Evidence map›Paper›PMID 32155994›Full record

ArticleInternational journal of molecular sciences2020

Perinuclear Lamin A and Nucleoplasmic Lamin B2 Characterize Two Types of Hippocampal Neurons through Alzheimer's Disease Progression.

Laura Gil, Sandra A Niño, Erika Chi-Ahumada, Ildelfonso Rodríguez-Leyva, Carmen Guerrero, Ana Belén Rebolledo, José A Arias, María E Jiménez-Capdeville

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  13. Nuclear face of Tau: an inside player in neurodegeneration.Acta neuropathologica communications · 2023
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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

8 authors at 4 institutions in 2 countries.

Laura GilDepartamento de Genética, Escuela de Medicina, Universidad "Alfonso X el Sabio", 28691 Madrid, Spain.
Sandra A NiñoDepartamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí 78210, Mexico.ORCID 0000-0001-7665-2468
Erika Chi-AhumadaDepartamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí 78210, Mexico.
Ildelfonso Rodríguez-LeyvaServicio de Neurología, Hospital Central "Ignacio Morones Prieto", San Luis Potosí 78290, Mexico.ORCID 0000-0002-3316-1471
Carmen GuerreroBanco de cerebros (Biobanco), Hospital Universitario Fundación Alcorcón, Alcorcón, 28922 Madrid, Spain.
Ana Belén RebolledoBanco de cerebros (Biobanco), Hospital Universitario Fundación Alcorcón, Alcorcón, 28922 Madrid, Spain.
José A AriasDepartamento de Genética, Escuela de Medicina, Universidad "Alfonso X el Sabio", 28691 Madrid, Spain.ORCID 0000-0001-5059-7667
María E Jiménez-CapdevilleDepartamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí 78210, Mexico.ORCID 0000-0002-8342-7063
Autonomous University of San Luis Potosí · MXHospital Universitario Fundación Alcorcón · ESUniversidad Alfonso X el Sabio · ESHospital Central Dr. Ignacio Morones Prieto · MX

Funding

Fundación Banco Santander 1.010.924
6 · The paper itself

Abstract

backgroundRecent reports point to a nuclear origin of Alzheimer's disease (AD). Aged postmitotic neurons try to repair their damaged DNA by entering the cell cycle. This aberrant cell cycle re-entry involves chromatin modifications where nuclear Tau and the nuclear lamin are involved. The purpose of this work was to elucidate their participation in the nuclear pathological transformation of neurons at early AD. METHODOLOGY: The study was performed in hippocampal paraffin embedded sections of adult, senile, and AD brains at I-VI Braak stages. We analyzed phospho-Tau, lamins A, B1, B2, and C, nucleophosmin (B23) and the epigenetic marker H4K20me3 by immunohistochemistry.

resultsTwo neuronal populations were found across AD stages, one is characterized by a significant increase of Lamin A expression, reinforced perinuclear Lamin B2, elevated expression of H4K20me3 and nuclear Tau loss, while neurons with nucleoplasmic Lamin B2 constitute a second population.

conclusionsThe abnormal cell cycle reentry in early AD implies a fundamental neuronal transformation. This implies the reorganization of the nucleo-cytoskeleton through the expression of the highly regulated Lamin A, heterochromatin repression and building of toxic neuronal tangles. This work demonstrates that nuclear Tau and lamin modifications in hippocampal neurons are crucial events in age-related neurodegeneration.

Indexed as

Alzheimer DiseaseCell CycleCellular SenescenceDisease ProgressionHippocampusHumansLamin Type ALamin Type BNeuronsNuclear Laminatau ProteinsLamin Type ALamin Type Btau ProteinsAlzheimer’s diseasecell-cycleheterochromatinhippocampusLamin ALamin B2neurofibrillary tanglesTau protein

Identifiers

PMID32155994
PMCPMC7084765
OpenAlexW3010209754

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.