Evidence map›Paper›PMID 37170361›Full record

ArticleActa neuropathologica communications2023

Rise and fall of peroxisomes during Alzheimer´s disease: a pilot study in human brains.

Eugen Semikasev, Barbara Ahlemeyer, Till Acker, Anne Schänzer, Eveline Baumgart-Vogt

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. bioRxiv : the preprint server for biology · 2025
    Article
  9. Review
  10. Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. 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 1 institution in 1 country.

Eugen Semikasev *Division of Medical Cell Biology, Institute for Anatomy and Cell Biology, Justus-Liebig University, Aulweg 123, 35385, Giessen, Germany.
Barbara Ahlemeyer *Division of Medical Cell Biology, Institute for Anatomy and Cell Biology, Justus-Liebig University, Aulweg 123, 35385, Giessen, Germany. Barbara.Ahlemeyer@anatomie.med.uni-giessen.de.
Till AckerInstitute of Neuropathology, Justus-Liebig University, Arndtstr. 16, 35392, Giessen, Germany.
Anne SchänzerInstitute of Neuropathology, Justus-Liebig University, Arndtstr. 16, 35392, Giessen, Germany.
Eveline Baumgart-VogtDivision of Medical Cell Biology, Institute for Anatomy and Cell Biology, Justus-Liebig University, Aulweg 123, 35385, Giessen, Germany. Eveline.Baumgart-Vogt@anatomie.med.uni-giessen.de.ORCID 0000-0002-8265-3763
Justus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peroxisomes are eukaryotic organelles that rapidly change in number depending on the metabolic requirement of distinct cell types and tissues. In the brain, these organelles are essential for neuronal migration and myelination during development and their dysfunction is associated with age-related neurodegenerative diseases. Except for one study analysing ABCD3-positive peroxisomes in neurons of the frontal neocortex of Alzheimer disease (AD) patients, no data on other brain regions or peroxisomal proteins are available. In the present morphometric study, we quantified peroxisomes labelled with PEX14, a metabolism-independent peroxisome marker, in 13 different brain areas of 8 patients each either with low, intermediate or high AD neuropathological changes compared to 10 control patients. Classification of patient samples was based on the official ABC score. During AD-stage progression, the peroxisome density decreased in the area entorhinalis, parietal/occipital neocortex and cerebellum, it increased and in later AD-stage patients decreased in the subiculum and hippocampal CA3 region, frontal neocortex and pontine gray and it remained unchanged in the gyrus dentatus, temporal neocortex, striatum and inferior olive. Moreover, we investigated the density of catalase-positive peroxisomes in a subset of patients (> 80 years), focussing on regions with significant alterations of PEX14-positive peroxisomes. In hippocampal neurons, only one third of all peroxisomes contained detectable levels of catalase exhibiting constant density at all AD stages. Whereas the density of all peroxisomes in neocortical neurons was only half of the one of the hippocampus, two thirds of them were catalase-positive exhibiting increased levels at higher ABC scores. In conclusion, we observed spatiotemporal differences in the response of peroxisomes to different stages of AD-associated pathologies.

Indexed as

Alzheimer DiseaseNeocortexCatalaseHumansPeroxisomesPilot ProjectsCatalaseCatalaseHippocampusNeocortexNeurodegenerative disorderPeroxisomePEX14Pyramidal neurons

Identifiers

PMID37170361
PMCPMC10176950
OpenAlexW4376224399

What OpenQuestion holds

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LicenceCC BY
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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.