Alzheimer’s disease (AD) exemplifies a looming epidemic lacking effective
treatment and manifests with the accumulation of neurofibrillary tangles, amyloid-β
plaques, neuroinflammation, behavioral changes, and acute cognitive impairments. It is
a complex, multifactorial disorder that arises from the intricate interaction between
environment and genetic factors, restrained via epigenetic machinery. Though the
research progress has improved the understanding of clinical manifestations and
disease advancement, the causal mechanism of detrimental consequences remains
undefined. Despite the substantial improvement in recent diagnostic modalities, it is
challenging to distinguish AD from other forms of dementia. Accurate diagnosis is a
major glitch in AD as it banks on the symptoms and clinical criteria. Several studies are
underway in exploring novel and reliable biomarkers for AD. In this direction,
epigenetic alterations have transpired as key modulators in AD pathogenesis with the
impeding inferences for the management of this neurological disorder. The present
chapter aims to discuss the significance of epigenetic modifications reported in the
pathophysiology of AD such as DNA methylation, hydroxy-methylation, methylation
of mtDNA, histone modifications, and noncoding RNAs. Additionally, the chapter also
describes the possible therapeutic avenues that target epigenetic modifications in AD.
Keywords: Alzheimer’s disease, DNA methylation, Epigenetic therapy, Histone modifications, Non-coding RNAs.
