Role of exercise on molecular mechanism in the treatment of depression

Mood disorders such as depression result enormous personal distress. Intrinsic depression has not fully verified, but is deliberated to from molecular and cellular singularities. Available antidepressants have significant limitations. Regular exercise reduces depressive-like behavior activation. The aim of the present study is to review the possibility whether exercise regulates depression-associated antidepressant effects in the brain. Increased hippocampal neurogenesis with exercise has potential significance for depression. Exercise promotes brain health in the molecular levels in the hippocampus and also affects behavior in a similar way to chronic antidepressant treatment. The neurotrophic/plasticity hypothesis of depression is now supported by multiple studies focused on the role of intracellular-signaling cascades that regulate neuroplasticity and neural proliferation. The neuroplastic changes of the brain linked to antidepressant effects promoted by exercise. Wnt and Fz signaling system plays an important role in cell proliferation, growth, and differentiation during development. Our results demonstrate complicated, differential effects of antidepressants on Wnt signaling system, and assume a role for selected signaling molecules in the neurogenic activity of antidepressant care. The present study showed evidences suggesting that exercise-induced enhancement in neuroplasticity and neurogenesis are linked with treatment of depression in the brain. Our review suggests that exercise may preserve brain function by increasing neurogenesis through activating Wnt signaling pathway in the psychiatric disorders, such as depression.