Evidence map›Paper›PMID 25297090›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Aβ selectively impairs mGluR7 modulation of NMDA signaling in basal forebrain cholinergic neurons: implication in Alzheimer's disease.

Zhenglin Gu, Jia Cheng, Ping Zhong, Luye Qin, Wenhua Liu, Zhen Yan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease.Frontiers in cell and developmental biology · 2020
    Review
  12. Role of Cofilin in Alzheimer's Disease.Frontiers in cell and developmental biology · 2020
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Negative Allosteric Modulators of mGluFrontiers in molecular neuroscience · 2018
    Article
  18. Glycinergic Input to the Mouse Basal Forebrain Cholinergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  19. Article
  20. Review
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

6 authors at 3 institutions in 2 countries.

Zhenglin GuDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214.
Jia ChengDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214.
Ping ZhongDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214, Veterans Administration Western New York Healthcare System, Buffalo, New York 14215, and.
Luye QinDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214.
Wenhua LiuDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214.
Zhen YanDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214, Veterans Administration Western New York Healthcare System, Buffalo, New York 14215, and Department of Neurobiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University, Beijing Institute for Brain Disorders, Beijing 100069, China zhenyan@buffalo.edu.
University at Buffalo, State University of New York · USChinese Institute for Brain Research · CNVA Western New York Healthcare System · US

Funding

A Novel Pathophysiological Mechanism of Alzheimer's DiseaseI01BX001633 · VA · VA WESTERN NEW YORK HEALTHCARE SYSTEM · PI YAN, ZHEN · 2013 to 2016
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BLRD VA I01 BX001633
6 · The paper itself

Abstract

Degeneration of basal forebrain (BF) cholinergic neurons is one of the early pathological events in Alzheimer's disease (AD) and is thought to be responsible for the cholinergic and cognitive deficits in AD. The functions of this group of neurons are highly influenced by glutamatergic inputs from neocortex. We found that activation of metabotropic glutamate receptor 7 (mGluR7) decreased NMDAR-mediated currents and NR1 surface expression in rodent BF neurons via a mechanism involving cofilin-regulated actin dynamics. In BF cholinergic neurons, β-amyloid (Aβ) selectively impaired mGluR7 regulation of NMDARs by increasing p21-activated kinase activity and decreasing cofilin-mediated actin depolymerization through a p75(NTR)-dependent mechanism. Cell viability assays showed that activation of mGluR7 protected BF neurons from NMDA-induced excitotoxicity, which was selectively impaired by Aβ in BF cholinergic neurons. It provides a potential basis for the Aβ-induced disruption of calcium homeostasis that might contribute to the selective degeneration of BF cholinergic neurons in the early stage of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCholine O-AcetyltransferaseNerve DegenerationNeuronsN-MethylaspartateParasympathetic Nervous SystemProsencephalonRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateSignal TransductionAmyloid beta-PeptidesCholine O-Acetyltransferasemetabotropic glutamate receptor 7N-MethylaspartateReceptors, Metabotropic Glutamateactinbasal forebrainbeta-amyloidcholinergicmGluRNMDA receptor

Identifiers

PMID25297090
PMCPMC6608374
OpenAlexW1963965739

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.