Evidence map›Paper›PMID 30186116›Full record

ReviewFrontiers in cellular neuroscience2018

Importance of GPCR-Mediated Microglial Activation in Alzheimer's Disease.

Md Ezazul Haque, In-Su Kim, Md Jakaria, Mahbuba Akther, Dong-Kug Choi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  2. Article
  3. The Role and Mechanisms of G protein-coupled receptors in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
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  9. Article
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  12. Review
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  15. Chemogenetic manipulation of CX3CR1Molecular psychiatry · 2023
    Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

5 authors at 1 institution in 1 country.

Md Ezazul HaqueDepartment of Applied Life Science, Graduate School, Konkuk University, Chungju, South Korea.
In-Su KimDepartment of Integrated Bioscience and Biotechnology, College of Biomedical and Health Science, Research Institute of Inflammatory Disease, Konkuk University, Chungju, South Korea.
Md JakariaDepartment of Applied Life Science, Graduate School, Konkuk University, Chungju, South Korea.
Mahbuba AktherDepartment of Applied Life Science, Graduate School, Konkuk University, Chungju, South Korea.
Dong-Kug ChoiDepartment of Applied Life Science, Graduate School, Konkuk University, Chungju, South Korea.
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with impairment of cognition, memory deficits and behavioral abnormalities. Accumulation of amyloid beta (Aβ) is a characteristic hallmark of AD. Microglia express several GPCRs, which, upon activation by modulators, mediate microglial activation and polarization phenotype. This GPCR-mediated microglial activation has both protective and detrimental effects. Microglial GPCRs are involved in amyloid precursor protein (APP) cleavage and Aβ generation. In addition, microglial GPCRs are featured in the regulation of Aβ degradation and clearance through microglial phagocytosis and chemotaxis. Moreover, in response to Aβ binding on microglial Aβ receptors, they can trigger multiple inflammatory pathways. However, there is still a lack of insight into the mechanistic link between GPCR-mediated microglial activation and its pathological consequences in AD. Currently, the available drugs for the treatment of AD are mostly symptomatic and dominated by acetylcholinesterase inhibitors (AchEI). The selection of a specific microglial GPCR that is highly expressed in the AD brain and capable of modulating AD progression through Aβ generation, degradation and clearance will be a potential source of therapeutic intervention. Here, we have highlighted the expression and distribution of various GPCRs connected to microglial activation in the AD brain and their potential to serve as therapeutic targets of AD.

Indexed as

acetylcholine receptorsadrenergic receptorsAlzheimer’s diseaseamyloid betadopamine receptorsGPCRmicrogliapurinergic receptors

Identifiers

PMID30186116
PMCPMC6110855
OpenAlexW2888540773

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.