Dementie onderzoek: kortzichtig!

Het onderzoek naar de behandeling van dementie (Alzheimer) richt zich al jaren op twee targets, beta-amyloid en tau. Er wordt zelfs gesproken van 2 scholen, de baptists en de tau-ists. Grote farmaceutische belangen gaan achter die twee schuil, want veel industrieen richten zich op de ene of de andere target. En nieuwe middelen uit de industrie helpen patienten zelfs van de wal in de sloot, zoals recent bleek...

Nu in de Lancet een sterke kritiek op de myopie van de wetenschap inzake dementie, en we citeren enkele zinnen n.a.v een recent artikel met de provocerende titel:

Why are drug trials in Alzheimer’s disease failing? [1] 

The dominant hypothesis in the field is the amyloid hypothesis and almost all trials of potential disease-modifying drugs are based on manipulation of β amyloid.

In the recently abandoned semagacestat trial, some patients on the drug got worse—ie, the drug, which was designed to inhibit formation of β amyloid, seemed to speed up cognitive decline. One interpretation is that the formation of β amyloid might be the brain’s protective mechanism against the disease process.

But this view is regarded as pure heresy.

Is that because so much research funding and such large drug development budgets are at stake?The review by Mangialasche and colleagues concluded that “the one protein, one drug, one disease hypothesis used as a basis of most Alzheimer’s disease therapy studies needs to be revised.”

Bron: citaat The Lancet Volume 376, Issue 9751, 30 October 2010-5 November 2010, Page 1466 

Modern dementie onderzoek: van de wal in de sloot 

It is time that we stopped looking for a “cure” but directed our research effort to the prevention of Alzheimer’s disease.

….the one protein, one drug, one disease hypothesis used as a basis of most Alzheimer’s disease therapy studies needs to be revised…. inderdaad, we zijn allemaal myope wezens en denken in monocausaliteiten. Dat helpt de patient niet, of van de wal in de sloot….[2]

November 2010, JMKH