Many neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia and amyotrophic lateral sclerosis, are devastating disorders that affect millions of people worldwide. However, the number of therapeutic options remains severely limited with only symptomatic management therapies available. Mounting evidence suggests that dysfunction in protein homeostasis network and protein misfolding in the brain may be the common pathogenic mechanisms for many neurodegenerative diseases. For example, accumulation of the amyloid beta peptide, the major component of amyloid plaques, is hypothesized to trigger a pathogenic cascade that ultimately leads to neuronal dysfunction and neurodegeneration in Alzheimer’s disease. Therefore, understanding the factors that induce cerebral Abeta aggregation and subsequent amyloidosis is critical for the development of effective therapy.