Resistance exercise improves short-term memory through inactivation of NF-κB pathway in mice with Parkinson disease.

Dysfunctions of Parkinson disease (PD) are classified into motor dysfunction, autonomic nervous system dysfunction, and nonmotor dysfunction, and clinical symptoms such as muscle stiffness, tremors, speech disorders, balance disorders, and slow movements appear. Resistance exercise is a main compartment of exercise programs for PD patient. The effect of resistant exercise on short-term memory in PD mice was studied in relation to the activation of nuclear factor (NF)-κB pathway. PD was induced by subcutaneous injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. For resistance exercise, mice performed ladder climbing 5 days per week for 5 weeks. Step-down avoidance test for short-term memory, enzyme-linked immunoassay for tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β, Western bot for NF-κB, NF-κB inhibitor (IκB)-α, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), and Bcl-2, and immunohistochemistry for cleaved caspase-3 were done. Latency time was shortened, TNF-α, IL-6, and IL-1β concentration was increased, NF-κB expression and IκB-α phosphorylation were increased, cleaved caspase-3 and Bax expression was enhanced, and Bcl-2 expression was suppressed by PD induction. Latency time was lengthened, TNF-α, IL-6, and IL-1β concentration was decreased, NF-κB expression and IκB-α phosphorylation were suppressed, cleaved caspase-3 and Bax expression was decreased, and Bcl-2 expression was increased in PD mice by resistance exercise or levodopa treatment. Resistance exercise improved short-term memory by inhibiting secretion of proinflammatory cytokines and apoptosis through inactivation of NF-κB. These effects of resistance exercise were similar to levodopa treatment.