Transmission des lésions amyloïdes de la maladie d’Alzheimer : apports des modèles animaux

Abstract

Transmission of amyloid lesions in Alzheimer’s disease : contributing data from animal models. Since the discovery of the transmissibility of prion diseases, other cerebral proteinopathies have been suspected to harbor similar transmissible properties. Alzheimer’s disease (AD) is characterized by the deposition of misfolded β-amyloid (Aβ) peptides and hyperphosphorylated Tau proteins, forming amyloid plaques and neurofibrillary tangles respectively in the brain. Although available epidemiological data suggest that AD is not transmitted between individuals, suspicion has recently been raised for iatrogenic β-amyloidosis transmission between humans. This suggests that Aβ misfolding and aggregation could occur through seeding and spreading mechanisms, virtually identical to those of prions. Here, we present a review of the literature focusing on the relevance of prion-like misfolding and aggregation mechanisms for Aβ in animal models.