ArticleNeuron2018
Tau Protein Disrupts Nucleocytoplasmic Transport in Alzheimer's Disease.
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Article in Neuron, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 262 papers, 1 of them a synthesis that pooled it.
0numbers the graph read from it
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262citing papers in PubMed, 1 pooled it
17.4field-weighted citation impact, top 1% of its field
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Who cites it
262 citing papers in PubMed, 1 synthesis or guideline pooled it, 442 citations in OpenAlex.
- Multi-omics integration reveals shared genetic architecture between metabolic markers and gray matter atrophy in Alzheimer's Disease.The journal of prevention of Alzheimer's disease · 2026Pooled it
- Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.Nucleus (Austin, Tex.) · 2026Article
- Importin-8 silencing reduces Ataxin-3 aggregation and alleviates Machado-Joseph disease/spinocerebellar ataxia type 3.iScience · 2026Article
- NAT10 inhibition corrects nuclear defects in tau mutant human neurons and extends lifespan in aiScience · 2026Article
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Nuclear Speckle Protein SRRM2 Co-localized with Pathological Tau (pTauS396) in Neuronal and Glial Cells in Progressive Supranuclear Palsy.Acta histochemica et cytochemica · 2026Article
- Article
- The nuclear basket nucleoporin MLP1 is required to maintain nuclear integrity, and mitotic fidelity in Trypanosoma brucei.PLoS neglected tropical diseases · 2026Article
- Regional and Cellular Distribution of Nuclear Phosphorylated Tau (AT100) in the Frontal Cortex and Cerebellum of Cetaceans.Biology · 2026Article
- IgLON5 autoimmune antibodies activate Tau via neuronal hyperactivity.Science advances · 2026Article
- Brainstem pathology in anti-IgLON5 disease: new insights into early events and tau progression.Brain : a journal of neurology · 2026Article
- Pathologies at the gateway: exploring the link between nucleoporins and inherited diseases.Cellular and molecular life sciences : CMLS · 2026Review
- TMEM106B C-terminal fragments drive nucleocytoplasmic transport failure and TDP-43 mislocalization in the aging human brain.bioRxiv : the preprint server for biology · 2026Article
- Tau oligomerization induces nuclear lamina invagination and chromatin remodeling in Alzheimer's disease.Acta neuropathologica · 2026Article
- Reversibility and β-sheet formation are decoupled in tau condensate aging.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Nuclear tau aggregates inhibit RNA export and form by secondary seeding from cytosolic tau aggregates.bioRxiv : the preprint server for biology · 2026Article
- Impaired nucleocytoplasmic transport in SOD1-mediated ALS.Molecular neurodegeneration · 2026Article
- The Nodding syndrome cerebrospinal fluid proteome: a lens into neurodevelopmental failure consistent with environmentally triggeredFrontiers in molecular neuroscience · 2026Article
- Biostimulants fromFrontiers in plant science · 2026Article
- Pyruvate kinase M2 in Alzheimer's disease: from dysregulation to therapeutic inhibition.Brain communications · 2026Review
202 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
30 authors at 9 institutions in 4 countries.
Bahareh EftekharzadehDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
J Gavin DaigleBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Larisa E KapinosBiozentrum, University of Basel, Basel 4056, Switzerland.
Alyssa CoyneBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Julia SchiantarelliDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Yari CarlomagnoDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Casey CookDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Sean J MillerBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Simon DujardinDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Ana S AmaralDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Jonathan C GrimaBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Rachel E BennettDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Katharina TepperDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Michael DeTureDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA.
Charles R VanderburgDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Bianca T CorjucDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Sarah L DeVosDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Jose Antonio GonzalezDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Jeannie ChewBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Svetlana VidenskyBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Fred H GageLaboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Jerome MertensLaboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Juan TroncosoDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA.
Eckhard MandelkowGerman Center for Neurodegenerative Diseases (DZNE) and CAESAR Research Center, 53175 Bonn, Germany.
Xavier SalvatellaInstitute for Research in Biomedicine, Barcelona 08028, Spain.
Roderick Y H LimBiozentrum, University of Basel, Basel 4056, Switzerland.
Leonard PetrucelliDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Susanne WegmannDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Jeffrey D RothsteinBrain Science Institute, Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. Electronic address: jrothstein@jhmi.edu.
Bradley T HymanDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA. Electronic address: bhyman@mgh.harvard.edu.
Harvard University · USJohns Hopkins Medicine · USJohns Hopkins University · USMassachusetts General Hospital · USMayo Clinic in Florida · USSalk Institute for Biological Studies · USUniversity of Basel · CHGerman Center for Neurodegenerative Diseases · DEInstitute for Research in Biomedicine · ES
Funding
THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1985 to 2019
$37.6MTHE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI BU, GUOJUN · 1999 to 2018
$36.9MProject 3: Neuropathology of the multi-proteinopathy of c9FTD/ALS.P01NS084974 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD · 2014 to 2024
$17.6MExpanding insights into FTD disease mechanismsR35NS097273 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD · 2017 to 2024
$10.6MValidation of r(G4C2)exp-binding small molecules in vivo and c9FTD/ALS biomarker developmentP01NS099114 · NINDS · UNIVERSITY OF FLORIDA · PI DISNEY, MATTHEW D · 2017 to 2021
$6.5MProject 2: Identifying genes and Pathways that impact Tau Toxicity in FTDU54NS100693 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD · 2016 to 2020
$6.2MNucleocytoplasmic transport and nuclear pore disruption in ALS/FTDR01NS094239 · NINDS · JOHNS HOPKINS UNIVERSITY · PI LLOYD, THOMAS E., ROTHSTEIN, JEFFREY D · 2016 to 2020
$3.4MOligodendroglial Dysfunction in C9orf72 ALS and FTDR01NS099320 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MORRISON, BRETT M., ROTHSTEIN, JEFFREY D · 2017 to 2021
$3.0MAssessing cellular aging in old and rejuvenated neurons from Alzheimer patientsR01AG056306 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI GAGE, FRED H · 2017 to 2021
$2.4MThe role of acetylation in regulating pathophysiology of tauR01NS089544 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD, WOLOZIN, BENJAMIN L · 2014 to 2018
$1.9MALS/FTD mutant C9orf72-induced genetic and nuclear pathology in iPS cell modelsR01NS085207 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ROTHSTEIN, JEFFREY D, SATTLER, RITA · 2013 to 2017
$1.8MNIA NIH HHS P50 AG005134NIA NIH HHS P50 AG005146NIA NIH HHS P50 AG016574NIA NIH HHS R01 AG056306NINDS NIH HHS F31 NS103360NINDS NIH HHS P01 NS084974NINDS NIH HHS P01 NS099114NINDS NIH HHS R01 NS085207NINDS NIH HHS R01 NS089544NINDS NIH HHS R01 NS094239NINDS NIH HHS R01 NS099320NINDS NIH HHS R21 NS094489NINDS NIH HHS R35 NS097273NINDS NIH HHS U54 NS100693
Abstract
Tau is the major constituent of neurofibrillary tangles in Alzheimer's disease (AD), but the mechanism underlying tau-associated neural damage remains unclear. Here, we show that tau can directly interact with nucleoporins of the nuclear pore complex (NPC) and affect their structural and functional integrity. Pathological tau impairs nuclear import and export in tau-overexpressing transgenic mice and in human AD brain tissue. Furthermore, the nucleoporin Nup98 accumulates in the cell bodies of some tangle-bearing neurons and can facilitate tau aggregation in vitro. These data support the hypothesis that tau can directly interact with NPC components, leading to their mislocalization and consequent disruption of NPC function. This raises the possibility that NPC dysfunction contributes to tau-induced neurotoxicity in AD and tauopathies.
Indexed as
Active Transport, Cell NucleusAlzheimer DiseaseAnimalsCell NucleusCytoplasmFemaleHumansMaleMiceMice, Transgenictau Proteinstau ProteinsAlzheimer’s diseasenuclear pore complexnucleocytoplasmic transportNup98tauopathies
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Read underepoch 390
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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.