Contribution of Multivesicular Bodies to the Prion-Like Propagation of Lesions in Alzheimer’s Disease

摘要: Alzheimer’s disease (AD) is a chronic developing dementing characterized by coexistence of two types lesions, the parenchymal amyloid deposits and intraneuronal neurofibrillary tangles. Amyloid are composed amyloid-beta peptides that derive from sequential cleavages its precursor named protein (APP). Neurofibrillary tangles (NFT) results aggregation abnormally modified microtubule-associated Tau proteins. A synergistic relationship between lesions may trigger progression disease. Thus, starting in entorhinal cortex slowly progressing through temporal, frontal, parietal occipital cortex, NFT well correlated with clinical expression However, little known about mechanism underlying spatiotemporal propagation these ultimately leading to growing number studies suggest prion-like diffusion NFT, which could even be extrapolate several other neurodegenerative diseases. In present chapter, we will develop current hypotheses regarding molecular cellular mechanisms driving development spreading involving multivesicular bodies.