Evidence map›Paper›PMID 34638632›Full record

ReviewInternational journal of molecular sciences2021

Phospho-Tau and Chromatin Landscapes in Early and Late Alzheimer's Disease.

Laura Gil, Sandra A Niño, Carmen Guerrero, María E Jiménez-Capdeville

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Structural and functional damage to neuronal nuclei caused by extracellular tau oligomers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  7. Nuclear face of Tau: an inside player in neurodegeneration.Acta neuropathologica communications · 2023
    Review
  8. Article
  9. Article
  10. 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 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 78210, Mexico.ORCID 0000-0001-7665-2468
Carmen GuerreroBanco de Cerebros (Biobanco), Hospital Universitario Fundación Alcorcón, Alcorcón, 28922 Madrid, Spain.
María E Jiménez-CapdevilleDepartamento de Bioquímica, Facultad de Medicina, Universidad Autónoma, de 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 · ES

Funding

Fundación Banco Santander 1.010.924.
6 · The paper itself

Abstract

Cellular identity is determined through complex patterns of gene expression. Chromatin, the dynamic structure containing genetic information, is regulated through epigenetic modulators, mainly by the histone code. One of the main challenges for the cell is maintaining functionality and identity, despite the accumulation of DNA damage throughout the aging process. Replicative cells can remain in a senescent state or develop a malign cancer phenotype. In contrast, post-mitotic cells such as pyramidal neurons maintain extraordinary functionality despite advanced age, but they lose their identity. This review focuses on tau, a protein that protects DNA, organizes chromatin, and plays a crucial role in genomic stability. In contrast, tau cytosolic aggregates are considered hallmarks of Alzheimer´s disease (AD) and other neurodegenerative disorders called tauopathies. Here, we explain AD as a phenomenon of chromatin dysregulation directly involving the epigenetic histone code and a progressive destabilization of the tau-chromatin interaction, leading to the consequent dysregulation of gene expression. Although this destabilization could be lethal for post-mitotic neurons, tau protein mediates profound cellular transformations that allow for their temporal survival.

Indexed as

Alzheimer DiseaseChromatinDNADNA DamageEpigenesis, GeneticGenomic InstabilityHistone CodeHumansNucleosomesPhosphorylationtau ProteinsTime FactorsChromatinDNAMAPT protein, humanNucleosomestau ProteinsagingAlzheimer’s diseasecell nucleuschromatin architectureepigenetic markseuchromatinheterochromatinhistone codenuclear lamintau protein

Identifiers

PMID34638632
PMCPMC8509045
OpenAlexW3202063286

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.