Epigenetic Modification in Alzheimer Disease

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder characterized by progressive cognitive decline and memory loss, imposing a significant burden on affected individuals and their families. Despite the recent promising progress in therapeutic approaches, more needs to be done to understand the intricate molecular mechanisms underlying the development and progression of AD. Alzheimer’s disease is characterized by the formation and deposit abnormal peptides such as amyloid plaques and neurofibrillary tangles in the Brain. There are currently no validated biomarkers which can be used to accurately diagnose Alzheimer’s disease (AD) or to distinguish it from other dementia-causing neuropathologies.As of right now, there are no verified biomarkers that can be used to reliably diagnose Alzheimer’s disease (AD) or differentiate it from other neuropathologies that cause dementia. Epigenetic changes have become recognised as significant players in the pathophysiology of AD in the hunt for novel, more trustworthy biomarkers and effective treatment alternatives. Numerous studies have indicated that histone posttranslational modifications, non-coding RNA regulation (with a focus on microRNAs), DNA methylation and hydroxymethylation, and these processes are crucial for the progression and development and accumulation of aberrant peptides in the brain, such as amyloid plaques and neurofibrillary tangles, is what defines Alzheimer’s disease. Treatment plans intended to stop these deposits from forming have not proved effective. As of right now, the condition has no viable remedies. Treatments targeted at reversing these alterations by interfering with DNA methylation, histone acetylation, and microRNA expression may represent potential avenues of research in the future, given the multitude of epigenetic changes found in Alzheimer’s disease.Extensive research has suggested an important role of DNA methylation and hydroxymethylation, histone posttranslational modifications, and non-coding RNA regulation in the course and development of AD