The roles of long non-coding RNAs in Alzheimer's disease diagnosis, treatment, and their involvement in Alzheimer's disease immune responses

Abstract

Alzheimer's disease (AD) is the most frequent type of dementia, presenting a substantial danger to the health and well-being of the aged population. It has arisen as a significant public health problem with considerable socioeconomic repercussions. Unfortunately, no effective treatments or diagnostic tools are available for Alzheimer's disease. Despite substantial studies on the pathophysiology of Alzheimer's, the molecular pathways underpinning its development remain poorly understood. Long non-coding RNAs (lncRNAs) vary in size from 200 nucleotides to over 100 kilobytes and have been found to play critical roles in various vital biological processes that play critical in developing Alzheimer's disease. This review intends to examine the functions of long non-coding RNAs in diagnosing and treating Alzheimer's disease and their participation in immunological responses associated with AD.

Keywords: Alzheimer's disease; Diagnosis; Long non-coding RNA; Progression; Treatment.

Fig. 1

Long non-coding RNAs molecular mechanisms involved in Alzheimer Disease: Downregulation of MEG3 increases neuroinflammation through PI3/Akt pathway. The increased expression of MALAT1 reduces neuroinflammation by lowering IL-6 and TNF-. NEAT1 and linc00507 have been identified as Tau proteins. Increased expression of NEAT1 increased Tau protein phosphorylation by sponging miR-107, whilst increased linc00507 levels increase Tau protein hyperphosphorylation via modulating the miR-181c-5p/MAPT/TTBK1 pathway. MALAT1 upregulation increased cell death via targeting miR-125b. Furthermore, EBF3-AS is involved in the regulation of neuron apoptosis. BACE1 activity is linked to BACE1-AS, BC200, and BDNF-AS overexpression. Elevated 51A levels in AD patients changed the splicing mode of SORL1, causing harm to APP processing and promoting Aβ accumulation. BC1 upregulation promotes APP mRNA translation via binding to FMRP. NDM29 overexpression promotes APP production.