Evidence map›Paper›PMID 23656989›Full record

Trial reportJournal of neuropathology and experimental neurology2013

Differential relationships of reactive astrocytes and microglia to fibrillar amyloid deposits in Alzheimer disease.

Alberto Serrano-Pozo, Alona Muzikansky, Teresa Gómez-Isla, John H Growdon, Rebecca A Betensky, Matthew P Frosch, Bradley T Hyman

Open access · hybridAbstract readComparative StudyRandomized Controlled Trial
In one paragraph

Trial report in Journal of neuropathology and experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 4% 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

150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 222 citations in OpenAlex.

  1. Pooled it
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  10. In vivo mapping of cortical amyloid beta-myelin coupling in preclinical Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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90 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

7 authors at 2 institutions in 1 country.

Alberto Serrano-PozoMass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Massachusetts Alzheimer Disease Research Center, and Harvard Medical School, Charlestown, Massachusetts, USA.
Alona Muzikansky
Teresa Gómez-Isla
John H Growdon
Rebecca A Betensky
Matthew P Frosch
Bradley T Hyman
Massachusetts General Hospital · USMaineGeneral Medical Center · US

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
NEUROPATHOLOGICAL ALTERATIONS IN ALZHEIMERS DISEASER01AG008487 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1995 to 2010
$5.4M
PATHOLOGICAL ALTERATIONS IN ALZHEIMER'S DISEASER29AG008487 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T · 1989 to 1993
–
NIA NIH HHS AG008487NIA NIH HHS P30 AG062421NIA NIH HHS P50 AG005134NIA NIH HHS R01 AG008487
6 · The paper itself

Abstract

Although it is clear that astrocytes and microglia cluster around dense-core amyloid plaques in Alzheimer disease (AD), whether they are primarily attracted to amyloid deposits or are just reacting to plaque-associated neuritic damage remains elusive. We postulate that astrocytes and microglia may differentially respond to fibrillar amyloid β. Therefore, we quantified the size distribution of dense-core thioflavin-S (ThioS)-positive plaques in the temporal neocortex of 40 AD patients and the microglial and astrocyte responses in their vicinity (≤50 μm) and performed correlations between both measures. As expected, both astrocytes and microglia were clearly spatially associated with ThioS-positive plaques (p = 0.0001, ≤50 μm vs. >50 μm from their edge), but their relationship to ThioS-positive plaque size differed: larger ThioS-positive plaques were associated with more surrounding activated microglia (p = 0.0026), but this effect was not observed with reactive astrocytes. Microglial response to dense-core plaques seems to be proportional to their size, which we postulate reflects a chemotactic effect of amyloid β. By contrast, plaque-associated astrocytic response does not correlate with plaque size and seems to parallel the behavior of plaque-associated neuritic damage.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAstrocytesBrainFemaleHumansMaleMicrogliaPlaque, Amyloid

Identifiers

PMID23656989
PMCPMC3661683
OpenAlexW1995111570

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.