Evidence map›Paper›PMID 35610289›Full record

ArticleScientific reports2022

Pyramidal cell axon initial segment in Alzheimer´s disease.

Alejandro Antón-Fernández, Gonzalo León-Espinosa, Javier DeFelipe, Alberto Muñoz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. The Primary Cilia are Associated with the Axon Initial Segment in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Extracellular Tau Oligomers Damage the Axon Initial Segment.Journal of Alzheimer's disease : JAD · 2023
    Article
  12. Article
  13. 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

4 authors at 3 institutions in 1 country.

Alejandro Antón-FernándezDepartment of Functional and Systems Neurobiology, Instituto Cajal, CSIC, Madrid, Spain.
Gonzalo León-EspinosaLaboratorio Cajal de Circuitos Corticales (CTB), Universidad Politécnica de Madrid, Madrid, Spain. gonzalo.leonespinosa@ceu.es.
Javier DeFelipeDepartment of Functional and Systems Neurobiology, Instituto Cajal, CSIC, Madrid, Spain.
Alberto MuñozDepartment of Functional and Systems Neurobiology, Instituto Cajal, CSIC, Madrid, Spain.
Universidad Politécnica de Madrid · ESInstituto Cajal · ESUniversidad Complutense de Madrid · ES

Funding

Alzheimer's Association ZEN-15-321663
6 · The paper itself

Abstract

The axon initial segment (AIS) is a region of the neuron that is critical for action potential generation as well as for the regulation of neural activity. This specialized structure-characterized by the expression of different types of ion channels as well as adhesion, scaffolding and cytoskeleton proteins-is subjected to morpho-functional plastic changes in length and position upon variations in neural activity or in pathological conditions. In the present study, using immunocytochemistry with the AT8 antibody (phospho-tau S202/T205) and 3D confocal microscopy reconstruction techniques in brain tissue from Alzheimer's disease patients, we found that around half of the cortical pyramidal neurons with hyperphosphorylated tau showed changes in AIS length and position in comparison with AT8-negative neurons from the same cortical layers. We observed a wide variety of AIS alterations in neurons with hyperphosphorylated tau, although the most common changes were a proximal shift or a lengthening of the AISs. Similar results were found in neocortical tissue from non-demented cases with neurons containing hyperphosphorylated tau. These findings support the notion that the accumulation of phospho-tau is associated with structural alterations of the AIS that are likely to have an impact on normal neuronal activity, which might contribute to neuronal dysfunction in AD.

Indexed as

Alzheimer DiseaseAxon Initial SegmentHumansNeuronsPyramidal Cellstau Proteinstau Proteins

Identifiers

PMID35610289
PMCPMC9130508
OpenAlexW4281397082

What OpenQuestion holds

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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.