This study reflects that Neurological disorders are the leading cause of disability worldwide, and Parkinson’s disease (PD) is the fastest growing. Neurodegeneration in PD is relentlessly progressive, creating a compelling need to find effective and safe disease-modifying therapies. Considerable evidence supports the critical role of neuroinflammation in the degenerative process,1 which is known to be orchestrated by interactions of glial cells, peripheral lymphocytes, proinflammatory cytokines/chemokines, and changes in growth factors.2-5 The inflammatory condition of the parkinsonian neuronal-glial microenvironment is well described in human postmortem tissue, in vivo models (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 6-hydroxydopamine, rotenone, lipopolysaccharide (LPS), and SNc extracts), and in vitro models. Inflammation also plays a significant role in toxin-induced and genetic models,6, 7 and epidemiological studies on the risk-lowering effects of anti-inflammatory drug regimens confirm its vital role.8, 9 Our group has studied the peripheral immune system in PD neurodegeneration by using LPS rat models,10, 11 glial cells,12, 13 and patient cerebrospinal fluid and blood.

Reference link-