Parkinson's disease is a common neurodegenerative disease, and its pathological manifestations include loss of dopaminergic neurons in the midbrain, pathological aggregation of alpha synuclein, and chronic neuroinflammation. Among them, overactivated neuroinflammation is an important pathological mechanism of Parkinson's disease, which not only accelerates the deposition of alpha synuclein, but also damages dopaminergic neurons. And what is the mechanism of overactivation of neuroinflammation? It is not immediately known. In addition to the resident immune cells of the central nervous system, peripheral immune cells are also receiving increasing attention. Previous studies have found that during the occurrence and development of Parkinson's disease, activated peripheral immune cells can pass through blood-cerebrospinal fluid, blood-leptomeningeal, blood-brain and other barriers or penetrate into the brain parenchyma through meningeal lymphatic vessels, and secrete different pro-inflammatory factors, thus leading to neuroinflammation. However, the role of peripheral inflammation on the progression of clinical symptoms in Parkinson's disease is unknown. In addition, peripheral inflammatory cells can destroy the integrity of the blood-brain barrier during the process of infiltration into the central nervous system, and then cause white matter damage, which is closely related to motor and non-motor symptoms of Parkinson's disease. Therefore, it is speculated that white matter integrity may be involved in the role of peripheral inflammation in the progression of clinical symptoms of Parkinson's disease.
