EJMS

Abstract

Toxoplasma gondii (T. gondii) is an intracellular parasite which chronically infects 30 to 50% of the human population. Several studies had suggested that such infection might contribute to neurological and psychiatric symptoms. The present study tested the hypothesis that T. gondii infection in mice might have a role in the development of Alzheimer’s disease (AD)-like pathology in the brain. Fifteen mice were infected at 3 months of age with T. gondii Me49 strain and sacrifice was done at 1, 3, and 6 months post-infection (PI). So, the experimental groups were: group I (one month PI), group II (3 month PI) and group III (6 month PI). Two age matched mice were used as uninfected control for each time point PI (control I, control II, control III). After sacrifice, specimens from temporal lobe of cerebral cortex were processed for H&E and immunohistochemical staining for detection of tissue parasitism, β-amyloid deposits, hyperphosphorylated tau protein and reactive astrocytes. In all the infected groups, tissue cysts of T. gondii were observed in the brain parenchyma using H & E and immunostaining. Cellular infiltration of pia mater and around the blood vessels (perivascular cuffing) was seen. Apparent increase in the number of neuroglial cells especially activated astrocytes and microglia was noticed. Degenerative changes in the neurons of temporal lobe in the form of apoptosis and necrosis were observed. Amyloid beta deposits were seen with the formation of neurofibrillary tangles derived from abnormal tau proteins in all the infected groups. It could be concluded that T. gondii infection has a possible correlation to the development of AD. Further studies are needed to explore the possible association between T. gondii infection and the symptoms and clinical course of AD.