The neuroinflammatory role of microRNAs in Alzheimer’s disease: pathological insights to therapeutic potential

Alzheimer’s disease (AD) is a neurodegenerative disease and the most common cause of dementia, contributing to around 60–80% of cases. The main pathophysiology of AD is characterized by an abnormal accumulation of protein aggregates extracellularly (beta-amyloid plaques) and intracellularly (neurofibrillary tangles of hyperphosphorylated tau). However, an increasing number of studies have also suggested neuroinflammation may have a crucial role in precipitating the cascade reactions that result in the development of AD neuropathology. In particular, several studies indicate microRNAs (miRNAs) can act as regulatory factors for neuroinflammation in AD, with potential to affect the occurrence and/or progression of AD inflammation by targeting the expression of multiple genes. Therefore, miRNAs may have potential as therapeutic targets for AD, which requires more research. This article will review the existing studies on miRNAs that have been identified to regulate neuroinflammation, aiming to gain further insights into the specific regulatory processes of miRNAs, highlight the diagnostic and therapeutic potential of miRNAs as biomarkers in AD, as well as current challenges, and suggest the further work to bridge the gap in knowledge to utilize miRNAs as therapeutic targets for AD.