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Toxoplasma gondii & Human Phenotype

Compendium of Known Effects and Ongoing Research

modulation

Latent Toxoplasma gondii infection leads to deficits in goal-directed behavior in healthy elderly

October 10, 2014
Beste, C., Getzmann, S., Gajewski, P. D., Golka, K., Falkenstein, M
Neurobiology of Aging 2014; 35: 1037-1044.
Click for abstract
The parasite Toxoplasma gondii has been found to manipulate the behavior of its secondary hosts to increase its own dissemination which is commonly believed to be to the detriment of the host (manipulation hypothesis). The manipulation correlates with an up-regulation of dopaminergic neurotransmission. In humans, different pathologies have been associated with T. gondii infections but most latently infected humans do not seem to display overt impairments. Since a dopamine plus does not necessarily bear exclusively negative consequences in humans, we investigated potential positive consequences of latent toxoplasmosis (and the presumed boosting of dopaminergic neurotransmission) on human cognition and behavior. For this purpose, we focused on action cascading which has been shown to be modulated by dopamine. Based on behavioral and neurophysiological (EEG) data obtained by means of a stop-change paradigm, we were able to demonstrate that healthy young humans can actually benefit from latent T. gondii infection as regards their performance in this task (as indicated by faster response times and a smaller P3 component). The data shows that a latent infection which is assumed to affect the dopaminergic system can lead to paradoxical improvements of cognitive control processes in humans.

Tagged: action cascading, animal behavior, attention, basal ganglia, cognitive flexibility, Dopamine, eeg, error, event-related potentials, executive function, executive functions, Human, latent toxoplasmosis, manipulation hypothesis, modulation, Parasite, parkinson's disease, stop-change paradigm, toxoplama gondii

Mental health

Latent Toxoplasma gondii infection leads to improved action control

October 10, 2014
Stock, A. K., von Heinegg, E. H., Kohling, H. L., Beste, C.
Brain Behavior and Immunity 2014; 37: 103-108
Click for abstract
The parasite Toxoplasma gondii has been found to manipulate the behavior of its secondary hosts to increase its own dissemination which is commonly believed to be to the detriment of the host (manipulation hypothesis). The manipulation correlates with an up-regulation of dopaminergic neurotransmission. In humans, different pathologies have been associated with T. gondii infections but most latently infected humans do not seem to display overt impairments. Since a dopamine plus does not necessarily bear exclusively negative consequences in humans, we investigated potential positive consequences of latent toxoplasmosis (and the presumed boosting of dopaminergic neurotransmission) on human cognition and behavior. For this purpose, we focused on action cascading which has been shown to be modulated by dopamine. Based on behavioral and neurophysiological (EEG) data obtained by means of a stop-change paradigm, we were able to demonstrate that healthy young humans can actually benefit from latent T. gondii infection as regards their performance in this task (as indicated by faster response times and a smaller P3 component). The data shows that a latent infection which is assumed to affect the dopaminergic system can lead to paradoxical improvements of cognitive control processes in humans. (C) 2013 Elsevier Inc. All rights reserved.

Tagged: action cascading, animal behavior, attention, basal ganglia, cognitive flexibility, Dopamine, eeg, error, event-related potentials, executive function, executive functions, Human, latent toxoplasmosis, manipulation hypothesis, modulation, Parasite, parkinson's disease, stop-change paradigm, toxoplama gondii

Cognitive functionsMental healthMotor functions

Paranoid Schizophrenia May Be Caused by Dopamine Hyperactivity of Ca1 Hippocampus

November 8, 1991
Krieckhaus EE, Donahoe JW, Morgan MA
Biological Psychiatry 1992; 31: 560-570
Click for abstract
Explicit consolidation of memory, or fixation of declarative belief, appears to be physically represented in changes of synaptic conductances of neurons in the parietal-temporal-occipital association cortex (PTO) of the mammalian forebrain. This fixation of belief in PTO is postulated to be critically dependent on a diffuse reinforcement signal via the inferior temporal cortex (ITC) ultimately caused by an increased output of the CA1 pyramidal cells of hippocampus. Analogous to the reinforcing mechanisms of other forebrain systems, this updating of the connection weights of the neural nets in PTO by the output of the critical neurons in CA1 is directly related to concentrations of dopamine (DA). We propose that the delusions (i.e., unreasonable beliefs) of paranoid schizophrenia are caused by a hyperactivity of the same DA-sensitive CA1 neurons that are responsible for the fixation of normal beliefs. The dramatic reduction in delusions with administration of neuroleptics, as DA D2 blockers, in schizophrenics may thus be explained by their acting to ameliorate the hyperactivity of these CA1 DA D2 receptors.

Tagged: amnesia, autoradiographic localization, brain, cortex, d2 receptors, disorder, long-term potentiation, memory impairment, modulation, psychosis

Mental health

Topics

  • Behavior 105
  • Cognitive functions 64
  • Mental health 439
  • Morphology 6
  • Motor functions 10
  • Personality 36
  • Physical health 134
  • Reproduction 36
  • Reviews 40
  • Sensory functions 3
  • Uncategorized 2

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Recent articles

  • Mortality Patterns of Toxoplasmosis and Its Comorbidities in Tanzania: A 10-Year Retrospective Hospital-Based Survey February 6, 2020
  • The role of latent toxoplasmosis in the aetiopathogenesis of schizophrenia–the risk factor or an indication of a contact with cat? February 6, 2020
  • The Association between Toxoplasma gondii Infection and Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis February 6, 2020

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