Cited by 1,133Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchAmyotrophic Lateral Sclerosis Research

Tau pathology and neurodegeneration

Spillantini, Maria Grazia, Goedert, Michel·2013·The Lancet Neurology

Abstract

The pathway leading from soluble and monomeric to hyperphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenerative diseases, collectively referred to as tauopathies. Dominantly inherited mutations in MAPT, the gene that encodes tau, cause forms of frontotemporal dementia and parkinsonism, proving that dysfunction of tau is sufficient to cause neurodegeneration and dementia. However, most cases of tauopathy are not inherited in a dominant manner. The first tau aggregates form in a few nerve cells in discrete brain areas. These become self propagating and spread to distant brain regions in a prion-like manner. The prevention of tau aggregation and propagation is the focus of attempts to develop mechanism-based treatments for tauopathies.

Integrity signals

Registry

Crossref · 10.1016/s1474-4422(13)70090-5

Cites

250 of 250 references verified0 citation errors · 0 not checkable

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Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Several tauopathies including PSP, CBD, FTDP-17, and AGD exclusively feature 4R tau deposits.

    “Aggregates composed of both 3R and 4R tau are seen in disease states, though curiously several tauopathies including PSP, CBD, FTDP-17, and AGD exclusively feature 4R tau deposits.”

    From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [1]

  • Pathological studies have shown deposition of abnormal proteins in FTD brain tissues, including TDP-43 (50% of cases), tau (40% of cases), and FUS (5-10% of cases).

    “Pathological studies have shown the deposition of abnormal proteins in the brain tissues of FTD patients, including TDP-43 (50% of cases), tau (40% of cases), and FUS (5–10% of cases).314,315”

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Authors
Spillantini, M. G., & Goedert, M.
Affiliations
  • University of Cambridge (GB)
  • MRC Laboratory of Molecular Biology (GB)
Venue
The Lancet Neurology
Publisher
Elsevier BV
Published
2013-06
Volume
12
Issue
6
Pages
609-622
ISSN
1474-4422 (ISSN-L)
OpenAlex
W2137140827
Cited by
1,133
References
250
Citations by year
2026: 60 · 2025: 89 · 2024: 69 · 2023: 78 · 2022: 97 · 2021: 102 · 2020: 99 · 2019: 113 · 2018: 87 · 2017: 89 · 2016: 80 · 2015: 88 · 2014: 60 · 2013: 19 · 2012: 1
FWCI
9.07
Type
journal article
Language
en
Open access
closed
Locations
  • The Lancet Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Parkinson's UK (K-1012)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
Keywords
tau pathology, tauopathy, neurodegeneration, tau aggregation, hyperphosphorylated tau, MAPT mutations, frontotemporal dementia, parkinsonism, prion-like propagation, tau-targeted therapy
MeSH terms
Animals, Brain, Humans, tau Proteins, Neurodegenerative Diseases, Tauopathies

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