Exercise-Induced Autophagy and Parkinson’s Disease

PD is the second most common neurodegenerative disease after Alzheimer’s disease (AD). The occurrence of PD is more common in the elderly, and the average age of onset is 60 years. The major pathological change in PD is the degeneration and death of dopamine (DA) neurons in the substantia nigra of the midbrain, which causes a significant decrease in DA content in the striatum. The exact cause of this pathological change is still unclear. Genetic factors, environmental factors, aging, oxidative stress, and other relevant factors may be involved in the degeneration and death of dopaminergic neurons in PD. In 1817, British doctor James Parkinson first provided a detailed description of this disease. Its clinical manifestations mainly include resting tremor, bradykinesia, muscle rigidity, and postural and gait disorders. Patients may also experience symptoms of depression, constipation, and sleep disorders. Diagnosis of PD primarily depends on the history, clinical symptoms, and signs of this disease. There are usually no abnormal changes identified during general auxiliary examinations. Levodopa, a natural chemical converted to dopamine in the brain, combined with carbidopa, a compound that prevents premature conversion of levodopa, is the current primary drug treatment strategy for PD, while surgical treatment is an effective supplemental treatment. Rehabilitation, psychotherapy, and nursing care can also alleviate the symptoms of PD to a certain extent. These currently available treatments can mitigate symptoms and significantly improve the quality of life of PD patients, but cannot cure or halt the progression of this disease. The life expectancy of PD patients is shorter than general population, especially those who have been diagnosed before the age of 70 [1].