Our feline friends may have earned a bad reputation as the moodiest common house pets, but can they be responsible for schizophrenia? While cats certainly cannot cause such severe mental illness, recent research has, in fact, revealed a link between a particular cat parasite and development of the disorder.
The parasitic Toxoplasma gondii can hitch a ride upon convenient feline carriers and infiltrate the central nervous systems of unsuspecting warm-blooded victims. Not all subjects infected with T. gondii develop schizophrenia, but the rate of illness is significantly higher among the T. gondii-infected population. Understanding the parasite’s influence is a critical step toward cracking schizophrenia’s biological code and pioneering more effective treatments.
Gondii in Mice Populations: Far-Reaching Implications
The sign of an ‘effective’ parasite lies in its ability to manipulate its host to suit its own needs. Clever T. gondii is therefore able to dampen a mouse’s natural fear of the predator cat; in this way, the mouse will approach the cat, become prey for the cat, and pass the parasite into the body of the cat where the parasite can multiply in peace; in fact, this parasite can only replicate within cats . Once T. gondii invades an unsuspecting mouse, the parasite actually instructs for DNA hypomethylation at the promoter region of the mouse’s arginine vasopressin gene; this pushes gene expression to an atypical height and is likely responsible for the fearlessness exhibited by T. gondii-infected mice. Since the parasite has demonstrated its capacity to change behavior patterns in the comparatively simpler rodent brain, it can wreak potentially devastating havoc on the sophisticated human brain.
Schizophrenia is a mental disorder characterized by relatively extreme distortions of thought, behavior, and perception. A genetic basis for the disease has been proposed and somewhat substantiated, but environmental factors definitely help shape the disorder progression; such factors may easily include viral or parasitic infection . If T. gondii invasion can influence mice to behave in fashions contrary to their innate animalistic instincts, the parasite can also play a role in schizophrenia’s mental and behavioral distortions.
Biological Building Blocks of Disorder
How does T. gondii, a microscopic parasitic agent, take the reins of the human brain? Again, while the parasite is not one hundred percent linked with schizophrenia, its presence does indicate an increased likelihood that an individual will develop the disorder. Scientific studies have demonstrated that T. gondii can traverse the blood-brain barrier, a sifting mechanism that typically wards off harmful pathogens and guards the brain against a potential threat. Once T. gondii sidesteps this protective checkpoint, it is free to directly infect host brain cells. Like an alien invader, it uses the host cell as a breeding ground and proceeds to conquer the surrounding areas. Cysts have been observed in critical brain structures such as the amygdala, olfactory bulb, cerebellum, and cortical regions, all of which relate to emotional state and sensory integration. This cellular takeover clearly sets the stage for T. gondii’s impact on schizophrenic symptoms. The question remains: what bodily processes are tweaked by T. gondii and how do these changes manifest as the abnormal schizophrenic behavioral shifts?
A partial key lies in T. gondii’s manipulation of its host’s dopamine levels. Dopamine is a neurotransmitter involved in several regulatory functions, including but not limited to controlling mood, memory, behavior, and pleasurable reward. When brain production centers churn out too much dopamine, cognition can be rewired and schizophrenic symptoms can become apparent . The link between schizophrenia and elevated dopamine levels has been recognized amidst the scientific community for quite some time, but researchers have now isolated two genes within the T. gondii genome which seem to cause a detrimental dopamine spike. These genes, labeled AAH1 and AAH2, encode for tyrosine and phenylalanine hydroxylases, enzymes which catalyze a chain reaction of chemical alterations that culminates in increased dopamine levels. Pinpointing the exact mechanism of T. gondii’s dopamine manipulation is a step toward engineering treatments that can restore equilibrium.
Beyond the Dopamine Hypothesis
T. gondii’s influence extends even beyond dopamine level interference. The parasite also amps up the influence of a proinflammatory cytokine called interferon gama which kicks the cell’s regular kynurenine pathway into high gear. Interferon gama, a cytokine integral to cell signaling, essentially directs this common cellular pathway to break down chemical tryptophan more quickly than usual- a process which results in increased levels of quinolinic and kynurenic acid. Both of these compounds have devastating effects on the brain; excess quinolinic acid causes neurodegeneration and the imbalanced kynurenic acid ratio produces cognitive symptoms reminiscent of schizophrenia.
While the full range of T. gondii-related damage is still under investigation, the parasite’s activity is certainly correlated with the onset of schizophrenia-type behaviors. It may even be able to alter the host cell’s patterns of transcription, thereby changing the cell’s expression of genetic material to suit the parasite’s needs. Although there are many proposed hypotheses to explain T. gondii’s action in both mice and humans, all concede that the parasite causes genetic, cognitive, and behavioral interference; these distortions are intimately linked to the exploration of schizophrenia’s biological underpinnings.
Will the study of T. gondii lead to any significant breakthroughs in schizophrenia research? Maybe yes, maybe no. After all, schizophrenia is not exclusive to T. gondii invasion and can befall individuals who have never before encountered the parasite. Since schizophrenia and T. gondii infection present similar symptoms, though, combating T. gondii infection may shed some light on the impenetrable puzzle that is schizophrenia. Bottom line, cats do not cause schizophrenia. But they can occasionally introduce an insidious parasite which is schizophrenia’s symptomatic partner.