There has been a lot of study done linking Toxoplasmosis so various neuropsychiatric disorders. These studies have shown a high positive correlation between these two conditions. A recent study has linked Schizophrenic and Toxoplasmosis indicating the infection to be causative agent in the increase of dopamine in brain of infected subjects (28). However Toxoplasmosis with respect to neurodegeneration has not been studied as much.
Most of the studies that have studied the link between toxoplasmosis and AD are scattered (29, 30) and have seroprevalnce data (31). From our analysis we find that the AD cholesterol and immune system pathway is significantly affected in correlation to toxoplasmosis. In the Cholesterol pathway tereponoid biosynthesis is affected which in turn affects lipid homeostasis along with disturbance in NO pathways (29, 30). Peroxisome proliferator activated receptors (PPARs) signaling is also affected. PPARs are shown to reduce inflammatory response in macrophages. The neuroinflammatory response of AD is activated by installation of the β-amyloid peptide in extracellular …show more content…
The first is highly virulent whereas the other two are lower. These fatal infections are arbitrated to Th1 cytokine response, such as, by TNF-α, IFN-γ, IL-12 and IL-18, whereas non-fatal infections are accounted for by diffident initiations of Th1 cytokines (38). These responses are highly beneficial for the parasite during acute phases of the infection to keep the host cells alive. However during the chronic and latent phases, the parasite initiates immune suppression (39). Hence we hypothesize that the parasite property to alter host immune responses could be directly linked to AD progression. Through our study we find correlation factors between AD and toxoplasmosis. These factors are mainly centered on immune responses and cholesterol regulation. However better analysis needs to be done to overcome the challenges from this
Most of the studies that have studied the link between toxoplasmosis and AD are scattered (29, 30) and have seroprevalnce data (31). From our analysis we find that the AD cholesterol and immune system pathway is significantly affected in correlation to toxoplasmosis. In the Cholesterol pathway tereponoid biosynthesis is affected which in turn affects lipid homeostasis along with disturbance in NO pathways (29, 30). Peroxisome proliferator activated receptors (PPARs) signaling is also affected. PPARs are shown to reduce inflammatory response in macrophages. The neuroinflammatory response of AD is activated by installation of the β-amyloid peptide in extracellular …show more content…
The first is highly virulent whereas the other two are lower. These fatal infections are arbitrated to Th1 cytokine response, such as, by TNF-α, IFN-γ, IL-12 and IL-18, whereas non-fatal infections are accounted for by diffident initiations of Th1 cytokines (38). These responses are highly beneficial for the parasite during acute phases of the infection to keep the host cells alive. However during the chronic and latent phases, the parasite initiates immune suppression (39). Hence we hypothesize that the parasite property to alter host immune responses could be directly linked to AD progression. Through our study we find correlation factors between AD and toxoplasmosis. These factors are mainly centered on immune responses and cholesterol regulation. However better analysis needs to be done to overcome the challenges from this