Background　Alzheimer's disease(AD) is the most common neurodegenerative disorder in the elderly with dementia as featured symptom. The microRNA(miRNA) are a class of non-coding single-stranded RNA composed of 22 nucleotides. They target coding miRNA and cause degradation of the miRNA, inhibiting their translation. Through these procedures, miRNA regulate various physiological functions, including the development and progress of AD.　Objective　To review the effects of miRNA on the levels of β-amyloid peptide(Aβ) and tau, neuroinflammation, and synaptic plasticity in AD.　Content　Amyloid plaques and neurofibrillary tangles are major pathophysiological hallmarks of AD. Amyloid plaques are formed by the accumulation of Aβ, while neurofibrillary tangles are generated by the excess phosphorylation of tau protein. Some miRNA were discovered to promote or reduce the accumulation of Aβ or production/phosphorylation of tau protein in certain stages of AD. Some miRNA modulate inflammation through TNF-α/NF-κB pathway or IL-1/IL-6 pathway, regulating the development and progress of AD. The levels of miRNA are also demonstrated to involve in the impairment of synaptic plasticity in AD.　Trend　Pathological evidence has demonstrated that miRNA may play important role in the progress of AD, suggesting that some miRNA can be potential biomarkers for stage classifications of AD. Further mechanistic investigations are required to clarify whether miRNA can be therapeutic targets to reverse or curb the deterioration of AD.