[The effect of DNA methylation on β-amyloid accumulation in Alzheimer's disease]

DNA methylation is the most intensively studied mechanism for epigenetic gene regulation. The functions of DNA methylation have recently drawn wide attention for investigation into the etiology of neurodegenerative disorders such as Alzheimer's disease (AD). It has been well established that β-amyloid (Aβ) accumulation leads to the formation of senile plaques, which is a hallmark of AD pathology. Aggregation of Aβ induces neurotoxicities manifested by apoptosis, neuroin-flammation, oxidative stress and mitochondrial dysfunction etc., which consequently provoke the pathological progression of AD. Previous studies have demonstrated that DNA methylation plays an important role in regulating genes associated with the production, clearance and aggregation of Aβ. DNA methylation is a reversible process, making it a promising target for AD therapeutics. Further studies of DNA methylation in the initiation and progression of AD would pave the road to explore improved approaches to treat this disease. In this review, we summarize the involvement of DNA methylation in Aβ accumulation as well as the associated pathological alterations during the initiation and progression of AD, which would help to fully appreciate the molecular basis of AD.