Cited by 177Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Tau protein and neurodegeneration

Goedert, Michel·2004·Seminars in Cell & Developmental Biology

Abstract

Tau protein is the major component of the intracellular filamentous deposits that define a number of neurodegenerative diseases. They include the largely sporadic Alzheimer's disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), Pick's disease (PiD), argyrophilic grain disease, as well as the inherited frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). The identification of mutations in Tau as the cause of FTDP-17 established that dysfunction or misregulation of tau protein is sufficient to cause neurodegeneration and dementia. At an experimental level, the new understanding is leading to the development of good transgenic animal models of the tauopathies.

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Crossref · 10.1016/j.semcdb.2003.12.015

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  • Tauopathies include neurological disorders such as Alzheimer disease, frontotemporal dementia and progressive supranuclear palsy, in which pathology is heavily associated with toxic accumulation of aberrant tau species, leading tau to aggregate into paired helical filaments and ultimately into neurofibrillary tangles that result in neuronal cell death.

    “Tauopathies include neurological disorders, such as Alzheimer disease, frontotemporal dementia (FTD) and progressive supranuclear palsy (PSP)182, in which pathology is heavily associated with toxic accumulation of aberrant tau species, leading tau to aggregate into paired helical filaments and ultimately into neurofibrillary tangles that result in neuronal cell death183.”

    From PROTAC targeted protein degraders: the past is prologue (2022) · cites this paper as [183]

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Authors
Goedert, M.
Affiliations
MRC Laboratory of Molecular Biology (GB)
Corresponding author
Goedert, Michel
Venue
Seminars in Cell & Developmental Biology
Publisher
Elsevier BV
Published
2004-02
Volume
15
Issue
1
Pages
45-49
ISSN
1084-9521 (ISSN-L)
OpenAlex
W2061265193
Cited by
177
References
33
Citations by year
2026: 3 · 2025: 15 · 2024: 11 · 2023: 6 · 2022: 7 · 2021: 6 · 2020: 4 · 2019: 9 · 2018: 6 · 2017: 8 · 2016: 4 · 2015: 9 · 2014: 10 · 2013: 10 · 2012: 13
FWCI
1.01
Type
journal article
Language
en
Open access
closed
Locations
  • Seminars in Cell and Developmental Biology (publishedVersion)
  • PubMed (publishedVersion)
  • Apollo (University of Cambridge) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
tau protein, neurodegeneration, tauopathy, Alzheimer's disease, progressive supranuclear palsy, corticobasal degeneration, Pick's disease, argyrophilic grain disease, FTDP-17, tau mutations, transgenic animal models, neurofibrillary tangles
MeSH terms
Amyloid, Animals, Brain, Dementia, Disease Models, Animal, Glycosaminoglycans, Humans, Mice, Transgenic, Microscopy, Electron, Microtubules, Mutation, Nerve Tissue Proteins, Protein Binding, Supranuclear Palsy, Progressive, tau Proteins, Alternative Splicing, Neurodegenerative Diseases, Protein Isoforms, Parkinsonian Disorders, Pick Disease of the Brain, Tauopathies, Mice

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