Are exosomes the vehicle for protein aggregate propagation in neurodegenerative diseases?

Abnormal protein aggregation has been implicated in neurodegenerative processes in human neurological disorders, such as Alzheimer's disease and Parkinson's disease. Recently, studies have established a novel concept that protein aggregates are transmitted among neuronal cells. By extension, such interneuronal aggregate transmission has been hypothesized to be the underlying mechanism for the pathological and clinical disease progression.

Amplification of distinct α-synuclein fibril conformers through protein misfolding cyclic amplification.

Amyloid fibril formation has been implicated in the pathogenesis of neurodegenerative diseases. Fibrillation generates numerous conformers. Presumably, the conformers may possess specific biological properties, thus providing a biochemical framework for strains of prions.