. Memory T cells persisting within the brain after local infection show functional adaptations to their tissue of residence. Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):17872-9. PubMed.

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  1. Joseph Prandota at the University Medical School in Wroclaw, Poland, suggests that Toxoplasma gondii (T. gondii), the parasitic protozoa hosted in cats, which causes cerebral toxoplasmosis (CT), may be implicated in the pathogenesis of Alzheimer's disease (AD).

    Prandota states that T. gondii affects chromatin structure and may cause dysregulation of the host cell cycle. Moreover, it seems that the accumulation of iron in senile plaques reflects a defense of the host against T. gondii because this transition metallic ion is necessary for proliferation of tachyzoites, which are part of the protozoan's life cycle.

    Prandota observes that the beneficial effects of ibuprofen in patients with AD, which restored cellular immunity, decreased production of proinflammatory cytokines, nitric oxide, and amyloid-β, and reduced lipid peroxidation and free radical generation, are consistent with the suggestion that congenital and/or acquired chronic latent CT plays a role in neurodegeneration.
     

    References:

    . Metabolic, immune, epigenetic, endocrine and phenotypic abnormalities found in individuals with autism spectrum disorders, Down syndrome and Alzheimer disease may be caused by congenital and/or acquired chronic cerebral toxoplasmosis. Research in Autism Spectrum Disorders, Volume 5, Issue 1, January-March 2011, pp. 14-59.

    View all comments by David Corbin

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  1. Brain T Cells Lie in Wait for Recurrent Infections