Evidence map›Paper›PMID 30319529›Full record

ReviewFrontiers in neurology2018

Elucidating the Interactive Roles of Glia in Alzheimer's Disease Using Established and Newly Developed Experimental Models.

Heejung Chun, Ian Marriott, C Justin Lee, Hansang Cho

Abstract readReview
In one paragraph

Review in Frontiers in neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

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  8. Rejuvenating aged microglia by p16Molecular neurodegeneration · 2024
    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

4 authors.

Heejung ChunCenter for Glia-Neuron Interaction, Brain Science Institute, Korea Institute of Science and Technology, Seoul, South Korea.
Ian MarriottDepartment of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC, United States.
C Justin LeeCenter for Glia-Neuron Interaction, Brain Science Institute, Korea Institute of Science and Technology, Seoul, South Korea.
Hansang ChoDepartment of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is an irreversible neurodegenerative illness and the exact etiology of the disease remains unknown. It is characterized by long preclinical and prodromal phases with pathological features including an accumulation of amyloid-beta (Aβ) peptides into extracellular Aβ plaques in the brain parenchyma and the formation of intracellular neurofibrillary tangles (NFTs) within neurons as a result of abnormal phosphorylation of microtubule-associated tau proteins. In addition, prominent activation of innate immune cells is also observed and/or followed by marked neuroinflammation. While such neuroinflammatory responses may function in a neuroprotective manner by clearing neurotoxic factors, they can also be neurotoxic by contributing to neurodegeneration

Indexed as

Alzheimer's diseaseanimal modelsastrogliosisastrogliosis-microgliosis axisbrain-on-a-chipmicrogliosisneuroinflammation

Identifiers

PMID30319529
PMCPMC6168676

What OpenQuestion holds

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Registered trials

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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.