ArticleBehavioural brain research2018
AAH2 gene is not required for dopamine-dependent neurochemical and behavioral abnormalities produced by Toxoplasma infection in mouse.
Article in Behavioural brain research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- From parasite-induced immune activation to neuroinflammation and behavioral dysfunction: convergent mechanisms across protozoa and helminths: a review.Journal of neuroinflammation · 2026Review
- The role of parasite-produced dopamine in Toxoplasma gondii-altered host behaviour.Nature communications · 2025Article
- Article
- Silent Infections are not So Silent: The Emerging Role of Combined Infections, Inflammation, and Vitamin Levels in OCD.Clinical neuropsychiatry · 2024Article
- Toxoplasma-induced behavior changes - is microbial dysbiosis the missing link?Frontiers in cellular and infection microbiology · 2024Review
- Article
- 4-Arylthiosemicarbazide Derivatives as Toxoplasmic Aromatic Amino Acid Hydroxylase Inhibitors and Anti-inflammatory Agents.International journal of molecular sciences · 2022Article
- Epigenetic Manipulation of Psychiatric Behavioral Disorders Induced byFrontiers in cellular and infection microbiology · 2022Review
- 4-Arylthiosemicarbazide derivatives as a new class of tyrosinase inhibitors and anti-Journal of enzyme inhibition and medicinal chemistry · 2021Article
- Social preference is maintained in mice with impaired startle reflex and glutamate/D-serine imbalance induced by chronic cerebral toxoplasmosis.Scientific reports · 2021Article
- Behavioral biology of Toxoplasma gondii infection.Parasites & vectors · 2021Review
- Neurological and Neurobehavioral Disorders Associated withJournal of parasitology research · 2021Review
- The molecular biology and immune control of chronic Toxoplasma gondii infection.The Journal of clinical investigation · 2020Review
- Pathophysiological Mechanisms of Cognitive Impairment and Neurodegeneration byBrain sciences · 2020Review
- Latent Toxoplasmosis Effects on Rodents and Humans: How Much is Real and How Much is Media Hype?mBio · 2020Review
- In Reply.Deutsches Arzteblatt international · 2019Article
- Efficient genome engineering of Toxoplasma gondii using the TALEN technique.Parasites & vectors · 2019Article
- Toxoplasma gondii: Biological Parameters of the Connection to Schizophrenia.Schizophrenia bulletin · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Infection with the protozoan parasite, Toxoplasma gondii (T. gondii), has been associated with the increased risk for several psychiatric disorders. The exact mechanisms of a hypothesized contribution of T. gondii infection are poorly understood. The T. gondii genome contains two aromatic amino acid hydroxylase genes (AAH1 and AAH2) that encode proteins that can produce L-DOPA. One popular hypothesis posits that these encoded enzymes might influence dopamine (DA) production and hence DA synaptic transmission, leading to neurobehavioral abnormalities in the infected host. Prior studies have shown that deletion of these genes does not alter DA levels in the brain or exploratory activity in infected mice. However, possible effects of AAH gene deficiency on infection-induced brain and behavior alterations that are directly linked to DA synaptic transmission have not been evaluated. We found that chronic T. gondii infection of BALB/c mice leads to blunted response to amphetamine or cocaine and decreased expression of Dopamine Transporter (DAT) and Vesicular Monoamine Transporter 2 (VMAT2). Deletion of AAH2 had no effects on these changes in infected mice. Both wild type and Δaah2 strains produced comparable levels of neuroinflammation. Our findings demonstrate that AAH2 is not required for T. gondii infection-produced DA-dependent neurobehavioral abnormalities.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.