Abstract
Alzheimer's disease is the primary cause of dementia and imposes a significant socioeconomic burden globally. Physical exercise, as an effective strategy for improving general health, has been largely reported for its effectiveness in slowing neurodegeneration and increasing brain functional plasticity, particularly in aging brains. However, the underlying mechanisms of exercise in cognitive aging remain largely unclear. Adiponectin, a cell-secreted protein hormone, has recently been found to regulate synaptic plasticity and mediate the antidepressant effects of physical exercise. Studies on the neuroprotective effects of adiponectin have revealed potential innovative treatments for Alzheimer's disease. Here, we reviewed the functions of adiponectin and its receptor in the brains of human and animal models of cognitive impairment. We summarized the role of adiponectin in Alzheimer's disease, focusing on its impact on energy metabolism, insulin resistance, and inflammation. We also discuss how exercise increases adiponectin secretion and its potential benefits for learning and memory. Finally, we highlight the latest research on chemical compounds that mimic exercise- enhanced secretion of adiponectin and its receptor in Alzheimer's disease.
Published Version
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