In the 23 Mar 06 issue of Nature (Vol. 440, No. 7083), researchers reveal how an enzyme called Pin1 plays a part in the pathogenesis of Alzheimer's disease.
Brain plaques, consisting of amyloid-beta peptides derived from amyloid precursor protein (APP), are one hallmark of Alzheimer's disease. Kun Ping Lu and his colleagues present evidence that Pin1 regulates the processing of APP into toxic forms of amyloid- beta.
The team shows that Pin1 directly binds to a specific region in APP, boosts - by 1,000-fold - its conversion from one conformation to another, and seems to suppress the production of amyloid- beta 42, a particularly toxic form of amyloid- beta. Further studies on this conformational change may help clarify the molecular events leading to Alzheimer's, the authors say.
Kung Ping Lu (Harvard Medical School, Boston, MA, USA)
(C) Nature press release.
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