J Biomol Struct Dyn 2007 Dec 01;253:271-4.

Rat's trick to escape Alzheimer's disease.

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Amyloid beta (Abeta) peptides fibril formation and deposition is considered to be the principal pathological hallmark of Alzheimer's disease (AD). However, it remains obscure why AD is precluded by rat/mouse despite the high sequence identity (97%) of rat/mouse Abeta to its human homologue. Based on the recently proposed redox chemistry-based pathogenic model of neurodegenerative diseases, we hypothesize that the lack of key residues of rat/mouse Abeta compared with the human counterpart may account for why rat/mouse is free of AD. At the same time, we propose a new possible redox chemistry-based pathogenic model of AD based on the experimental observations of certain residues in triggering Abeta aggregation. Moreover, it is also interesting to note that non-mammalian Xenopus Abeta contains all the redox chemistry-related key residues and whether it implies that Xenopus Abeta possesses high amyloidogenic potency remains to be determined by further experimental study.

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???displayArticle.link??? J Biomol Struct Dyn


GO keywords: amyloid-beta metabolic process

???displayArticle.disOnts??? Alzheimer's disease
???displayArticle.omims??? ALZHEIMER DISEASE, FAMILIAL, 1; AD1