Alzheimer’s disease (AD) is a neurodegenerative disease with progressive and persistent cognition and memory destruction. Its main pathological features are β-amyloid (Aβ) deposition and neurofibril tangles formed by hyperphosphorylated Tau protein, which is becoming a serious global health problem. Peroxisome proliferators-activated receptors (PPARs) is a nuclear receptor that expresses in the central nervous system and regulates energy metabolism, neurotransmission, redox homeostasis, mitochondrial function and other physiological processes. PPARα, as one of the subtypes, plays an important role in the control of synaptic plasticity and neuronal function. In this review, we discussed the possibility of PPARα as a therapeutic target for AD treatment. PPARα can reduce the production of soluble amyloid precursor protein (sAPP) and Aβ by regulating β secretase-1 (BACE-1) and reduce the accumulation of reactive oxygen species (ROS) by regulating the function of mitochondria, thereby decreasing oxidative stress damage. PPARα can down-regulate inflammatory factors and lessen neuroinflammation. It can also decrease blood lipids, alleviate insulin resistance, and regulate lipids metabolism. PPARα, as a promising target for the treatment of AD, is of great significance to new treatment strategies for AD.