Possible Link BetweenToxoplasma Gondiiand the Anosmia Associated With Neurodegenerative Diseases

Abstract

Toxoplasma gondii is an intracellular protozoan infecting 30% to 50% of global human population. Recently, it was suggested that chronic latent neuroinflammation caused by the parasite may be responsible for the development of several neurodegenerative diseases manifesting with the loss of smell. Studies in animals inoculated with the parasite revealed cysts in various regions of the brain, including olfactory bulb. Development of behavioral changes was paralleled by the preferential persistence of cysts in defined anatomic structures of the brain, depending on the host, strain of the parasite, its virulence, and route of inoculation. Olfactory dysfunction reported in Alzheimer's disease, multiple sclerosis, and schizophrenia was frequently associated with the significantly increased serum anti-T gondii immunoglobulin G antibody levels. Damage of the olfactory system may be also at least in part responsible for the development of depression because T gondii infection worsened mood in such patients, and the olfactory bulbectomized rat serves as a model of depression.

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

“…Masur et al [748] observed that even therapeutic concentrations of hydrocortisone rendered normal macrophages unresponsive to IFN-γ in Alzheimer's disease [720][721][722] . These findings are compatible with our earlier suggestions that latent chronic T. gondii infection may be at least in part responsible for the generation of amyloid plaques characteristic for the brains of patients with Alzheimer's disease and Down's syndrome [222,223] . In summary, infection of host vascular endothelial cells by T. gondii tachyzoites may become an additional source of cysteine cathepsin activities that are superimposing on the activity of similar enzymes physiopathologically present in the host cells, because the parasite's tachyzoites, bradyzoites, and sporozoites express several members of these proteases.…”

“…These cytoprotective actions may at least partly explain H 2 S beneficial effects in slowing down progression of experimental Alzheimer's disease [219] , as well as improving health in major cardiovascular diseases [220] . It was recently suggested that atherosclerosis and Alzheimer are diseases with a common cause [221] , and it seems that chronic T. gondii infection may be at least in part responsible for this causal relationship [222,223] .…”

Alzheimer’s disease and gut microbiota

“…Infections of Chlamydophila pneumoniae, Helicobacter pylori, Toxoplasma gondii, Herpes simplex virus (HSV), Human immunodeficiency virus (HIV), Human cytomegalovirus (HCMV) and other common pathogens are all considered to be associated with the pathogenesis of AD (Balin et al, 1998;Borjabad and Volsky, 2012;Itzhaki and Wozniak, 2008;Kountouras et al, 2012;Lurain et al, 2013;Prandota, 2014). In a prospective cohort of healthy individuals, Katan et al found a correlation between infectious burden and cognitive impairment assessed using the mini-mental state examination (MMSE) (Katan et al, 2013).…”

“…gondii is an intracellular parasite, which can cause encephalitis and nervous system dysfunction by promoting chronic inflammation in the brain and CNS. Studies found that serum anti-T. gondii immunoglobulin G antibody levels significantly increased in AD patients, suggesting a link between AD and T. gondii infection (Prandota, 2014).…”

Pathogenic microbes, the microbiome, and Alzheimer’s disease (AD)

“…Recently AD has been associated with significantly increased anti- T. gondii antibodies suggesting a possible mechanistic link between T. gondii infection and AD (Prandota, 2014). …”