Therapeutic trials in familial cases of Alzheimer's
(focus on the pre-symptomatic phase)
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Why do so many candidate drugs for Alzheimer's disease fail in clinical trials? The question hung over this week's annual Alzheimer's Association International Conference in Paris, where the post-mortem on semagacestat, a drug from pharmaceutical giant Eli Lilly that was pulled late last year, was a hot topic. Researchers are now rushing to study carriers of rare genetic forms of Alzheimer's disease in search of an answer — and of a therapy that could save not only people affected by these 'familial' forms of the disease, but also victims of the more common 'sporadic' form that affects millions worldwide. According to the consensus emerging from the conference, drugs fail because they are given too late, after the accumulation of amyloid-β peptides, which form sticky plaques in the brain, and other physiological changes have already destroyed the patient's neurons and neuronal networks. At that point, even removing the amyloid-β, the aim of many of the treatments, won't do much good. "There is already significant neuronal loss, so removing the amyloid is unlikely to reverse things," says Randall Bateman, a neurologist at Washington University in St Louis, Missouri. Continue to read: dailymail.co.uk
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