July 15, 2005
Study Suggests That Alzheimer's Damage May Be ReversibleTopics:
An interesting and provocative new study in mice suggests that some recovery of memory may be possible in the early stages of Alzheimer's disease. If their conclusions are correct, we could see a new two-pronged attack against the dibilitating disease.
The leading theory in Alzheimer's is that something spurs abnormal production of beta-amyloid, which forms sticky clumps that coat brain cells and kill them -- plaque that is the disease's hallmark. But tau clearly plays some role: A mutant form of this protein forms fibrous tangles in brain cells of Alzheimer's patients, and tau seems to be primarily responsible for another form of dementia.
(...) The research shows a mutant protein named tau is poisoning brain cells, and that blocking its production may allow some of those sick neurons to recover. It worked in demented mice who, to the scientists' surprise, fairly rapidly regained memory.Read more ...
(...) The work is years away from being useful in people. There are no drugs yet to block tau, and most of the recent search for Alzheimer's treatments has focused instead on another protein, called beta-amyloid.
(...) But the study, published in the journal Science, is sure to refocus attention on finding ways to attack this second culprit, too.
This study has more meaning when you consider that there is evidence that tau must be present for beta-amyloid to cause the degeneration of brain cells that occurs in Alzheimer’s disease. Experimental results have shown that neurons with normal amounts of tau degenerated in the presence of beta-amyloid, while neurons specially treated to be devoid of tau did not degenerate.
Another related link:
[A blurring of the traditional distinction between basic and applied research is increasingly evident in the study of neurodegeneration. Complex and previously enigmatic diseases of post-mitotic neurons, such as Parkinson's, Huntington's and Alzheimer's diseases, seem to share elements of a common pathogenic process: the misfolding and progressive polymerization of otherwise soluble proteins. Although the molecular and cellular details vary greatly among these disorders, the tendency for highly soluble neuronal proteins to develop altered conformations as a function of time or genetic mutation and then aggregate inside cells — and in the case of Alzheimer's disease, also outside cells — precedes the earliest clinical signs of these diseases and is associated with profound neuronal dysfunction and death.- more ... ]
Hat tip - Debra Donham Barr
Companion post at Hyscience
Posted by Richard at July 15, 2005 5:48 PM
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