Crosstalk between epigenetics and mTOR as a gateway to new insights in pathophysiology and treatment of Alzheimer's disease

Int J Biol Macromol. 2021 Dec 1:192:895-903. doi: 10.1016/j.ijbiomac.2021.10.026. Epub 2021 Oct 15.

Abstract

Epigenetics in the current times has become a gateway to acquire answers to questions that were left unanswered by classical and modern genetics, be it resolving the complex mystery behind neurodegenerative disorders or understanding the complexity behind life-threatening cancers. It has presented to the world an entirely new dimension and has added a dynamic angle to an otherwise static field of genetics. Alzheimer's disease is one of the most prevalent neurodegenerative disorders is largely found to be a result of alterations in epigenetic pathways. These changes majorly comprise an imbalance in DNA methylation levels and altered acetylation and methylation of histones. They are often seen to cross-link with metabolic regulatory pathways such as that of mTOR, contributing significantly to the pathophysiology of AD. This review focusses on the study of the interplay of the mTOR regulatory pathway with that of epigenetic machinery that may elevate the rate of early diagnosis and prove to be a gateway to the development of an efficient and novel therapeutic strategy for the treatment of Alzheimer's disease at an early stage.

Keywords: Acetylation; Alzheimer's; Epigenetics; Histone; Methylation; mTOR.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / etiology*
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Alzheimer Disease / therapy
  • Amyloidogenic Proteins / genetics
  • Animals
  • Autophagy / genetics
  • Biomarkers
  • DNA Methylation
  • Disease Management
  • Disease Susceptibility
  • Epigenesis, Genetic*
  • Gene Expression Regulation* / drug effects
  • Histones / metabolism
  • Humans
  • Molecular Targeted Therapy
  • Protein Processing, Post-Translational
  • Signal Transduction* / drug effects
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Amyloidogenic Proteins
  • Biomarkers
  • Histones
  • MTOR protein, human
  • TOR Serine-Threonine Kinases