Evidence map›Paper›PMID 33218044›Full record

ArticleInternational journal of molecular sciences2020

Impaired Expression of GABA Signaling Components in the Alzheimer's Disease Middle Temporal Gyrus.

Karan Govindpani, Clinton Turner, Henry J Waldvogel, Richard L M Faull, Andrea Kwakowsky

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Canonical Pathways Rewiring in Alzheimer's Disease.International journal of molecular sciences · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  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

5 authors at 1 institution in 1 country.

Karan GovindpaniCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand.ORCID 0000-0003-3796-1983
Clinton TurnerCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand.
Henry J WaldvogelCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand.
Richard L M FaullCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand.
Andrea KwakowskyCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand.ORCID 0000-0002-3801-4956
University of Auckland · NZ

Funding

Alzheimers New Zealand 3718869Alzheimers New Zealand Charitable Trust 3720863Aotearoa Foundation, Centre for Brain Research, University of Auckland 3705579Auckland Medical Research Foundation 3712563 and 3715590Brain Research New Zealand NAFreemasons New Zealand 3719321Health Research Council of New Zealand 3627373
6 · The paper itself

Abstract

γ-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter, playing a central role in the regulation of cortical excitability and the maintenance of the excitatory/inhibitory (E/I) balance. Several lines of evidence point to a remodeling of the cerebral GABAergic system in Alzheimer's disease (AD), with past studies demonstrating alterations in GABA receptor and transporter expression, GABA synthesizing enzyme activity and focal GABA concentrations in post-mortem tissue. AD is a chronic neurodegenerative disorder with a poorly understood etiology and the temporal cortex is one of the earliest regions in the brain to be affected by AD neurodegeneration. Utilizing NanoString nCounter analysis, we demonstrate here the transcriptional downregulation of several GABA signaling components in the post-mortem human middle temporal gyrus (MTG) in AD, including the GABA

Indexed as

Signal TransductionAgedAged, 80 and overAlzheimer DiseaseAutopsyFemaleGABA Plasma Membrane Transport Proteinsgamma-Aminobutyric AcidGene ExpressionGlutamate DecarboxylaseHumansMaleProtein IsoformsReceptors, GABAReceptors, GABA-ATemporal Lobebetaine plasma membrane transport proteinsGABA Plasma Membrane Transport Proteinsgamma-Aminobutyric AcidGlutamate Decarboxylaseglutamate decarboxylase 1Protein IsoformsReceptors, GABAReceptors, GABA-AAlzheimer’s diseaseGABAGABAergic systemGABA receptorsGABA transportersmiddle temporal gyrus

Identifiers

PMID33218044
PMCPMC7698927
OpenAlexW3100852457

What Socratic 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 Socratic graph.