Evidence map›Paper›PMID 32121669›Full record

ReviewBiomolecules2020

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia.

Amira Bryll, Justyna Skrzypek, Wirginia Krzyściak, Maja Szelągowska, Natalia Śmierciak, Tamas Kozicz, Tadeusz Popiela

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 2 countries.

Amira BryllDepartment of Radiology, Jagiellonian University Medical College, Kopernika 19, 31-501 Krakow, Poland.
Justyna SkrzypekDepartment of Medical Diagnostics, Jagiellonian University, Medical College, Medyczna 9, 30-688 Krakow, Poland.
Wirginia KrzyściakDepartment of Medical Diagnostics, Jagiellonian University, Medical College, Medyczna 9, 30-688 Krakow, Poland.
Maja SzelągowskaDepartment of Medical Diagnostics, Jagiellonian University, Medical College, Medyczna 9, 30-688 Krakow, Poland.
Natalia ŚmierciakDepartment of Child and Adolescent Psychiatry, Faculty of Medicine, Jagiellonian University, Medical College, Kopernika 21a, 31-501 Krakow, Poland.
Tamas KoziczDepartment of Clinical Genomics, Center for Individualized Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Tadeusz PopielaDepartment of Radiology, Jagiellonian University Medical College, Kopernika 19, 31-501 Krakow, Poland.
Jagiellonian University · PLMayo Clinic · US

Funding

Uniwersytet Jagielloński Collegium Medicum N41/DBS/000292
6 · The paper itself

Abstract

Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

Indexed as

Energy MetabolismSynaptic TransmissionAdenosine TriphosphateAnimalsAntioxidantsBrainCognitionGlucoseHumansOxidation-ReductionSchizophreniaTOR Serine-Threonine KinasesAdenosine TriphosphateAntioxidantsGlucoseMTOR protein, humanTOR Serine-Threonine Kinasesglucose metabolismmitochondrial dysfunctionreactive oxygen speciesschizophrenia

Identifiers

PMID32121669
PMCPMC7175146
OpenAlexW3009462395

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.