Alzheimer's disease (AD) is an insidious, progressive, and irreversible neurodegenerative disease characterized by the deposition of extracellular amyloid β-protein (Aβ) to form senile plaques and abnormal phosphorylation of intracellular tau protein to form neuronal fiber tangles. The pathogenesis of AD is complex, and there are several hypotheses, primarily including the Aβ cascade hypothesis, the neurofibrillary tangle hypothesis, the inflammatory hypothesis, and the cholinergic hypothesis. It has been suggested that the dysregulation of multiple energy metabolic pathways, especially mitochondria metabolism, may be related to the severity of AD pathology and disease symptoms in the brain. The modification of histone (lysine) methylation, an actively regulated and reversible process, is closely related to energy metabolism and plays a crucial role in AD development. In summary, histone methylation, energy metabolism, and AD restricted and regulated each other. Here, we review the advances in the correlation between histone methylation, energy metabolism, and AD. This can provide further insights into the mechanisms underlying AD pathogenesis and its control.