Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Genetics & Heredity, Alzheimer's disease, long non-coding RNAs, gene expression, GENOME-WIDE ASSOCIATION, LONG NONCODING RNAS, RISK LOCI, A-BETA, COMMON VARIANTS, EXPRESSION, PROMOTES, PROTEIN, CD33, MICRORNA-125B, Alzheimer’s disease, Aging, Alzheimer Disease, Animals, Brain, Genome-Wide Association Study, Humans, RNA, Long Noncoding, 0604 Genetics, 3105 Genetics

Abstract:

With the ongoing demographic shift towards increasingly elderly populations, it is estimated that approximately 150 million people will live with Alzheimer's disease (AD) by 2050. By then, AD will be one of the most burdensome diseases of this and potentially next centuries. Although its exact etiology remains elusive, both environmental and genetic factors play crucial roles in the mechanisms underlying AD neuropathology. Genome-wide association studies (GWAS) identified genetic variants associated with AD susceptibility in more than 40 different genomic loci. Most of these disease-associated variants reside in non-coding regions of the genome. In recent years, it has become clear that functionally active transcripts arise from these non-coding loci. One type of non-coding transcript, referred to as long non-coding RNAs (lncRNAs), gained significant attention due to their multiple roles in neurodevelopment, brain homeostasis, aging, and their dysregulation or dysfunction in neurological diseases including in AD. Here, we will summarize the current knowledge regarding genetic variations, expression profiles, as well as potential functions, diagnostic or therapeutic roles of lncRNAs in AD. We postulate that lncRNAs may represent the missing link in AD pathology and that unraveling their role may open avenues to better AD treatments.