Evidence map›Paper›PMID 31010726›Full record

ArticleJournal of autoimmunity2019

Sex-specific Tau methylation patterns and synaptic transcriptional alterations are associated with neural vulnerability during chronic neuroinflammation.

Alessandro Didonna, Ester Cantó, Hengameh Shams, Noriko Isobe, Chao Zhao, Stacy J Caillier, Carlo Condello, Hana Yamate-Morgan, Seema K Tiwari-Woodruff, Mohammad R K Mofrad and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Loss of ADAP1/CentA1 Protects Against Autoimmune Demyelination.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. TopoDB: a novel multifunctional management system for laboratory animal colonies.Database : the journal of biological databases and curation · 2020
    Article
  15. 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

12 authors.

Alessandro DidonnaDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA. Electronic address: alessandro.didonna@ucsf.edu.
Ester CantóDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.
Hengameh ShamsDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.
Noriko IsobeDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.
Chao ZhaoDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.
Stacy J CaillierDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.
Carlo CondelloDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA; Institute for Neurodegenerative Diseases, University of California, San Francisco, CA, 94158, USA.
Hana Yamate-MorganDivision of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, CA, 92521, USA; Neuroscience Graduate Program, University of California Riverside, Riverside, CA, 92521, USA.
Seema K Tiwari-WoodruffDivision of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, CA, 92521, USA; Neuroscience Graduate Program, University of California Riverside, Riverside, CA, 92521, USA; Center for Glial-Neuronal Interactions, UCR School of Medicine, CA, 92506, USA.
Mohammad R K MofradMolecular Cell Biomechanics Laboratory, Departments of Bioengineering and Mechanical Engineering, University of California, Berkeley, CA, 94720, USA; Physical Biosciences Division, Lawrence Berkeley National Lab, Berkeley, CA, 94720, USA.
Stephen L HauserDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.
Jorge R OksenbergDepartment of Neurology and Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, 94158, USA.

Funding

GENE LINKAGE STUDY OF MULTIPLE SCLEROSIS SIBLING PAIRSR01NS026799 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HAUSER, STEPHEN L, OKSENBERG, JORGE R. · 1989 to 2018
$6.8M
Stimulating oligodendrocyte progenitor cell differentiation and remyelinationR01NS081141 · NINDS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI TIWARI-WOODRUFF, SEEMA K · 2014 to 2017
$1.3M
NINDS NIH HHS R01 NS026799NINDS NIH HHS R01 NS081141
6 · The paper itself

Abstract

The molecular events underlying the transition from initial inflammatory flares to the progressive phase of multiple sclerosis (MS) remain poorly understood. Here, we report that the microtubule-associated protein (MAP) Tau exerts a gender-specific protective function on disease progression in the MS model experimental autoimmune encephalomyelitis (EAE). A detailed investigation of the autoimmune response in Tau-deficient mice excluded a strong immunoregulatory role for Tau, suggesting that its beneficial effects are presumably exerted within the central nervous system (CNS). Spinal cord transcriptomic data show increased synaptic dysfunctions and alterations in the NF-kB activation pathway upon EAE in Tau-deficient mice as compared to wildtype animals. We also performed the first comprehensive characterization of Tau post-translational modifications (PTMs) in the nervous system upon EAE. We report that the methylation levels of the conserved lysine residue K306 are significantly decreased in the chronic phase of the disease. By combining biochemical assays and molecular dynamics (MD) simulations, we demonstrate that methylation at K306 decreases the affinity of Tau for the microtubule network. Thus, the down-regulation of this PTM might represent a homeostatic response to enhance axonal stability against an autoimmune CNS insult. The results, altogether, position Tau as key mediator between the inflammatory processes and neurodegeneration that seems to unify many CNS diseases.

Indexed as

Gene Expression RegulationAnimalsAutoimmunityCell LineDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Regulatory NetworksMaleMethylationMiceMice, KnockoutModels, MolecularMultiple SclerosisNeuronsSignal Transductiontau ProteinsLysine methylationMultiple sclerosisNeuroinflammationPost-translational modifications (PTMs)Tau

Identifiers

PMID31010726
PMCPMC6561733

What OpenQuestion holds

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Registered trials

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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.