Evidence map›Paper›PMID 32714136›Full record

ReviewFrontiers in neuroscience2020

GABAergic Inhibitory Interneuron Deficits in Alzheimer's Disease: Implications for Treatment.

Yilan Xu, Manna Zhao, Yuying Han, Heng Zhang

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

Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 3 pooled it
11.6field-weighted citation impact, top 1% 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

132 citing papers in PubMed, 3 syntheses or guidelines pooled it, 195 citations in OpenAlex.

  1. Meta-Analysis of Transcriptomic Studies of Blood and Six Brain Regions Identifies a Consensus of 15 Cross-Tissue Mechanisms in Alzheimer's Disease and Suggests an Origin of Cross-Study Heterogeneity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2025
    Pooled it
  2. The Footprint ofCurrent Alzheimer research · 2025
    Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. A compact GAD67 promoter enables inhibitory neuron-targeted AAV gene therapy for seizure suppression.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  7. Article
  8. Aurantio-Obtusin Attenuates Aβ-Induced Cognitive Impairment and Synaptic Dysfunction by Suppressing Neuroinflammation in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
  14. BDCD: a comprehensive Brain Disease Cell-cell communication Database.Database : the journal of biological databases and curation · 2026
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

72 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

4 authors at 1 institution in 1 country.

Yilan XuNeurodegeneration and Neuroregeneration Laboratory, Department of Basic Medicine, School of Medicine, Shaoxing University, Shaoxing, China.
Manna ZhaoNeurodegeneration and Neuroregeneration Laboratory, Department of Basic Medicine, School of Medicine, Shaoxing University, Shaoxing, China.
Yuying HanNeurodegeneration and Neuroregeneration Laboratory, Department of Basic Medicine, School of Medicine, Shaoxing University, Shaoxing, China.
Heng ZhangNeurodegeneration and Neuroregeneration Laboratory, Department of Basic Medicine, School of Medicine, Shaoxing University, Shaoxing, China.
Shaoxing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by severe cognitive deficits and pathologically by amyloid plaques, neuronal loss, and neurofibrillary tangles. Abnormal amyloid β-protein (Aβ) deposition in the brain is often thought of as a major initiating factor in AD neuropathology. However, gamma-aminobutyric acid (GABA) inhibitory interneurons are resistant to Aβ deposition, and Aβ decreases synaptic glutamatergic transmission to decrease neural network activity. Furthermore, there is now evidence suggesting that neural network activity is aberrantly increased in AD patients and animal models due to functional deficits in and decreased activity of GABA inhibitory interneurons, contributing to cognitive deficits. Here we describe the roles played by excitatory neurons and GABA inhibitory interneurons in Aβ-induced cognitive deficits and how altered GABA interneurons regulate AD neuropathology. We also comprehensively review recent studies on how GABA interneurons and GABA receptors can be exploited for therapeutic benefit. GABA interneurons are an emerging therapeutic target in AD, with further clinical trials urgently warranted.

Indexed as

Alzheimer’s diseaseamyloid β-proteincognitive deficitsGABA inhibitory interneuronsPV inhibitory interneurons

Identifiers

PMID32714136
PMCPMC7344222
OpenAlexW3038338923

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.