Research Progress of the AMPK/PINK1/Parkin Pathway in Alzheimer’s Disease Mechanism and Therapeutic Potential

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by β-amyloid (Aβ) plaque deposition, tau pathology, and mitochondrial dysfunction. Recent studies have found that the AMP-activated protein kinase (AMPK)/PTEN-induced kinase 1 (PINK1)/Parkin pathway plays a key role in the pathogenesis of AD by regulating energy metabolism, mitophagy, and neuroinflammation. As a core regulator of energy metabolism, AMPK enhances the efficiency of mitochondrial autophagy by phosphorylating PINK1, while inhibiting β-site amyloid precursor protein cleaving enzyme (BACE1) and reducing Aβ production. The PINK1/Parkin pathway selectively clears damaged mitochondria and alleviates oxidative stress and neuronal damage. This article systematically reviews the molecular mechanism of the AMPK/PINK1/Parkin pathway and its multi-target regulatory role in AD, and discusses the therapeutic strategies based on this pathway, to provide new directions for AD drug development.