Elsevier

Journal of Physiology-Paris

Volume 92, Issues 3–4, June–August 1998, Pages 289-292
Journal of Physiology-Paris

The role of Aβ42 in Alzheimer's diseaseRôle de l'Aβ42 dans la maladie d'Alzheimer

https://doi.org/10.1016/S0928-4257(98)80035-1Get rights and content

Abstract

Our recent studies of plasma, fibroblasts, transfected cells and transgenic mice show that a fundamental effect of the mutations linked to familial Alzheimer's disease (FAD) is to increase the extracellular concentration of Aβ42. This effect of the FAD-linked mutations is likely to be directly related to the pathogenesis of Alzheimer's disease (AD) because Aβ42 is deposited early and selectively in the senile plaques that are an invariant feature of all forms of AD. Thus our results provide strong evidence that the FAD-linked mutations all cause AD by increasing the extracellular concentration of Aβ42 (43), thereby fostering Aβ deposition, and they support the hypothesis that cerebral Aβ deposition is an essential early event in the pathologenesis of all forms of AD. Interactions between the basal forebrain cholinergic system and Aβ that could influence AD pathogenesis are discussed.

Résumé

Des études récentes effectuées sur le plasma, des fibroblastes, des cellules transfectées et des souries transgéniques montrent que les mutations liées à la maladie d'Alzheimer familial (FAD) augmentent la concentration extracellulaire d'Aβ42. Cet effet des mutations liées à la FAD est probablement directement lié à la pathogénocité de la maladie d'Alzheimer puisque Aβ42 est présent plus tôt et plus sélectivement dans les plaques séniles par rapport aux autres formes d'AD. Ces résultats confortent l'hypothèse que le dépôt d'Aβ est un événement essentiel dans toutes les formes d'AD.

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