Autism and ADHD may be linked with the parasite Toxoplasma gondii
Toxoplasma gondii is the parasite that causes toxoplasmosis. This parasitical infection is largely asymptomatic, but its been known to cause chronic oxidative stress in the brain of the host, which plays an essential role in the pathogenesis of neurological disorders like autism and ADHD.
This has been further discussed in a recent review that suggested there is a correlation between Autism and the reactivation of latent toxoplasmosis, which can be caused via environmental triggering factors like pregnancy, viral/bacterial infections, vaccinations, medications, and other substances. The profuse multiplication of Toxoplasma gondii in the brain is associated with persistent neuro-inflammation. It also causes chronic overproduction of pro- inflamatory and antiinflammatory cytokines and nitric oxide, which increases oxidative stress in the parasite host.
In what way does Toxoplasma gondii causes disruption in the neurological system?
1)It affects testosterone production
The neurological aspects of a toxoplasmosis infection have been detailed in many studies that demonstrated that toxoplasmosis, even in its latent stage, can induce different hormonal and behavioral and cognitive alterations in humans and rodents. There have also been reports of a significantly higher concentration of testosterone in women with latent toxoplasmosis.
Interestingly, several complex neuro-developmental disorders may be associated with higher levels of testosterone, including antisocial, aggressive behavior and ADHD symptoms. Correspondently, some of these neuro-developmental disorders have been reported in individuals with latent toxoplasmosis and ASD probands.
2) It affects the size, function of areas of the brain responsible for behaviour and cognition.
A research on The Distribution of Toxoplasma gondii Cysts in the Brain of mice with latent toxoplasmosis, revealed the areas of the brain that were mostly infested corresponded to the olfactory bulb, the entorhinal, somatosensory, motor and orbital, frontal association cortex and visual cortices, and, importantly, the hippocampus and the amygdala. All brain regions that are responsible for behaviour and cognitive skills. These affected areas have been shown to either be of abnormal size or function abnormally in ADHD patients.
It is know that connectivity of these prefrontal regions, especially the ventromedial prefrontal cortex, with the hippocampus and amygdala regulates a variety of attentional, memory, and emotional. Circuits connecting the amygdala and orbitofrontal cortex (OFC) support decision - making and reward reinforcement. So, disturbances of these circuits cause behavioral disinhibition and impulsivity.
3) It affects the connectivity between neurons
It is well established by the scientific community that parasitical infestations that cross the blood brain barrier disrupt neurotransmitter pathways. A recent article on the Toxoplasma gondii and its implications in many neurological disorders, explained that to be infected with this parasite, affects the Erbb signaling networks, which regulate the assembly of neural circuitry, myelination, neurotransmission, and synaptic plasticity. The myelination of cells, is a highly relevant process to a number of psychiatric disorders such as autism and ADHD. It consists in the process of coating the axon of each neuron with a fatty coating called myelin, which protects the neuron and helps it conduct signals more efficiently.
An investigation based on a possible pathological relationship of autoimmunity to autism found that 58% of the subjects involved had Myelin Basic Protein anti – bodies. This dysfunction implicates in a pathological effect of under connectivity between neurons, a pathological feature of autism.
4) It caused oxidative stress and changes the behaviour of the host
Myelin is sensitive to oxidative stress and glutathione depletion caused by oxidative stress. Glutathione is natural substance made from glutamate, and a recent study on rodents revealed that there is a significant reduction in the primary astrocytic glutamate transporter, GLT-1, following infection with Toxoplasma. The Glutathione precursor N-acetylcysteine, has been shown to be in involved in the pathogenesis of autism.