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This is a drug development company in the late stages of developing a drug to retard alzheimers disease. Proof of principle has been acknowledged by a leading US neurological scientific journal. The foundational work has been carried out by Prof Ashley Bush of the Massachussetts General Hospital which is the research arm of Harvard Medical School. In Australia Ashley Bush and Professor Colin Masters began the work in 1997. Profesor Bush just signed on for another extended period with Prana.


The basic drug is Clioquinol. It had another use some time back so it does not need to be demonstrated as safe for human use.


The web-sites above, one NASDAQ, give a full picture.


There are two streams of activity. First is the development of a drug to retard Alzheimers. It has been suggested tentatively that it may even allow limited rehabilitation. The second is the development of a vaccine. The latter is being done in partnership with Prima Biomed, PRR, PRROB.


Price has oscillated between 50 and 60c in recent times but can be expected to move significanrly when results of current work are available.


Worth a look!



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If PBT is getting to expensive, don't forget that it has a deal with PRR to develop a vaccine and share the royalties.


PRR has options, PRROB that are convertible in June. Options are a little cheap at 6.8c. There's a cent in it at least.



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Stealing your memories

By Steve Rotherham

May 01, 2004


FOUR years ago, Alan was a successful medical specialist with his own practice in suburban Perth. Today this once hardworking professional is almost helpless.


Alan can no longer read and write or drive a car. His food must be cut for him and he needs help to get dressed. He has great difficulty using keys or a telephone or finding the words to express his ideas, and he has been on a maintenance dose of an anti-depressant for years.


"Depression is often one of the first signs of Alzheimer's," Alan's wife, Jenny says. She and Alan (who prefer not to give their full names) have had to make many adjustments over the last four years.


The speed of the disease's progression is not always predictable ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ it can last for three to 20 years from diagnosis until death ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ but it does inevitably advance, spreading through the brain, killing neurons, destroying skills, faculties, memories and identity.


"Alzheimer's always gets worse ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ it's a progressive and terminal disease," Jenny says.


Jenny is only 52 and Alan was just 53 when Alzheimer's struck him. The symptoms became apparent in 2000 and were soon so bad that he had to give up his practice.


"The first symptoms were increased forgetfulness, an inability to spell common words and trouble reading," Jenny says. "He knew something was very wrong and he became depressed."


The first phase of Alzheimer's is usually is about three to four years, characterised by vagueness and mild memory loss, especially of recent events. People developing Alzheimer's can also lose enthusiasm for activities they once enjoyed and take longer to do routine tasks.


Personality changes can emerge ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ the sufferer can become obsessive or more aggressive.


Four years on, Alan's deterioration is marked and Jenny believes he has entered the middle stage of Alzheimer's. "My husband isn't like my husband anymore," she says.


"I can't rely on him for protection and support. Our children have had to go from having a father figure to being carers for their father."


She knows there is worse to come. As Alzheimer's progresses, functioning regresses and family ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ often partners ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ must assist with the forgotten skills of daily living.


In the advanced stages, communication problems continue to worsen ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ vocabulary shrinks and misinterpretations become common. Delusional thinking and hallucinations can occur. Eventually, well-learned skills are lost ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ patients can no longer dress, eat or walk. At this stage, severe sleep problems, weight loss and incontinence will require high levels of specialised care.


Alan is still witty, can have meaningful conversations and still recognises friends.


But Jenny is aware that little by little, all of these faculties will slip away, and one day ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ perhaps in just a few years ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ he will die.


"I don't know if he will be around when our daughter gets married or if he will see his first grandchildren ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ and if he does see them, will he understand what he is seeing?"


With Australia's population ageing rapidly and life expectancies growing, more and more people will find themselves facing the same problems as Alan and Jenny.


An Access Economics report ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ The Dementia Epidemic ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ commissioned by Alzheimer's Australia and published last year, found 160,000 Australians were living with Alzheimer's and other forms of dementia. Unless a cure or preventative treatment can be found the number will reach 500,000 by 2040.


The likelihood of being affected by dementia doubles each five years after the age of 60.


By the time the time you are 90, it is more likely than not that you will have some form of dementia, according to Alzheimer's Australia National Executive Director Glenn Rees.


"The prevalence of dementia has increased 62 per cent in the last decade, and will be the number-one cause of disability for our ageing baby boomer population ahead of cardiovascular disease, cancer and depression," Rees says.


The report highlights the snowballing social and economic burden of dementia on an already under-resourced aged-care system, and the growing number of elderly Australians with dementia living without effective treatment and care.


Dementia is already Australia's most costly mental health problem.


By the end of this decade the current $6.6 billion annual cost to Australia will double, and costs from the dementia epidemic will probably exceed 3 per cent of GDP, according to the report.


It argues that Australia will save money by providing better services for people with dementia and their carers, including more well resourced, dementia-specific community and support programs, as well as early diagnosis and treatment. This will delay institutionalisation.


The Alzheimer's Australia report also calls for significant financial investment into research on the causes of and treatments for it and other forms of dementia.


It argues that federal investment in finding a cure should be boosted from the current $2.5 million a year to about $49 million a year, which would bring Australia in line with US expenditure.


And Alzheimer's, constituting about 60 per cent of dementia cases, should get the bulk of research dollars. But the Commonwealth has committed no extra funding to dementia research.


Australia has excellent research organisations producing cutting-edge work, but these bodies rely on financial donations and struggle to fund their work.


One organisation, the McCusker Foundation, warns that its research team may soon have to break up due to lack of funding.


There is broad agreement on how Alzheimer's develops.


In healthy people a protein known as beta-amyloid exists in small amounts in the brain and build-ups of this protein are cleared away. But in people with Alzheimer's, beta-amyloid builds up to form abnormal plaque deposits between nerve cells.


This plaque somehow induces "neurofibrilliary tangles" (NFTs), in which twisted filaments disrupt nerve cells' transport systems and cause malfunctions in communication between nerve cells.


In combination with toxins released by the plaque, the NFTs seem to kill brain cells.


As Alzheimer's progresses, nerve cells die in parts of the brain that control memory and learning. The brain shrinks as gaps develop in these areas.


Then tissue loss moves across the brain like a bushfire, consuming all before it, spreading relentlessly until it burns itself out.


The relationship between plaques and the NFTs is not well understood, says Professor Jillian Kril, a research neuropathologist at the University of Sydney's Ageing & Alzheimer's Research Foundation.


Nor is there agreement on the specific ways the plaque affects the brain, but increasingly researchers are concluding that beta-amyloid plaque deposition is central to the development of Alzheimer's.


"We probably won't develop a 'cure' for Alzheimer's, because we can't repair existing damage," Professor Kril says. But ways could be found to halt the progress of the disease and to prevent it occurring in new patients.


"The most promising direction for research would be looking at reducing the formation of beta-amyloid and the laying down of plaques," he says.


"But it may not be the whole answer ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ effective treatment and prevention may require a complex of medicines."


Currently the most common treatments for Alzheimer's are aimed at improving the function of the remaining living brain cells.


Most of these reduce the breakdown of acetylcholine, an important neurotransmitter that helps carry messages between nerve cells. Other less commonly used drugs work on other neurotransmitters.


These drugs buy precious time ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ sometimes months, sometimes a year or more, depending on the progress of the disease ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ for patients and their carers. But they do nothing to address the underlying causes of Alzheimer's nor halt the progress of the disease.


New treatments are needed and some researchers in Australia and overseas believe they are making significant headway in developing ways to stop the disease in its tracks and prevent it emerging in as yet unaffected people.


Some medicines and other treatments are already emerging, and despite inadequate funding Australia is punching well above its weight in Alzheimer's research.


"This is an exciting time right now ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ we are rapidly pulling the pieces together," says Ralph Martins, director of research at the McCusker Foundation for Alzheimer's Research at Perth's Edith Cowan University.


In 1985, Professor Martins and other University of Western Australia researchers working under Colin Masters first showed that brain plaques in Alzheimer's patients were formed from beta-amyloid. The following year, Martins was the first person in the world to publish material showing that oxidation was occurring in Alzheimer's, which has led to studies on how antioxidants could be used to mitigate the progress and effects of the disease.


A few years later in Melbourne, he supervised Ashley Bush, a promising student, in the first year of his PhD. Today all three men are leaders in developing treatments for Alzheimer's.


While Martins has returned to Western Australia, Professor Masters is head, Alzheimer's Disease Research, at the Mental Health Research Institute of Victoria (MHRI)and Professor Bush now divides his time between Melbourne, where he works as Director of the Oxidation Disorders Laboratory at the MHRI, and the US, where he is Associate Professor of Psychiatry at Harvard Medical School.


Bush says beta-amyloid is a normal protein and his research shows that plaques and associated problems occur when a damaged form of beta-amyloid reacts with zinc and copper.


But he warns that while reducing amyloid levels is desirable, shutting down amyloid production altogether could be harmful, as amyloid has some important functions.


"Zinc promotes aggregation of beta-amyloid plaques and copper then promotes the toxicity of these plaques," he says. This is a controversial theory but it is supported by recent evidence, he claims.


"We have been dealing with scepticism for nearly 15 years," Bush says. "While we have built up a large amount of evidence to support the science, the proof of the pudding will only be in making drugs. The correct theory will be the one that provides drugs."


Bush is referring to one drug in particular ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ clioquinol ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ which he says binds zinc and copper ions, shuts down the beta-amyloid's reaction with these metals and leads to the plaque dissolving into soluble, non-toxic protein.


MHRI's affiliated company, Prana Biotechnology, has conducted two studies into this drug ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ a 36-week clinical trial and a subsequent extension study over 48 weeks involving nine of the 18 patients from the first study.


The results of the extension study were released last week.


According to Prana, using clioquinol over 18 months markedly slowed the decline in cognitive function in Alzheimer's patients compared with the predicted level of decline available from the scientific literature.


In addition, the longer-term treatment was well tolerated.


"The drug significantly lowered plasma amyloid and was the first drug ever reported in humans to achieve this effect," Bush says.


"The results are clearly in the right direction, and the hope is that if we scale up with larger numbers that the results will be a major improvement in treating Alzheimer's disease."


The next step is a larger trial, probably involving larger doses now that it has been shown that clioquinol is well tolerated. Bush expects that it could even possibly be used for people at high risk of developing Alzheimer's as part of a preventative strategy.


Martins agrees that clioquinol is an important step forward, but he is now conducting research into molecules that neutralise beta-amyloid's tendency to bind with metal ions and thus neutralise its toxicity. But such a drug is many years away and even clioquinol will not be available to the Australian public until 2009.


So what can Alzheimer's patients, their carers and people at risk of developing the disease do right now? Plenty, says Martins.


Cardiovascular disease, stroke and diabetes are all risk factors for Alzheimer's, and the risk factors for these diseases ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ smoking, heavy alcohol use, poor diet and physical inactivity ÃÆâ€â„¢ÃƒÆ’ƒâہ¡ÃƒÆ’‚¢ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â€š¬Ã…¡Ãƒâ€šÃ‚¬ÃƒÆ’…¡Ãƒâہ¡ÃƒÆ’‚¬ÃƒÆ’¢Ã¢Ã¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã‚¡ÃƒÆ’‚¬Ãƒâ€Â¦ÃƒÆ’¢Ã¢Ã¢â‚¬Å¡Ã‚¬Ãƒâ€¦Ã¢â‚¬Å“ also increase the chances of getting Alzheimer's.


Martins believes a good diet and supplementation with antioxidants such as vitamin E, gingko and pycnogenol are important. And so is exercise.


"Exercise increases blood flow through the body and brain, it regulates cholesterol and it enhances clearance," he says.


By clearance he means the brain's ability to clear beta-amyloid proteins and excessive levels of zinc so that plaques do not form.


The toll that an unhealthy lifestyle has taken on an individual can be measured to some extent by measuring levels of the amino acid homocysteine, and cholesterol.


High levels mean you are more likely to develop health problems and it has been shown that high homocysteine and high cholesterol increase beta-amyloid production, making them risk factors for Alzheimers.


Kril argues that exercising, modifying diet and reducing homocysteine levels would be helpful but could only have a limited effect.


"They are modifying factors rather than the core causation of Alzheimer's," she says.


But Martins maintains that for people without a genetic predisposition towards Alzheimer's, cholesterol and homocysteine are the core causal factors.


"Lipitor (a cholesterol-lowering drug) has now been shown to slow the progression of Alzheimer's," he said, brandishing a press release dated April 14.


According to this report, two-thirds of participants in a 63-person trial at Arizona's Sun Health Research Institute derived some clinical benefit from Lipitor. Half of the patients stabilised or actually improved.


"And Professor Leon Flicke at the University of Western Australia has recently shown a positive association between homocysteine and beta amyloid levels in the blood," he adds.


Research in Wales has also shown that reducing homocysteine helps Alzheimer's patients.


Andrew McCaddon is a GP who has conducted research with the University of Wales.


"We were initially disappointed by the results we saw from lowering homocysteine levels by simple supplementation with B12 and folate," Dr McCaddon told The Weekend Australian.


"However, the addition of the glutathione precursor N-acetylcysteine to this regime has resulted in prompt, striking, and sustained clinical improvement in nearly all of our patients."


The N-acetylcysteine helps produce glutathione, an antioxidant with powerful detoxifying properties, he says.


But homocysteine and cholesterol are not determined solely by lifestyle.


About half the Alzheimer's population have been found to have a genetic basis to their disease. The APO-E4 gene is found in 16 per cent of the general population but in about 50 per cent of people with Alzheimer's, Martins says.


"These people have a strong predisposition towards Alzheimer's, but it doesn't mean they will inevitably develop the disease."


For many of them, a healthy lifestyle might be enough to ward off Alzheimer's, while others will need treatments to reduce their cholesterol and homocysteine, Martins says.


And less than 3 per cent of the Alzheimer's population have one of the presenilin genes. People with one of these genes can build up amyloid plaques and develop Alzheimer's as early as their 20s.


They can benefit from lifestyle changes and homocysteine and cholesterol treatments, but they will also need drugs such as clioquinol, and Martins' proposed anti-amyloid drug.


"But for the vast majority of us, lifestyle factors are going to play a major role in keeping Alzheimer's at bay," he says.


from http://www.theaustralian.news.com.au/commo...5E23289,00.html

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  • 2 months later...

PBT 'holders' may be interested in my post on the CGS board just now.



Great 'info' Cotton Eyed Joe!! - I note that PBT 'fell' overnight. In spite of 'their' good Dr Bush was addressing the conferance again throughout the day. (below) - (Although, UP in the A/Hrs?)




"Also at ICAD, on Wednesday July 21, Dr. Bush is scheduled to give an invited lecture that will review the basic neuroscience describing the involvement of brain copper and zinc in Alzheimer pathology. New data is expected to be presented on the interaction of cholesterol with beta-amyloid and brain metals, which may play a key role in the sequence of events that leads to dementia. "


I've just checked the A/Hrs for PRAN (PBT) and note a 'buy' @ 16:13:46 @ $4.473 for 4000 shares. Interesting??? - In the above announcement they quote that "New data is expected to be presented" by Dr Bush! - I wonder IF he did his 'spool' late in the afternoon and someone has run out and bought the 4000?? LOL (I mean .... It IS .453cps above the 'close' of $4.02c ????)


PRAN - (As shown on Wall Street City)




Last: 4.473c

Close: 4.02c

High: 4.330

Low: 4.010

Open: 4.180

Change: +0.34

Volume: 122,400



Bid: 0.010

Ask: 9000.000

Bid/Ask Size: 357,700 / 100



52 Wk High: 10.500

52 Wk Low: 2.950

%Change: -2.7%



Market Cap: 29M

Price/Sales: 16.0

EPS: $-0.50

P/E Ratio: N/A


Time Price Volume Exchange Info



16:13:46 4.473 4000 Nasdaq Small Cap

15:59:03 4.020 500 Nasdaq Small Cap at Bid

15:55:02 4.020 500 Cincinnati at Ask

15:55:02 4.010 500 Nasdaq Small Cap at Bid

15:54:58 4.040 400 NASDAQ at Bid

15:54:24 4.040 300 Pacific at Bid

15:54:14 4.060 600 Nasdaq Small Cap at Bid

15:54:12 4.050 200 Nasdaq Small Cap

15:54:09 4.060 100 Pacific

15:54:04 4.060 200 Nasdaq Small Cap at Bid


I have bought some PBT anticipating an UP night tonight, maybe.


Thanks Cotton Eye Joe, once again!





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