Evidence map›Paper›PMID 33325389›Full record

ReviewJournal of Alzheimer's disease : JAD2020

Metabotropic Glutamate Receptors in Alzheimer's Disease Synaptic Dysfunction: Therapeutic Opportunities and Hope for the Future.

Akriti Srivastava, Brati Das, Annie Y Yao, Riqiang Yan

Open access · greenAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Discovery of VU6052959/BI'7927: A Selective mGluACS medicinal chemistry letters · 2026
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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.

Akriti SrivastavaDepartment of Neuroscience, University of Connecticut Health, Farmington, CT, USA.
Brati DasDepartment of Neuroscience, University of Connecticut Health, Farmington, CT, USA.
Annie Y YaoDepartment of Neuroscience, University of Connecticut Health, Farmington, CT, USA.
Riqiang YanDepartment of Neuroscience, University of Connecticut Health, Farmington, CT, USA.
UConn Health · US

Funding

Roles of reticulon proteins in neurodegenerative disordersR01AG025493 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2005 to 2024
$5.9M
Supplement for BACE1 in neurodegeneration and neuronal dysfunctionR01NS074256 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RIQIANG YAN · 2011 to 2026
$5.8M
Role of the CX3CL1 C-terminus in reversing age-dependent Alzheimers neurodegenerationRF1AG058261 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2017 to 2023
$5.0M
Inhibition of BACE1 for benefiting Alzheimer's patientsR01AG046929 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RIQIANG YAN · 2013 to 2026
$3.9M
Inhibition of BACE1 for benefiting Alzheimer's patientsRF1AG046929 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2018 to 2018
$3.3M
Roles of reticulon proteins in neurodegenerative disordersRF1AG025493 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2020 to 2020
$3.0M
BACE1 in neurodegeneration and neurological dysfunctionRF1NS074256 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2021 to 2021
$2.1M
NIA NIH HHS R01 AG025493NIA NIH HHS R01 AG046929NIA NIH HHS RF1 AG025493NIA NIH HHS RF1 AG046929NIA NIH HHS RF1 AG058261NINDS NIH HHS R01 NS074256NINDS NIH HHS RF1 NS074256
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the presence of neuritic plaques and neurofibrillary tangles. The impaired synaptic plasticity and dendritic loss at the synaptic level is an early event associated with the AD pathogenesis. The abnormal accumulation of soluble oligomeric amyloid-β (Aβ), the major toxic component in amyloid plaques, is viewed to trigger synaptic dysfunctions through binding to several presynaptic and postsynaptic partners and thus to disrupt synaptic transmission. Over time, the abnormalities in neural transmission will result in cognitive deficits, which are commonly manifested as memory loss in AD patients. Synaptic plasticity is regulated through glutamate transmission, which is mediated by various glutamate receptors. Here we review recent progresses in the study of metabotropic glutamate receptors (mGluRs) in AD cognition. We will discuss the role of mGluRs in synaptic plasticity and their modulation as a possible strategy for AD cognitive improvement.

Indexed as

Neuronal PlasticityAlzheimer DiseaseAmyloid beta-PeptidesHumansReceptors, Metabotropic GlutamateSynapsesAmyloid beta-PeptidesReceptors, Metabotropic GlutamateAlzheimer’s diseasecognitionionotropic glutamate receptorslong term depressionlong term potentiationmetabotropic glutamate receptorssynapsesynaptic plasticity

Identifiers

PMID33325389
PMCPMC8439550
OpenAlexW3111515297

What OpenQuestion holds

Textmetadata
LicenceTDM
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.