Evidence map›Paper›PMID 22738374›Full record

ArticleJournal of anatomy2012

Astrocytic cytoskeletal atrophy in the medial prefrontal cortex of a triple transgenic mouse model of Alzheimer's disease.

Magdalena Kulijewicz-Nawrot, Alexei Verkhratsky, Alexander Chvátal, Eva Syková, José J Rodríguez

Open access · greenAbstract read
In one paragraph

Article in Journal of anatomy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 158 citations in OpenAlex.

  1. Diffusion MRI reveals amyloid plaque-associated cellular signatures through spatial transcriptomic integration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    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
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  12. Amyloid precursor protein induces reactive astrogliosis.bioRxiv : the preprint server for biology · 2023
    Article
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  14. Article
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  17. Microglia-Astrocyte Communication in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023
    Review
  18. Review
  19. Article
  20. Review

22 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

5 authors at 2 institutions in 3 countries.

Magdalena Kulijewicz-NawrotInstitute of Experimental Medicine, ASCR, Videnska, Prague, Czech Republic.
Alexei Verkhratsky
Alexander Chvátal
Eva Syková
José J Rodríguez
Czech Academy of Sciences, Institute of Experimental Medicine · CZUniversity of the Basque Country · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the loss of cognitive functions, reflecting pathological damage to the medial prefrontal cortex (mPFC) as well as to the hippocampus and the entorhinal cortex. Astrocytes maintain the internal homeostasis of the CNS and are fundamentally involved in neuropathological processes, including AD. Here, we analysed the astrocytic cytoskeletal changes within the mPFC of a triple transgenic mouse model of AD (3 × Tg-AD) by measuring the surface area and volume of glial fibrillary acidic protein (GFAP)-positive profiles in relation to the build-up and presence of amyloid-β (Aβ), and compared the results with those found in non-transgenic control animals at different ages. 3 × Tg-AD animals showed clear astroglial cytoskeletal atrophy, which appeared at an early age (3 months; 33% and 47% decrease in GFAP-positive surface area and volume, respectively) and remained throughout the disease progression at 9, 12 and 18 months old (29% and 36%; 37% and 35%; 43% and 37%, respectively). This atrophy was independent of Aβ accumulation, as only a few GFAP-positive cells were localized around Aβ aggregates, which suggests no direct relationship with Aβ toxicity. Thus, our results indicate that the progressive reduction in astrocytic branching and domain in the mPFC can account for the integrative dysfunction leading to the cognitive deficits and memory disturbances observed in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesAtrophyCytoskeletonDisease Models, AnimalDisease ProgressionImmunohistochemistryMiceMice, TransgenicPrefrontal CortexAmyloid beta-Peptides

Identifiers

PMID22738374
PMCPMC3458630
OpenAlexW2162110855

What OpenQuestion holds

Textmetadata
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.