Evidence map›Paper›PMID 29237809›Full record

ReviewOpen biology2017

The role of astrocytes in amyloid production and Alzheimer's disease.

Georgia R Frost, Yue-Ming Li

Open access · goldAbstract readReview
In one paragraph

Review in Open biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 247 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
247citing papers in PubMed, 3 pooled it
18.2field-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

247 citing papers in PubMed, 3 syntheses or guidelines pooled it, 435 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Prolonged systemic inflammation worsens impairments to astrocyte CaAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  19. RNA-binding activity of PHGDH drives amyloid-beta production in a human brain organoid model of sporadic Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  20. Review

187 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

2 authors at 1 institution in 1 country.

Georgia R FrostChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA frostg@mskcc.org.
Yue-Ming LiChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-2633-3730
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Regulation and Function of Gamma-SecretaseR01AG026660 · NIA · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI LI, YUEMING · 2005 to 2015
$3.5M
Mechanism and therapy of AB-42-specific gamma-secretaseR01NS076117 · NINDS · SLOAN-KETTERING INST CAN RESEARCH · PI LI, YUEMING, ZHENG, HUI · 2011 to 2015
$2.8M
Mechanism and Synergy of gamma-Secretase ModulatorsR01NS096275 · NINDS · SLOAN-KETTERING INST CAN RESEARCH · PI LI, YUEMING · 2016 to 2020
$2.1M
NCI NIH HHS P30 CA008748NIA NIH HHS R01 AG026660NINDS NIH HHS R01 NS076117NINDS NIH HHS R01 NS096275
6 · The paper itself

Abstract

Alzheimer's disease (AD) is marked by the presence of extracellular amyloid beta (Aβ) plaques, intracellular neurofibrillary tangles (NFTs) and gliosis, activated glial cells, in the brain. It is thought that Aβ plaques trigger NFT formation, neuronal cell death, neuroinflammation and gliosis and, ultimately, cognitive impairment. There are increased numbers of reactive astrocytes in AD, which surround amyloid plaques and secrete proinflammatory factors and can phagocytize and break down Aβ. It was thought that neuronal cells were the major source of Aβ. However, mounting evidence suggests that astrocytes may play an additional role in AD by secreting significant quantities of Aβ and contributing to overall amyloid burden in the brain. Astrocytes are the most numerous cell type in the brain, and therefore even minor quantities of amyloid secretion from individual astrocytes could prove to be substantial when taken across the whole brain. Reactive astrocytes have increased levels of the three necessary components for Aβ production: amyloid precursor protein, β-secretase (BACE1) and γ-secretase. The identification of environmental factors, such as neuroinflammation, that promote astrocytic Aβ production, could redefine how we think about developing therapeutics for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesAstrocytesHumansAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanAlzheimer's diseaseamyloid betaastrogliosisneuroinflammation

Identifiers

PMID29237809
PMCPMC5746550
OpenAlexW2774835162

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.