The role of PrPc in Alzheimer's disease related Amyloid-β hypothesis: a systematic review

Abstract

Alzheimer's disease (AD) is characterized mainly by the accumulation of Amyloid-β oligomers (Aβo) in the brain that leads to hyperphosphorylation and polymerization of the Tau protein in neurofibrillary tangles, which is associated with neuronal death. The initial stage of the disease is due to the production and accumulation of Aβo which is produced from the cleavage of the Amyloid-β precursor protein (APP) by the β-secretase (BACE1) enzyme. Growing evidences indicate that the cellular prion (PrPc) can restrict the activity of BACE1 and, therefore, interrupt the production and toxicity of Aβo. Studies also suggest that the Aβo-PrPc interaction is necessary to trigger the synaptotoxic effects, which depend on the Aβo stimulus. Here we presented an in-depth review of PrPc and its involvement with AD to understand if PrPc can be a marker or target in AD.

Keywords

• Prion
• Alzheimer
• Neurodegeneration
• Amyloid-β
• Aβo
• BACE1