Biomolecular Changes and Cortical Neurodegenerative Lesions in Infected BALB/c Mice: A Preliminary Study Elucidating a Potential Relationship Between Systemic Helminthic Infections and Idiopathic Parkinson's.

Idiopathic Parkinson's (IP) is a neurodegenerative disease that is suspected to be due to exposure to infections during early life. Toxoplasmosishas been the only suspected parasitic infection in IP (Celik et al., 2010). Recently, some non-central nervous system bacterial and viral infections have been incriminated in IP (Çamcı & Oğuz, 2016). So in the current study, we tried to explore if the systemic inflammatory reactions triggered by some helminths like can induce Parkinsonian lesions in the brain, especially that the cerebral complications have been reported in 10-20% of infected patients . An experimental study was designed to assess the neurodegenerative and biomolecular changes that may occur in infected BALB/C mice in comparison to rotenone induced PD model and apparently healthy ones. The motor affection was significantly lesser in the infected mice than the Parkinson's model, but when the catalepsy score was calculated (through the grid and bar tests) it was found to be significantly higher in the infected mice than in the healthy ones. A significant increase in the blood advanced oxidative protein products (AOPP), IFN-γ, TGF-β, and brain DNA fragmentation was also detected in the infected mice. After histopathological examination, a significant increase in the cortical apoptotic neurons and Lewy's body were observed in the infected and the rotenone induced Parkinson's model sections. A significant decrease in the immunohistochemical expression of the tyrosine hydroxylase expression in the brain sections and the ELISA measured dopamine level in the brain homogenate was also reported in the infected mice group. This study findings may collectively suggest that the systemic inflammatory reactions and the oxidative stresses associated with some systemic helminthic infections like trichinellosis are possible to precipitate neurodegenerative lesions and biomolecular changes in the brain , and manifest with IPD later in life.