Recovery of memory decline during aging - role of epigenetics

Abstract

Aging is a natural phenomenon associated with the accumulation of multiple alterations, including memory loss. Such deterioration of memory is based on the susceptibility of specific brain regions and the disorders that coincide with aging in those areas. Previous findings suggest that the optimal expression of synaptic plasticity-related genes is essential for memory formation and consolidation. Epigenetic modifications are one of the most crucial factors that cause memory deterioration by inducing the differential expression of synaptic plasticity-related genes. Understanding the fundamental cause of cognitive alterations that arise with aging is very essential for the development of therapeutic and/or preventive approaches. Several strategies have been employed to restore or reverse the memory decline caused by age-associated epigenetic alterations. The present article emphasizes the role of epigenetic alterations caused by histone modifications, DNA methylation, and non-coding ribonucleic acids (RNAs) on memory during aging. Also, we highlight the mechanistic switches of brain aging, including physical exercise, nutraceuticals, epigenetic modifiers, modulators of non-coding RNAs, and associated targets for therapeutic interventions. The emerging field of neuropharmacology and pharmacoepigenomics provides evidence that small drug molecules are currently employed to treat memory loss associated with aging, particularly by targeting epigenetic systems like DNA methylation, chromatin remodeling, histone modifications, and small non-coding RNAs. Therefore, targeting epigenetic modifications could be a potential therapeutic approach for the improvement of synaptic plasticity, neuronal activities, memory, and other brain functions during aging.