Targeting Novel microRNAs in Developing Novel Alzheimer's Disease Treatments

Alzheimer's disease (AD) is considered a multifactorial disease and a significant cause of dementia during aging. This neurodegenerative disease process is classically divided into two different pathologies cerebral accumulation of amyloid-beta and hyperphosphorylated neurofibrillary tau tangles. In recent years, massive efforts have been made to treat AD by decreasing amyloid-beta and tau in the brains of patients with AD, with no success. The dysfunction of a wide range of microRNAs promotes the generation and insufficient clearance of amyloid-beta (A beta) and increases tau plaques which are the pathophysiological markers of AD. Disturbance of these microRNAs is associated with mitochondrial dysfunction, oxidative damage, inflammation, apolipoprotein E4 (APOE4) pathogenic process, synaptic loss, and cognitive deficits induced by AD. Targeting a specific microRNA to restore AD-induced impairments at multiple stages might provide a promising approach for developing new drugs and therapeutic strategies for patients with AD. This review focuses on different mechanisms of microRNAs in AD pathophysiology.

Automated summary

Alzheimer's disease is a multifactorial neurodegenerative disease that causes dementia in aging individuals. The abnormal accumulation of amyloid-beta and tau protein and the dysfunction of microRNAs play important roles in the pathophysiology of this disease. Targeting microRNAs could be a promising approach for developing new treatments for Alzheimer's disease.