Evidence map›Paper›PMID 32744952›Full record

ReviewCurrent neuropharmacology2021

Tetrahydrobioterin (BH4) Pathway: From Metabolism to Neuropsychiatry.

H Fanet, L Capuron, N Castanon, F Calon, S Vancassel

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
2.5field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

94 citing papers in PubMed, 115 citations in OpenAlex.

  1. Trial
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  8. Vitamin D and Vitamin BDiseases (Basel, Switzerland) · 2026
    Review
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  13. Research progress of ferroptosis in obesity and its complications.Journal of physiology and biochemistry · 2026
    Review
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  15. Ironing out mechanisms of ferroptotic death to tailor new stroke therapies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

H FanetINRAe, Nutrition and Integrated Neurobiology, UMR 1286, Bordeaux, France.
L CapuronINRAe, Nutrition and Integrated Neurobiology, UMR 1286, Bordeaux, France.
N CastanonINRAe, Nutrition and Integrated Neurobiology, UMR 1286, Bordeaux, France.
F CalonFaculty of Pharmacy, Universite Laval, Quebec City, QC, Canada.
S VancasselINRAe, Nutrition and Integrated Neurobiology, UMR 1286, Bordeaux, France.
NutriNeuro · FRUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tetrahydrobipterin (BH4) is a pivotal enzymatic cofactor required for the synthesis of serotonin, dopamine and nitric oxide. BH4 is essential for numerous physiological processes at periphery and central levels, such as vascularization, inflammation, glucose homeostasis, regulation of oxidative stress and neurotransmission. BH4 de novo synthesis involves the sequential activation of three enzymes, the major controlling point being GTP cyclohydrolase I (GCH1). Complementary salvage and recycling pathways ensure that BH4 levels are tightly kept within a physiological range in the body. Even if the way of transport of BH4 and its ability to enter the brain after peripheral administration is still controversial, data showed increased levels in the brain after BH4 treatment. Available evidence shows that GCH1 expression and BH4 synthesis are stimulated by immunological factors, notably pro-inflammatory cytokines. Once produced, BH4 can act as an anti- inflammatory molecule and scavenger of free radicals protecting against oxidative stress. At the same time, BH4 is prone to autoxidation, leading to the release of superoxide radicals contributing to inflammatory processes, and to the production of BH2, an inactive form of BH4, reducing its bioavailability. Alterations in BH4 levels have been documented in many pathological situations, including Alzheimer's disease, Parkinson's disease and depression, in which increased oxidative stress, inflammation and alterations in monoaminergic function are described. This review aims at providing an update of the knowledge about metabolism and the role of BH4 in brain function, from preclinical to clinical studies, addressing some therapeutic implications.

Indexed as

NeuropsychiatryBiopterinsGTP CyclohydrolaseHumansNitric OxideSerotoninBiopterinsGTP CyclohydrolaseNitric OxidesapropterinSerotoninAlzhemiercofactordepressionguanosine-triphosphate-cyclohydrolase-1 (GCH1)monoaminesParkinsontetrahydrobiopterin (BH4)

Identifiers

PMID32744952
PMCPMC8573752
OpenAlexW3048028461

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.