Evidence map›Paper›PMID 37730895›Full record

ArticleBrain structure & function2023

Prominent and conspicuous astrocyte atrophy in human sporadic and familial Alzheimer's disease.

J J Rodríguez, F Zallo, E Gardenal, Joan Cabot, X Busquets

Open access · hybridAbstract read
In one paragraph

Article in Brain structure & function, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Perisynaptic Astrocytic Processes as Communication Hubs and Early Sites of Dysfunction.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Astrocytic KFrontiers in aging neuroscience · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
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 3 institutions in 1 country.

J J RodríguezFunctional Neuroanatomy Group; IKERBASQUE, Basque Foundation for Science, Department of Neurosciences, Medical Faculty, University of the Basque Country (UPV/EHU), 48009/48940, Bilbao/Leioa, Vizcaya, Spain. j.rodriguez-arellano@ikerbasque.org.
F ZalloFunctional Neuroanatomy Group; IKERBASQUE, Basque Foundation for Science, Department of Neurosciences, Medical Faculty, University of the Basque Country (UPV/EHU), 48009/48940, Bilbao/Leioa, Vizcaya, Spain.
E GardenalFunctional Neuroanatomy Group; IKERBASQUE, Basque Foundation for Science, Department of Neurosciences, Medical Faculty, University of the Basque Country (UPV/EHU), 48009/48940, Bilbao/Leioa, Vizcaya, Spain.
Joan CabotLaboratory of Molecular Cell Biomedicine, Department of Biology, University of the Balearic Islands, 07122, Palma, Spain.
X Busquets *Laboratory of Molecular Cell Biomedicine, Department of Biology, University of the Balearic Islands, 07122, Palma, Spain.
Achucarro Basque Center for Neuroscience · ESUniversitat de les Illes Balears · ESUniversity of the Basque Country · ES

Funding

Government of the Basque Country AE-2010-1-28Grantová Agentura České Republiky GACR 309/09/1696Spanish Ministerio de Economía y Competitividad, RETOS Colaboración co-financed by FEDER and by the Ministry of Italian University and Research RTC-2015-3542-1the Spanish Government Plan Nacional de I+D+I 2008-2011, and ISCIII Subdirección General de Evaluación y Fomento de la investigación co-financed by FEDER PI10/02738
6 · The paper itself

Abstract

Pathophysiology of sporadic Alzheimer's disease (SAD) and familial Alzheimer's disease (FAD) remains poorly known, including the exact role of neuroglia and specifically astroglia, in part because studies of astrocytes in human Alzheimer's disease (AD) brain samples are scarce. As far as we know, this is the first study of a 3-D immunohistochemical and microstructural analysis of glial fibrillary acidic protein (GFAP)- and glutamine synthetase (GS)-positive astrocytes performed in the entorhinal cortex (EC) of human SAD and FAD samples. In this study, we report prominent atrophic changes in GFAP and GS astrocytes in the EC of both SAD and FAD characterised by a decrease in area and volume when compared with non-demented control samples (ND). Furthermore, we did not find neither astrocytic loss nor astrocyte proliferation or hypertrophy (gliosis). In contrast with the astrogliosis classically accepted hypothesis, our results show a highly marked astrocyte atrophy that could have a major relevance in AD pathological processes being fundamental and key for AD mnesic and cognitive alterations equivalent in both SAD and FAD.

Indexed as

Alzheimer DiseaseAstrocytesAtrophyEntorhinal CortexGlial Fibrillary Acidic ProteinHumansNeurogliaGlial Fibrillary Acidic ProteinAlzheimer’s diseaseAstrocytesAtrophyEntorhinal CortexFamilial Alzheimer’sGFAPGSSporadic Alzheimer’s

Identifiers

PMID37730895
PMCPMC10587264
OpenAlexW4386886680

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.