Evidence map›Paper›PMID 22691495›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Loss of functional GABA(A) receptors in the Alzheimer diseased brain.

Agenor Limon, Jorge Mauricio Reyes-Ruiz, Ricardo Miledi

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 3 pooled it
5.6field-weighted citation impact, top 3% 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

159 citing papers in PubMed, 3 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Use of Drugs Affecting GABAMolecular neurobiology · 2025
    Pooled it
  2. Pooled it
  3. Use of Benzodiazepines in Alzheimer's Disease: A Systematic Review of Literature.The international journal of neuropsychopharmacology · 2015
    Pooled it
  4. Article
  5. Review
  6. The role of GABANeuroscience and biobehavioral reviews · 2026
    Review
  7. Review
  8. Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Molecular assemblies and pharmacology of cerebellar GABAProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Neural Circuit Mapping and Neurotherapy-Based Strategies.Cellular and molecular neurobiology · 2025
    Review
  19. Review
  20. Article

99 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

3 authors at 1 institution in 1 country.

Agenor LimonLaboratory of Cellular and Molecular Neurobiology, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA. alimonru@uci.edu
Jorge Mauricio Reyes-Ruiz
Ricardo Miledi
University of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cholinergic and glutamatergic neurotransmission systems are known to be severely disrupted in Alzheimer's disease (AD). GABAergic neurotransmission, in contrast, is generally thought to be well preserved. Evidence from animal models and human postmortem tissue suggest GABAergic remodeling in the AD brain. Nevertheless, there is no information on changes, if any, in the electrophysiological properties of human native GABA receptors as a consequence of AD. To gain such information, we have microtransplanted cell membranes, isolated from temporal cortices of control and AD brains, into Xenopus oocytes, and recorded the electrophysiological activity of the transplanted GABA receptors. We found an age-dependent reduction of GABA currents in the AD brain. This reduction was larger when the AD membranes were obtained from younger subjects. We also found that GABA currents from AD brains have a faster rate of desensitization than those from non-AD brains. Furthermore, GABA receptors from AD brains were slightly, but significantly, less sensitive to GABA than receptors from non-AD brains. The reduction of GABA currents in AD was associated with reductions of mRNA and protein of the principal GABA receptor subunits normally present in the temporal cortex. Pairwise analysis of the transcripts within control and AD groups and analyses of the proportion of GABA receptor subunits revealed down-regulation of α1 and γ2 subunits in AD. In contrast, the proportions of α2, β1, and γ1 transcripts were up-regulated in the AD brains. Our data support a functional remodeling of GABAergic neurotransmission in the human AD brain.

Indexed as

AgingAlzheimer DiseaseBrainCase-Control StudiesDown-RegulationHumansReceptors, GABA-AReceptors, GABA-A

Identifiers

PMID22691495
PMCPMC3382476
OpenAlexW2091712128

What OpenQuestion holds

Textmetadata
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.