Role Of Lncrna In Alzheimer’s Diseases

Long noncoding RNA (lncRNA) are a family of RNA molecules with over 200 nucleotides in size. They cannot code for proteins but still have biological activities. lncRNAs are abundantly expressed in the pathogenic process of neurological diseases like Alzheimer’s. The lncRNA EBF3-AS is more expressed in the brains of older Alzheimer's disease patients called late onset Alzheimer’s disease. NAT-Rad18, a lncRNA over synthesized in specific areas of the brain in AD rats. The lncRNA n336694 targets miR-106b which increases its expression. MiR-106b leads to apoptosis markers in cells. oxidative stress-induced injury to the neurons is caused by the lncRNA SOX21-AS1. The lncRNA-ATB is involved in AD pathophysiology and reducing its expression helps with oxidative stress-induced injury. lncRNA MEG3 inhibits inflammatory injury and oxidative stress in individuals suffering from AD. The increase of lncRNA 17A in cerebral tissues of AD patients affects Aβ secretion. BACE1-AS suppression reduces Aβ and BACE1 levels and inhibits tau protein phosphorylation (3). The lncRNA BC200, also known as BCYRN1 upregulates Aβ production through BACE1 modulation which leads to AD pathogenesis. NEAT1 regulates the miR-124/BACE1 axis and plays a role in AD development. Reduced SORL1 expression increases neurotoxic Aβ formation in AD brains. LRP1-AS negatively regulates systemic Aβ clearance during AD progression. GAS5 regulates insulin signaling, neuronal survival, tau phosphorylation, and neuroinflammation. MAGI2-AS3-miR-374b-5p axis modulates neuroinflammation and neurotoxicity caused by Aβ fragment. Upregulation of WT1-AS inhibits the miR-375/SIX4 axis, OSI, and neuronal apoptosis in AD. BDNF-AS is found to be important in AD though the mechanism has yet to be determined. This review study aims to enhance comprehension of the disease progression of Alzheimer's disease (AD) in relation to various long non-coding RNAs (lncRNA).