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Biotech / Medical : Neuroscience -- Ignore unavailable to you. Want to Upgrade?


To: Jim Oravetz who wrote (252)7/30/2003 8:55:17 AM
From: scott_jiminez  Respond to of 278
 
Haven't read this PNAS article yet...the ß-amyloid/tau association is not news, the caspase correlation (distinct from 'causal' semantics) is more intriguing but not altogether novel. 'Elucidated' implies nothing more than an association was found and does not necessarily suggest that blocking the specific caspase (there are many) will greatly alter the course of amyloid-induced cellular dysfunction and destruction.

Anti-caspase abs to block this implied cascade is likely to lead to a plethora of unintended side effects.

While the NPR report accurately depicted the isolationist and self-serving character of the Alzheimer research 'camps', the gravitas granted this finding is misplaced. The role of caspase is another interesting aspect of the Alz pathology; it is neither a cornerstone of the etiology nor will it provide an avenue of treatment.

In short, NPR's random weekly search of the science literature - a process whose results will always find someone to provide a glowingly supportive interview - should always be absorbed with a good deal of skepticism.



To: Jim Oravetz who wrote (252)8/5/2003 11:27:31 AM
From: Jim Oravetz  Read Replies (2) | Respond to of 278
 
Myriad Genetics comments on Alzheimer's disease candidate drug (MYGN) 14.55: Co announces that its Alzheimer's disease candidate drug, MPC-7869 (R-flurbiprofen) reduces levels of Abeta42 more effectively than any other compound tested, according to a new study. Abeta42 is the primary constituent of senile plaques that accumulate in the brains of patients with Alzheimer's disease.

Briefing.com