CanToxoplasma gondiiPave the Road for Dementia?

Abstract

Dementia is an ominous neurological disease. Scientists proposed a link between its occurrence and the presence ofToxoplasma gondii(T. gondii). The long-term sequels of anti-Toxoplasmapremunition, chiefly dominated by TNF-α, on the neurons and their receptors as the insulin-like growth factor-1 receptor (IGF-1R), which is tangled in cognition and synaptic plasticity, are still not clear. IGF-1R mediates its action via IGF-1, and its depletion is incorporated in the pathogenesis of dementia. The activated TNF-αsignaling pathway induces NF-κβthat may induce or inhibit neurogenesis. This study speculates the potential impact of anti-Toxoplasmaimmune response on the expression of IGF-1R in chronic cerebral toxoplasmosis. The distributive pattern ofT. gondiicysts was studied in association with TNF-αserum levels, the in situ expression of NF-κβ, and IGF-1R in mice using the low virulent ME-49T. gondiistrain. There was an elevation of the TNF-αserum level (pvalue ≤ 0.004) and significant upsurge in NF-κβwhereas IGF-1R was of low abundance (pvalue < 0.05) compared to the controls. TNF-αhad a strong positive correlation with the intracerebral expression of NF-κβ(rvalue ≈ 0.943,pvalue ≈ 0.005) and a strong negative correlation to IGF-1R (rvalue -0.584 and -0.725 for area% and O.D., respectively). This activated TNF-α/NF-κβkeepsT. gondiiunder control at the expense of IGF-1R expression, depriving neurons of the effect of IGF-1, the receptor’s ligand. We therefore deduce thatT. gondiiimmunopathological reaction may be a road paver for developing dementia.