ReviewMetabolic brain disease2021
Experimental evidence of tyrosine neurotoxicity: focus on mitochondrial dysfunction.
Review in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 38 citations in OpenAlex.
- White matter disorders at the intersection of transcription, RNA processing and translation.Nature reviews. Neurology · 2026Review
- In-depth characterization of the CaScientific reports · 2026Article
- Shared Plant-human Biology: Herbicide Effects and New Biomarkers Perspectives.Current environmental health reports · 2026Review
- Beyond Protein Building Blocks: A Review of Biological Roles and Therapeutic Potential of Free Amino Acids.International journal of molecular sciences · 2025Review
- Highly Sensitive Detection of Tyrosine and Neurotransmitters by Stereoselective Biosynthesis and Photochemically Induced Dynamic Nuclear Polarization.Journal of the American Chemical Society · 2025Article
- Behavioral Alterations and Cholinergic Modulation in Zebrafish Acutely Exposed To Tyrosine.Neurotoxicity research · 2025Article
- Transfer RNA and small molecule therapeutics for aminoacyl-tRNA synthetase diseases.The FEBS journal · 2025Review
- Association between human blood metabolites and cerebral cortex architecture: evidence from a Mendelian randomization study.Frontiers in neurology · 2024Article
- Correlation between gut microbiome and cognitive impairment in patients undergoing peritoneal dialysis.BMC nephrology · 2023Article
- Neurocognitive outcome and mental health in children with tyrosinemia type 1 and phenylketonuria: A comparison between two genetic disorders affecting the same metabolic pathway.Journal of inherited metabolic disease · 2022Article
- Integrated Brain Metabolomics and Network Pharmacology Analysis to Reveal the Improvement Effect of Bai Chan Ting on Parkinson's Disease.BioMed research international · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue exposure to high levels of tyrosine, which is characteristic of an inborn error of metabolism named Tyrosinemia, is related to severe symptoms, including neurological alterations. The clinical manifestations and pathogenesis of tyrosine neurotoxicity can be recapitulated in experimental models in vivo and in vitro. A widely used experimental model to study brain tyrosine damage is the chronic and acute administration of this amino acid in infant rats. Other research groups and we have extensively studied the pathogenic events in the brain structures of rats exposed to high tyrosine levels. Rats administered acutely and chronically with tyrosine presented decreased and inhibition of the essential metabolism enzymes, e.g., Krebs cycle enzymes and mitochondrial respiratory complexes in the brain structures. These alterations induced by tyrosine toxicity were associated with brain oxidative stress, astrocytes, and, ultimately, cognitive impairments. Notably, in vivo data were corroborated by in vitro studies using cerebral regions homogenates incubated with tyrosine excess. Considering metabolism's importance to brain functioning, we hypothesized that mitochondrial and metabolic dysfunctions are closely related to neurological alterations induced by tyrosine neurotoxicity. Herein, we reviewed the main mechanisms associated with tyrosine neurotoxicity in experimental models, emphasizing the role of mitochondrial dysfunction.
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.