Schizophrenia and bipolar disorders: The Toxoplasma connection

Abstract

The infectious etiology of psychiatric illnesses has remained an unexplored area till recently. During the past two decades, numerous studies from multiple angles have tried to link chronic toxoplasmosis with schizophrenia and bipolar disorders, among others. Most of the evidence has come from serological studies in the patient population, but other facets have also been explored. This review examines the various areas from which a causal link has been deduced and includes: (a) serological studies, (b) effect of maternal toxoplasmosis on children, (c) neurotransmitter studies, (d) parasite localization in the brain, (e) role of cytokines, and (f) psychotherapy and its effect on Toxoplasma. However, multiple factors may play a role in the etiopathogenesis of psychiatric illnesses, and chronic Toxoplasma infection may be considered an important risk factor for the genesis and symptomatology of schizophrenia and bipolar disorders.

Toxoplasma gondii: An Underestimated Threat?

“…Dopamine dysregulation, which has received the most research attention, results partly from the parasite's ability to synthesise tyrosine hydrolase (an enzyme involved in dopamine biosynthesis) [24]. T. gondii also alters the expression of a range of other neurotransmitters, including γ-aminobutyric acid (GABA), glutamate, serotonin, and norepinephrine [25]. These effects might be mediated by the encystment of bradyzoites in neuraland most often microglial or neuronalcells, thereby causing considerable alterations, both in host neurobiochemistry and in the expression of specific receptors/transporters [24,25].…”

“…T. gondii also alters the expression of a range of other neurotransmitters, including γ-aminobutyric acid (GABA), glutamate, serotonin, and norepinephrine [25]. These effects might be mediated by the encystment of bradyzoites in neuraland most often microglial or neuronalcells, thereby causing considerable alterations, both in host neurobiochemistry and in the expression of specific receptors/transporters [24,25]. For example, it has been shown, in chronically infected mice, that T. gondii decreases the expression of the glutamate transporter GLT-1, resulting in a twofold increase in extracellular glutamate concentrations [26].…”

Emerging Therapeutic Targets Against Toxoplasma gondii: Update on DNA Repair Response Inhibitors and Genotoxic Drugs

“…Toxoplasmosis has two clinical phases in intermediate hosts: (i) acute, in which the highly replicative tachyzoite stage spreads throughout the body, and (ii) chronic phase, which involves the formation of tissue cysts, preferentially in the nervous system and skeletal muscle, which remain in the host for a lifetime (Delgado Betancourt et al, 2019;Stelzer et al, 2019). Chronic toxoplasmosis has been correlated with a variety of neuropsychiatric disorders that include memory loss, bipolarism, attention deficit hyperactivity disorder and schizophrenia (Chaudhury and Ramana, 2019;Tyebji et al, 2019).…”

Latent Toxoplasma gondii infections are associated with elevated biomarkers of inflammation and vascular injury

“…Latent T. gondii infections in humans have been associated with various adverse neuropsychiatric outcomes including suicide and increased risk of traffic accidents [ 50 ], schizophrenia and bipolar disorder [ 11 , 13 ], obsessive compulsive disorder [ 39 ], and increased aggression and impulsivity [ 14 ]. Other studies linked latent infections with an increased risk of type 2 diabetes [ 36 ], rheumatoid arthritis [ 28 ] and Alzheimer’s disease [ 40 ].…”