Harnessing the potential of long non-coding RNAs in the pathophysiology of Alzheimer's disease

Abstract

Alzheimer's disease (AD), a diverse neurodegenerative disease, is the leading cause of dementia, accounting for 60-80 % of all cases. The pathophysiology of Alzheimer's disease is unknown, and there is no cure at this time. Recent developments in transcriptome-wide profiling have led to the identification of a number of non-coding RNAs (ncRNAs). Among these, long non-coding RNAs (lncRNAs)-long transcripts that don't seem to be able to code for proteins-have drawn attention because they function as regulatory agents in a variety of biological processes. Recent research suggests that lncRNAs play a role in the pathogenesis of Alzheimer's disease by modulating tau hyperphosphorylation, amyloid production, synaptic impairment, neuroinflammation, mitochondrial dysfunction, and oxidative stress, though their precise effects on the disorder are unknown. The biology and modes of action of the best-characterized lncRNAs in AD will be outlined here, with an emphasis on their possible involvement in the pathophysiology of the disease. As lncRNAs may offer prospective prognostic/diagnostic biomarkers and therapeutic targets for the treatment of AD, a greater comprehension of the molecular processes and the intricate network of interactions in which they are implicated could pave the way for future research.

Keywords: Alzheimer's disease; Amyloid β peptide; Biomarker; Tau protein; lncRNA.