trials. A biomarker will also accelerate drug development by facilitating decisions as to whether to pursue or abandon agents in the early stages of clinical development.
Currently, Alzheimers disease (AD) is diagnosed based on patient clinical history and exclusion of other neurological disorders. Because early signs of AD are hard to distinguish from normal signs of aging, most patients are not diagnosed until neuronal damage is extensive. A diagnostic marker would enable physicians to diagnose more AD patients earlier and begin drug treatment when it could be most effective. The AD therapeutics market would also benefit: early diagnosis and treatment translates to more therapy sales over longer treatment periods.
In this Decision Resources report, we review AD diagnostic markers currently in use and in development, the main players in the AD diagnostics arena, and the impact that these markers will have on the U.S. AD market over the next ten years.

What kind of research has been carried out?

Carers are naturally always on the lookout for information about treatment. However, although there is as yet no curative treatment, there are numerous experiments underway, aimed at discovering new treatments, possible causes, protective factors and risk factors associated with Alzheimer's disease. As it is not possible to provide full details of all the research being or having been carried out, details are given below of just a few areas of research.

Aluminium
Aluminium can be found in tap water, antiperspirants, tea and indigestion tablets. Researchers have been studying the possible effects of aluminium in connection with Alzheimer's disease for over 30 years. However, although research is continuing, there is still no conclusive evidence for a causal link between aluminium and Alzheimer's disease.

Anti-inflammatory drugs
It has been observed that Alzheimer's disease is less prevalent in people suffering from rheumatoid arthritis. Such people tend to take anti-inflammatory drugs over a lengthy period of time. It is therefore suspected that these drugs might reduce the risk, delay onset and hinder development of the disease. Research is continuing.

Carers and Caring
Research has been carried out into the problems and needs of carers, e.g. the kind of support needed, difficulties encountered in providing care, problems obtaining a diagnosis and making difficult decisions, stress and depression. Such research is extremely important if the appropriate support, advice and services are to be provided for carers.

Estrogen
Studies have shown that women who took estrogen (a hormone) after their menopause, had a lower risk of getting Alzheimer's disease than those who did not. Another small scale study revealed that women who already had Alzheimer's disease and who took estrogen showed marked improvements in memory and attention which then diminished when it was withdrawn. Researchers are currently carrying out an in-depth, large-scale study into the effects of estrogen on Alzheimer's disease.

Genetics
Researchers have investigated genetic factors, which might lead to Alzheimer's disease (either a defect, which would directly cause the disease or an abnormality, which would increase the possibility of getting the disease). Abnormalities in 4 genes on the chromosomes 1, 14, 19 and 21 have been identified and further research is underway.

Pharmaceutical drugs
Extensive research is being carried out by pharmaceutical companies into drugs, which might slow down the progression of the disease or improve symptoms such as memory loss.

Smoking
Some European studies have found that in families with the inherited form of Alzheimer's disease, smoking cigarettes seems to protect them for a few years longer. However, Canadian research has indicated that heavy smokers had more than double the risk of developing Alzheimer's disease, whereas light smokers were at the same risk as non-smokers.

Powerful New Tool For Studying Brain Development

Source: St. Jude Children's Research Hospital
Scientists at St. Jude Children's Research Hospital have given investigators around the world free access to a powerful tool for studying brain development. The Internet-based tool, called the mouse Brain Gene Expression Map (BGEM), is one of the largest gene expression maps of an organ ever developed, according to the St. Jude researchers. They say the map will likely help scientists discover the genetic origins of brain cancers, which could speed development of novel drugs to treat them.
The continual updating and completion of the BGEM Web site will be crucial to scientists. More than half of the approximately 25,000 genes in the mouse are thought to be involved in the development and function of the nervous system, but scientists have determined the function of only 30 percent of them. Many brain disorders, such as tumors and some psychiatric diseases, are also believed to be caused by gene mutations that arise during development of this complex organ.
A report on the development and availability of the BGEM appears in the March 28 issue of PLoS Biology. The Web site is http://www.stjudebgem.org/

Researchers Team Up To Break Down Causes Of Alzheimer's

An enzyme previously associated with preventing the dementia of Alzheimer's disease now appears to play an even bigger role in safeguarding against the disease, bringing the promise of new targets for drug therapies. While scientists already knew that the enzyme known as Pin1 can prevent the tangles of knotlike brain lesions associated with Alzheimer's, new research, published in the March issue of Nature, finds the enzyme also plays a pivotal role in guarding against a second type of lesion, the buildup of plaque, or flat deposits on the surface of brain cells. Alzheimer's is caused by the two types of lesions, or alterations in brain tissue, occurring simultaneously. Researchers at Cornell University, Beth Israel Deaconess Medical Center (BIDMC) and Harvard Medical School authored the study. "The new finding provides a very specific molecular interaction that can be used as a target in drug discovery," said Linda Nicholson, co-principal investigator on the study and a Cornell associate professor of molecular biology and genetics. Nicholson and her Cornell team observed Pin1 acting on a protein called amyloid precursor protein (APP), which appears to be the primary cause of Alzheimer's. When APP gets a phosphate group attached to its tail (a process called phosphorylation), it toggles slowly back and forth between two forms. Like a kind of molecular Dr. Jekyll and Mr. Hyde, one form leads to buildup of plaque and disease, while the other form is part of normal function and helps neurons grow and survive. Using a powerful microscopic technique called nuclear magnetic resonance spectroscopy, Nicholson and colleagues found that Pin1 acts as a kind of molecular accelerator, allowing APP to toggle back and forth between its good and bad forms 1,000 times faster than if Pin1 were not present. In the absence of Pin1, the Hyde-like, disease-causing form of APP has a chance to build up to high levels toxic to cells, which leads to plaque lesions. "The really important thing here is that this research opens up entirely new therapeutic approaches to treating Alzheimer's," said Nicholson. One therapy to block the pathway that leads to plaque buildup might be to create small molecules that resemble the bad form of APP, which could then flood receptors and hinder the pathway, she said. Another way might be to create a molecule that attaches to this form of APP, which would also prevent binding to receptor sites, thereby interrupting the pathway. Nicholson and former graduate student Theresa Ramelot previously discovered the molecular switch in 2001.

Tea's brain health benefit link gets more support

Both green and black tea could protect against age-related diseases like Alzheimer's, says a new study, adding yet more support to the benefits of tea extract on brain health.“We looked at the protective effects of two tea extracts and their main constituents, called catechins, on dying nerve cells,” explained senior author Rémi Quirion from Douglas Hospital Research Centre, Quebec.
The research, published in the European Journal of Neuroscience (Vol. 23, pp. 55-64), claims to be the first to show beneficial effects of both green and black tea on cell cultures treated with amyloid proteins. Amyloid proteins are associated with the onset of Alzheimer’s disease, the most common form of dementia and currently affects over 13 million people worldwide.
The direct and indirect cost of Alzheimer care is over $100 billion (€81 billion) in the US alone. The direct cost of Alzheimer care in the UK was estimated at £15 billion (€22 billion).
Although the mechanism of Alzheimer’s is not clear, more support is gathering for the build-up of plaque from amyloid deposits. The deposits are associated with an increase in brain cell damage and death from oxidative stress.
The researchers used rat hippocampal cells as models for human cells, and found that addition of the beta-amyloid protein was toxic and killed the cells.
However, both green and black tea extracts, with concentration levels between five and 25 micrograms per millilitre, were found protective activity against the effects of the amyloid protein.
“These effects were shared by [tea extracts] gallic acid, epicatechin gallate (ECG), and epigallocatechin gallate (EGCG), the former being the most potent flavon-3-ol. In contrast, epicatechin and epigallocatechin (ECG) were ineffective in the same range of concentrations,” reported lead author Stéphanie Bastianetto.
Both EGCG and gallic acid were found to stop the amyloid aggregation, which could result in plaque formation, and also stopped potentially poisonous amyloid derivatives that would be diffusible across cell membranes.
“These data support the hypothesis that not only green but also black teas may reduce age-related neurodegenerative diseases, such as Alzheimer’s disease,” concluded Bastianetto.
It is known that the catechins can be extracted from both green and black teas, but the yield from the unfermented green tea leaf is significantly higher. Green tea is said to contains about 70 mg catechins per 100 mL, whereas black tea contains only about 15 mg per 100 mL.
This is further support for both the tea market and the tea extract market. European demand for tea extracts is currently surging, having reached 500 metric tonnes by 2003.
The global tea market is worth about €790 (£540, $941) million. Green tea accounts for about 20 per cent of total global production, while black tea (green tea that has been oxidized by fermentation) accounts for about 78 per cent.
Eisai, DNAVEC Join in Drug Discovery Research for Alzheimer's ...Japan Corporate News (press release) - Tokyo,Japan... signed an agreement with DNAVEC on drug discovery research for Alzheimer's disease (AD ... that can selectively induce the production of anti-beta amyloid antibodies ...