Evidence map›Paper›PMID 33634529›Full record

SynthesisGlia2021

Reactive astrocytes as treatment targets in Alzheimer's disease-Systematic review of studies using the APPswePS1dE9 mouse model.

Tamar Smit, Natasja A C Deshayes, David R Borchelt, Willem Kamphuis, Jinte Middeldorp, Elly M Hol

Open access · bronzeAbstract readSystematic Review
In one paragraph

Synthesis in Glia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Astrocyte reactivity across the AD continuum measured by [European journal of nuclear medicine and molecular imaging · 2026
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  11. Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025
    Review
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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

6 authors at 3 institutions in 2 countries.

Tamar SmitDepartment of Translational Neuroscience, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0003-0479-471X
Natasja A C DeshayesDepartment of Translational Neuroscience, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands.
David R BorcheltCenter for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, Department of Neuroscience, University of Florida College of Medicine, Gainesville, Florida, USA.ORCID 0000-0002-0813-6979
Willem KamphuisNetherlands Institute for Neuroscience, An Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.
Jinte MiddeldorpDepartment of Translational Neuroscience, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-9198-8020
Elly M HolDepartment of Translational Neuroscience, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0001-5604-2603
Netherlands Institute for Neuroscience · NLUtrecht University · NLUniversity of Florida · US

Funding

University of Florida - Mt. Sinai Medical Center AD Research CenterP50AG047266 · NIA · UNIVERSITY OF FLORIDA · PI GOLDE, TODD E · 2015 to 2019
$7.3M
NIA NIH HHS P50 AG047266
6 · The paper itself

Abstract

Astrocytes regulate synaptic communication and are essential for proper brain functioning. In Alzheimer's disease (AD) astrocytes become reactive, which is characterized by an increased expression of intermediate filament proteins and cellular hypertrophy. Reactive astrocytes are found in close association with amyloid-beta (Aβ) deposits. Synaptic communication and neuronal network function could be directly modulated by reactive astrocytes, potentially contributing to cognitive decline in AD. In this review, we focus on reactive astrocytes as treatment targets in AD in the APPswePS1dE9 AD mouse model, a widely used model to study amyloidosis and gliosis. We first give an overview of the model; that is, how it was generated, which cells express the transgenes, and the effect of its genetic background on Aβ pathology. Subsequently, to determine whether modifying reactive astrocytes in AD could influence pathogenesis and cognition, we review studies using this mouse model in which interventions were directly targeted at reactive astrocytes or had an indirect effect on reactive astrocytes. Overall, studies specifically targeting astrocytes to reduce astrogliosis showed beneficial effects on cognition, which indicates that targeting astrocytes should be included in developing novel therapies for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesDisease Models, AnimalGliosisMiceMice, TransgenicAmyloid beta-PeptidesAD mouse modelAlzheimer's diseaseamyloid-betaAPPswePS1dE9reactive astrocytes

Identifiers

PMID33634529
PMCPMC8247905
OpenAlexW3129946102

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.