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Mounting evidence over the past decade has underscored that mitophagy deficiency and calcium dyshomeostasis play pivotal regulatory roles in AD pathological progression, with these two abnormalities persisting throughout the entire course of disease onset and development. Mitophagy impairment can result in the accumulation of dysfunctional mitochondria, thereby further exacerbating calcium dyshomeostasis which can suppress autophagic flux in turn. This reciprocal interaction establishes a vicious cycle that can synergistically accelerate A\u03b2 plaque and neurofibrillary tangle formation, impair synaptic structure and function, and ultimately elicit neuronal programmed cell death and cognitive decline. This review systematically summarizes the biological basis of mitophagy and calcium homeostasis, as well as their mutual regulatory networks. 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