Autophagy in Alzheimer’s disease

Abstract

Autophagy is a degradation pathway for the turnover of dysfunctional organelles or aggregated proteins in cells. Extensive literature exists supporting a causative role of mitochondrial dysfunction and amyloid-β protein in the pathogenesis of Alzheimer’s disease (AD). Furthermore, a link between mitochondrial dysfunction, amyloid-β levels and autophagy has been reported to occur in AD. However, it is not yet clear if autophagy plays a causative role, a protective role or is a consequence of the disease process itself. Understanding the exact role of autophagy in different stages of AD progression may help to design more effective therapeutic strategies. A central issue in developing therapies for neurodegenerative diseases involves understanding why and when responses to stress or injury can help prevent neuronal degeneration and death.

Keywords::

• Alzheimer’s disease
• autophagy
• death
• neurodegeneration
• protection
• therapeutic target

Financial & competing interests disclosure

George Perry is, or has in the past been, a paid consultant for and/or owns equity or stock options in Neurotez Pharmaceuticals, Panacea Pharmaceuticals, Takeda Pharmaceuticals and Voyager Pharmaceuticals. Mark A Smith is, or has in the past been, a paid consultant for, owns equity or stock options in and/or receives grant funding from Anavex, Canopus BioPharma, Medivation, Neurotez, Neuropharm, Panacea Pharmaceuticals and Voyager Pharmaceuticals. Xiongwei Zhu is a paid Advisory Board member for Medivation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.