Evidence map›Paper›PMID 39187706›Full record

ArticleNature neuroscience2024

Tau is required for glial lipid droplet formation and resistance to neuronal oxidative stress.

Lindsey D Goodman, Isha Ralhan, Xin Li, Shenzhao Lu, Matthew J Moulton, Ye-Jin Park, Pinghan Zhao, Oguz Kanca, Ziyaneh S Ghaderpour Taleghani, Julie Jacquemyn and 5 more

Abstract read
In one paragraph

Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Tau protein as a regulator of mitochondrial function and dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. GSK-3β coordinates axonal microtubule organization through Shot and Tau.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

15 authors.

Lindsey D GoodmanDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Isha RalhanDepartment of Physiology, University of Alberta, Edmonton, Alberta, Canada.ORCID http://orcid.org/0000-0002-6890-2620
Xin LiCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Shenzhao LuDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0003-3117-3900
Matthew J MoultonDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0003-0228-7669
Ye-Jin ParkDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0002-8066-4194
Pinghan ZhaoJan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX, USA.
Oguz KancaDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Ziyaneh S Ghaderpour TaleghaniDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0001-9399-6502
Julie JacquemynDepartment of Physiology, University of Alberta, Edmonton, Alberta, Canada.ORCID http://orcid.org/0000-0002-4524-5728
Joshua M ShulmanDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Kanae AndoDepartment of Biological Sciences, Tokyo Metropolitan University, Hachioji, Tokyo, Japan.
Kai SunCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Maria S IoannouDepartment of Physiology, University of Alberta, Edmonton, Alberta, Canada.
Hugo J BellenDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA. hbellen@bcm.edu.ORCID http://orcid.org/0000-0001-5992-5989

Funding

Vascular Structure and Function in Cognitive AgingP01AG003949 · NIA · YESHIVA UNIVERSITY · PI Charles B Hall · 1985 to 2026
$73.9M
Alzheimer's Disease Genetics ConsortiumU01AG032984 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SCHELLENBERG, GERARD DAVID · 2009 to 2024
$60.4M
SUPPLEMENT TO ALZHEIMERS DISEASE PATIENT REGISTRYU01AG006786 · NIA · MAYO CLINIC ROCHESTER · PI GRAFF-RADFORD, JONATHAN, JACK, CLIFFORD R. · 1986 to 2023
$49.6M
SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI LEURGANS, SUE E. · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
THE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI PETERSEN, RONALD C · 1999 to 2018
$36.9M
UNDERSTANDING FXTAS AMONG MALES WITH THE FMR1 PREMUTATIONP30HD024064 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI ROSENMUND, CHRISTIAN · 1988 to 2013
$29.4M
Integrating the exposome and methylome to inform brain molecular changes in ADRD across established diverse cohorts.U01AG046139 · NIA · UNIVERSITY OF FLORIDA · PI ERTEKIN-TANER, NILUFER, FUNK, CORY · 2013 to 2022
$24.6M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Transposon induced disruption of most Drosophila genesR01GM067858 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI BELLEN, HUGO J · 2003 to 2020
$15.7M
Pathway discovery, validation and compound identification for Alzheimer's disease - SupplementU01AG046152 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2013 to 2017
$13.6M
Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Canada Research Chairs (Chaires de recherche du Canada) 2021-00027NIA NIH HHS P01 AG003949NIA NIH HHS P01 AG017216NIA NIH HHS P30 AG010161NIA NIH HHS P50 AG016574NIA NIH HHS P50 AG025711NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG018023NIA NIH HHS R01 AG030146NIA NIH HHS R01 AG032990NIA NIH HHS R01 AG036836NIA NIH HHS R01 AG073260NIA NIH HHS RF1 AG078660NIA NIH HHS U01 AG006786NIA NIH HHS U01 AG032984NIA NIH HHS U01 AG046139NIA NIH HHS U01 AG046152NIA NIH HHS U01 AG072439NICHD NIH HHS P30 HD024064NICHD NIH HHS P50 HD103555NICHD NIH HHS U54 HD083092NIDDK NIH HHS R01 DK129815NIGMS NIH HHS R01 GM067858NIH HHS P40 OD018537NIH HHS R24 OD022005NIH HHS R24 OD031447NINDS NIH HHS R01 NS080820NINDS NIH HHS T32 NS043124U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) T32-NS043124-18
6 · The paper itself

Abstract

The accumulation of reactive oxygen species (ROS) is a common feature of tauopathies, defined by Tau accumulations in neurons and glia. High ROS in neurons causes lipid production and the export of toxic peroxidated lipids (LPOs). Glia uptake these LPOs and incorporate them into lipid droplets (LDs) for storage and catabolism. We found that overexpressing Tau in glia disrupts LDs in flies and rat neuron-astrocyte co-cultures, sensitizing the glia to toxic, neuronal LPOs. Using a new fly tau loss-of-function allele and RNA-mediated interference, we found that endogenous Tau is required for glial LD formation and protection against neuronal LPOs. Similarly, endogenous Tau is required in rat astrocytes and human oligodendrocyte-like cells for LD formation and the breakdown of LPOs. Behaviorally, flies lacking glial Tau have decreased lifespans and motor defects that are rescuable by administering the antioxidant N-acetylcysteine amide. Overall, this work provides insights into the important role that Tau has in glia to mitigate ROS in the brain.

Indexed as

Lipid DropletsNeurogliaNeuronsOxidative Stresstau ProteinsAnimalsAstrocytesCells, CulturedCoculture TechniquesDrosophilaHumansRatsReactive Oxygen SpeciesReactive Oxygen Speciestau Proteins

Identifiers

PMID39187706
PMCPMC11809452

What OpenQuestion holds

Textmetadata
LicenceTDM
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.