ArticleNature neuroscience2025
In vivo hyperphosphorylation of tau is associated with synaptic loss and behavioral abnormalities in the absence of tau seeds.
Abstract read
In one paragraph
Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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.
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.
Who cites it
36 citing papers in PubMed.
- Site-specific phosphorylation of Ser352 drives aggregation of Tau R4 under acidosis conditions.Chemical science · 2026Article
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Neuroinflammatory and molecular pathways in Alzheimer's disease: mechanistic crosstalk and emerging therapeutic opportunities.Inflammopharmacology · 2026Review
- Selective degradation of DAPK1 via a novel hydrophobic tagging attenuates tau pathology in Alzheimer's disease.Journal of advanced research · 2026Article
- Tau Aggregate Imaging and Transcriptomics of Alzheimer's Disease Brain at Different Stages of Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Small-Molecule DEPTAC Rescues Cognitive Deficits by Targeted Dephosphorylation of Pathological Tau.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Scalable human neuronal models of tauopathy producing endogenous seed-competent 4R tau.Science advances · 2026Article
- The Interactions of Tau, RNA, and Stress Granules in Neurodegenerative Disease: A Comprehensive Review.Cells · 2026Review
- Patient-derived tau-seeded human neuronal chimeras recapitulate mature Alzheimer's tau pathology and uncover human-specific neuronal vulnerability.bioRxiv : the preprint server for biology · 2026Article
- Tau acetylation at K331 has limited impact on tau pathology in vivo.FEBS letters · 2026Article
- Impaired spatial coding and neuronal hyperactivity in the medial entorhinal cortex of aged APP knock-in mice.Cell reports · 2026Article
- Frontotemporal dementia associated CHCHD10Cell death & disease · 2026Article
- Considerations for the selection and phenotyping of mouse models for the study of Alzheimer's disease.STAR protocols · 2026Review
- Dysregulation of autophagosome-mitochondria contacts contributes to autophagy dysfunction and neurodegeneration in tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Proteoform medicine: characterizing and targeting protein forms in human disease.Nature reviews. Genetics · 2026Review
- The Mitochondrial Guardian α-Amyrin Mitigates Alzheimer's Disease Pathology via Modulation of the DLK-SARM1-ULK1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Methods for studying the effects of phosphorylation patterns in proteins.Biochemical Society transactions · 2026Review
- Aberrant medial entorhinal cortex dynamics link tau pathology to spatial memory impairment.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors.
Naoto Watamura *Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan. n.watamura@ucl.ac.uk.ORCID http://orcid.org/0000-0001-7971-7378
Martha S Foiani *UK Dementia Research Institute at University College London, London, UK. martha.foiani@ukdri.ac.uk.ORCID http://orcid.org/0000-0003-4157-2606
Sumi BezUK Dementia Research Institute at University College London, London, UK.ORCID http://orcid.org/0000-0002-8971-5103
Mathieu BourdenxUK Dementia Research Institute at University College London, London, UK.
Alessia SantambrogioDepartment of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge, UK.
Claire FrodshamUK Dementia Research Institute at University College London, London, UK.
Elena CamporesiDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology,The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Gunnar BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology,The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID http://orcid.org/0000-0001-6958-2393
Henrik ZetterbergUK Dementia Research Institute at University College London, London, UK.ORCID http://orcid.org/0000-0003-3930-4354
Saisha PatelUK Dementia Research Institute at University College London, London, UK.
Naoko KamanoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan.
Mika TakahashiLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan.
Javier Rueda-CarrascoUK Dementia Research Institute at University College London, London, UK.
Loukia KatsouriSainsbury Wellcome Centre for Neural Circuits and Behaviour, University College London, London, UK.ORCID http://orcid.org/0000-0003-0186-6116
Stephanie FowlerUK Dementia Research Institute at University College London, London, UK.ORCID http://orcid.org/0000-0001-6693-9959
Emir TurkesUK Dementia Research Institute at University College London, London, UK.
Shoko HashimotoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan.
Hiroki SasaguriLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan.ORCID http://orcid.org/0000-0003-2550-9156
Takashi SaitoDepartment of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.ORCID http://orcid.org/0000-0002-9659-9251
Afm Saiful IslamQueen Square Institute of Neurology, University College London, London, UK.
Seico BennerCenter for Health and Environmental Risk Research, National Institute for Environmental Studies, Tsukuba, Japan.
Toshihiro EndoPhenovance LLC, Chiba, Japan.
Katsuji KobayashiDepartment of Psychiatry, Awazu Neuropsychiatric Hospital, Ishikawa, Japan.
Chiho IshidaDepartment of Neurology, NHO Iou National Hospital, Iwade-machi, Japan.ORCID http://orcid.org/0000-0002-1948-5381
Michele VendruscoloDepartment of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-3616-1610
Masahito YamadaDepartment of Internal Medicine, Division of Neurology, Kudanzaka Hospital, Tokyo, Japan.
Karen E DuffUK Dementia Research Institute at University College London, London, UK. k.duff@ucl.ac.uk.ORCID http://orcid.org/0000-0002-6177-868X
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Japan. takaomi.saido@riken.jp.ORCID http://orcid.org/0000-0003-1970-6903
Funding
Research Education ComponentP30AG062677 · NIA · MAYO CLINIC ROCHESTER · PI NILUFER ERTEKIN-TANER · 2019 to 2026
$33.5MDifferential vulnerability to tauopathy in Alzheimer's disease and Frontotemporal Lobe DementiaRF1AG063521 · NIA · UNIVERSITY COLLEGE LONDON · PI DUFF, KAREN · 2019 to 2019
$2.1MSystems Genetics Analysis of Resilience to Tauopathy in ADRDR01AG085446 · NIA · UNIVERSITY COLLEGE LONDON · PI Karen Duff, Amy Dunn · 2025 to 2026
$2.0MJapan Agency for Medical Research and Development (AMED) JP20dm0207001MEXT | Japan Society for the Promotion of Science (JSPS) 21K15378NIA NIH HHS P30 AG062677NIA NIH HHS R01 AG085446NIA NIH HHS RF1 AG063521U.S. Department of Health & Human Services | National Institutes of Health (NIH) AG063521
Abstract
Tau pathology is a hallmark of several neurodegenerative diseases, including frontotemporal dementia and Alzheimer's disease. However, the sequence of events and the form of tau that confers toxicity are still unclear, due in large part to the lack of physiological models of tauopathy initiation and progression in which to test hypotheses. We have developed a series of targeted mice expressing frontotemporal-dementia-causing mutations in the humanized MAPT gene to investigate the earliest stages of tauopathy. MAPT
Indexed as
SynapsesTauopathiestau ProteinsAnimalsBehavior, AnimalDisease Models, AnimalFrontotemporal DementiaHippocampusHumansMiceMice, Inbred C57BLMice, TransgenicMutationPhosphorylationtau Proteins
Identifiers
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.