Monday, August 4, 2008

Alzheimer's Research Shows Improvement

Recently, researchers have made improvement in the search for treatments against Alzheimer's disease.

An older drug called dimebon has significantly improved Alzheimer's symptoms. However, in a second report, a once-promising vaccine failed to prevent the progression of Alzheimer's. Even though, the drug has cleared dementia-linked amyloid plaques in the brain.

Recently, the research has been made to find out the causes and treatment of dementia, including Alzheimers disease. According to the United States National Institutes of Health, an estimated 4.5 million Americans have Alzheimer's disease that thought to influence one in 20 people between the ages of 65 and 74. Moreover, the estimated rate goes up to nearly half of those aged 85 and older.

Dr. Clive Holmes, a leader of British researchers from the Memory Assessment and Research Centre at Moorgreen Hospital in Southampton, in a study has analyzed data on 80 Alzheimer's patients who were treated with an experimental vaccine that for now is dubbed AN1792.

The vaccine of AN1792 is targeted at the removal of amyloid protein plaques, which is clump around brain cells in increasing numbers as Alzheimer's progresses. The theory was that dementia could be reversed or slowed once the plaques were cleared. The experiments with the animals have shown that removing these plaques can improve brain function.

According to Holmes, long-term follow-up of Alzheimer's patients treated with AN1792 did show a reduction in the number of plaques in the brains of patients. In addition, in some cases there was a virtually complete removal of plaques. However, there was no proof that the patients benefited by the removal of plaques and even those subjects with virtually complete removal continued to deteriorate and had severe end-stage dementia prior to their death.

The researcher has made simple conclusion based on these results that removing plaques (at least by this method) is unlikely to make a significant difference to the clinical outcome of patients with established Alzheimer's disease. In addition, it strongly suggests that plaques are not sufficient on their own to account for disease progression. Holmes said treatments should move towards preventing plaques from building up in the first place or in established Alzheimer's disease. Moreover, he added treatments should focus more on non-plaque therapies.

According to Dr. Sam Gandy, chairperson of the Alzheimer's Association's National Medical and Scientific Advisory Council, the new finding suggests that other forces besides plaque build-up are driving disease progression. Gandy said, "If you do not start with your vaccine until you are at a later stage of disease and other processes are already established, the horse may be already out of the barn.” Moreover, he said it is possible that amyloid is like a match lighting a fire and once the fire is out of control, dealing with the match is not that effective."

However, there was better news in a second study. Dr. Rachelle S. Doody, a professor of neurology at the Alzheimer's Disease and Memory Disorders Center at Baylor College of Medicine in Houston, and her colleagues have studied in that work about the effects of the drug dimebon on 183 patients in Russia with mild to moderate Alzheimer's disease. Currently, the drug is not marketed anywhere, and was previously used in Russia as an antihistamine. After six months, Doody's team found that patients on dimebon had significant improvement in cognitive ability, compared with those receiving placebo.

Those patients were evaluated using ADAS-cog, a battery of tests that assesses a person's ability to track dates, comprehend instructions, memorize word lists, follow commands, and complete simple tasks such as addressing an envelope or copying drawings.

The researchers report that at six months, patients receiving dimebon showed an improvement of 1.9 points on the ADAS-cog scale from the beginning of the study, while those on placebo continued to decline. After a year, those patients who have received dimebon showed a 6.9-point increase on the ADAS-cog scale.

The study was settled and done in Russia because dimebon had been approved there as an antihistamine. Dimebon is made by Medivation, the San Francisco-based biopharmaceutical firm. Doody is on the Scientific and Clinical Advisory Board of Medivation and has stock options in the firm.

According to Doody, this first trial was promising. The result is not a cure for Alzheimer's disease, but the benefits could last for a long time. The drug appears to slow the clinical progression of the disease. However, he is still awaiting the completion of the next study, so that he and his team can see if this drug could potentially be approved for treating Alzheimer's patients. On the other hand, Gandy said the drug does appear to be superior to the currently approved medicines for Alzheimer's disease. Gandy said that this is the first new promising symptomatic therapy in a long time. In addition, the drug could potentially add to the impacts of other drugs such as Namenda, Aricept and Exelon.

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