Evidence map›Paper›PMID 34572962›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Exacerbated Age-Related Hippocampal Alterations of Microglia Morphology, β-Amyloid and Lipofuscin Deposition and Presenilin Overexpression in

Jan Hendrik Börner, Oliver Rawashdeh, Abdelhaq Rami

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024
    Review
  6. Article
  7. Review
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

3 authors at 2 institutions in 2 countries.

Jan Hendrik BörnerInstitut für Experimentelle Neurobiologie (Anatomie II), Klinikum der Johann Wolfgang von Goethe-Universität, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Oliver RawashdehChronobiology & Sleep Lab, Faculty of Medicine, School of Biomedical Sciences, The University of Queensland Brisbane, Brisbane 4072, Australia.ORCID 0000-0002-7147-4778
Abdelhaq RamiInstitut für Experimentelle Neurobiologie (Anatomie II), Klinikum der Johann Wolfgang von Goethe-Universität, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Goethe University Frankfurt · DEThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In humans, alterations of circadian rhythms and autophagy are linked to metabolic, cardiovascular and neurological dysfunction. Autophagy constitutes a specific form of cell recycling in many eukaryotic cells. Aging is the principal risk factor for the development of neurodegenerative diseases. Thus, we assume that both the circadian clock and autophagy are indispensable to counteract aging. We have previously shown that the hippocampus of

Indexed as

agingautophagyhippocampuslipofuscinmicrogliaoxidative stressPer1−/−-miceß-amyloid

Identifiers

PMID34572962
PMCPMC8469021
OpenAlexW3194375273

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.