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Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide. Several findings suggest that correcting the dysregulated signaling pathways may offer a potential therapeutic approach in this disease. Extracellular signal-regulated kinase 1/2 (ERK1/2), a member of the mitogen-activated protein kinase family, plays a major role in regulation of cell proliferation, autophagy process, and protein synthesis. The available literature suggests dysregulated ERK1/2 in AD patients with potential implications in the multifaceted underlying pathologies of AD, including amyloid-β plaque formation, tau phosphorylation, and neuroinflammation. In this regard, in the current review, we aim to summarize the reports on the potential roles of ERK1/2 in AD pathophysiology.