The coexpression of CD157/CD11b/CD18 in an experimental model of Parkinson's disease

Neurodegeneration is progressive neuronal death. Research on neuroinflammation mechanisms is necessary for understanding of the pathogenesis of acute and chronical neurodegeneration. The purpose of this research was to evaluate the coexpression of neuroinflammation molecules (CD157, CD11b/CD18) in the midbrain of animals under physiological conditions and in an experimental model of Parkinson's disease. Immunohistochemical evaluation of the coexpression of CD157 and MAC-1 was performed in rat midbrain sections. A significant increase in the number of cells that coexpress CD157/MAC-1 (CD11b/CD18) was found in the midbrain during Parkinson's disease. The possible roles of the neuroinflammatory molecules CD157 and MAC-1 in the pathogenesis of Parkinson's disease may include activation of microglial cells and performance of the neuroinflammatory response.