Cited by 2,174Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Tau-mediated neurodegeneration in Alzheimer’s disease and related disorders

Ballatore, Carlo, Lee, Virginia M.-Y., Trojanowski, John Q.·2007·Nature Reviews Neuroscience

Abstract

Advances in our understanding of the mechanisms of tau-mediated neurodegeneration in Alzheimer's disease (AD) and related tauopathies, which are characterized by prominent CNS accumulations of fibrillar tau inclusions, are rapidly moving this previously underexplored disease pathway to centre stage for disease-modifying drug discovery efforts. However, controversies abound concerning whether or not the deleterious effects of tau pathologies result from toxic gains-of-function by pathological tau or from critical losses of normal tau function in the disease state. This Review summarizes the most recent advances in our knowledge of the mechanisms of tau-mediated neurodegeneration to forge an integrated concept of those tau-linked disease processes that drive the onset and progression of AD and related tauopathies.

Integrity signals

Registry

Crossref · 10.1038/nrn2194

Cites

105 of 105 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • Tau becomes hyperphosphorylated and aggregated and contributes to neurodegeneration.

    “WPC2 also contains numerous cytoskeletal proteins, as exemplified by tau that is hyperphosphorylated and aggregated to contribute to neurodegeneration (Ballatore et al., 2007).”
  • The most widely used transgenic models express mutant forms of APP, with or without PSEN1/2, associated with autosomal-dominant early-onset AD, or MAPT mutations, which cause familial frontotemporal dementia.

    “The most widely used transgenic models express mutant forms of the amyloid precursor protein (APP) gene, with or without presenilin-1/2 (PSEN1/2), which are associated with autosomal-dominant, early-onset AD, or, alternatively, MAPT mutations, which cause familial frontotemporal dementia (FTD).”
  • These models recapitulate features of AD neuropathology, including plaques or tangles, along with variable neuronal dysfunction or loss and progressive behavioral impairment.

    “These models recapitulate features of AD neuropathology, including plaques or tangles, along with variable degree of neuronal dysfunction or loss and progressive behavioral impairment (Ballatore et al., 2007; Esquerda-Canals et al., 2017).”
  • Chronic neuroinflammation could provoke tau pathology thereby worsening neuronal injury and long-term outcome.

    “Together, these studies indicate that chronic neuroinflammation could provoke tau pathology thereby worsening neuronal injury and long-term outcome.”
  • A robust and persistent neuroinflammatory response may be sufficient to promote phosphorylation, aggregation, and subsequent neurodegeneration; key features of AD.

    “A robust and persistent neuroinflammatory response may then be sufficient to promote phosphorylation, aggregation, and subsequent neurodegeneration; key features of AD (149–151).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Ballatore, C., Lee, V. M.-Y., & Trojanowski, J. Q.
Affiliations
University of Pennsylvania (US)
Corresponding author
Trojanowski, John Q.
Venue
Nature Reviews Neuroscience
Published
2007-09
Volume
8
Issue
9
Pages
663-672
ISSN
  • 1471-003X (ISSN-L)
  • 1471-0048
OpenAlex
W2034286717
Cited by
2,174
References
105
Citations by year
2026: 70 · 2025: 94 · 2024: 113 · 2023: 108 · 2022: 129 · 2021: 117 · 2020: 161 · 2019: 138 · 2018: 135 · 2017: 139 · 2016: 137 · 2015: 117 · 2014: 123 · 2013: 102 · 2012: 104
FWCI
9.22
Type
journal article
Language
en
Open access
closed
Locations
  • Nature reviews. Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute for Health and Care Research
  • National Institutes of Health (5u01ag024904-10)
  • National Institute on Aging (P01AG014382, P01AG011542, P01AG014449, U01AG24904, P30AG010124, P01AG009215, P01AG017586, P01AG019724)
  • National Institute of Neurological Disorders and Stroke (P01NS044233)
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, Alzheimer's disease, tauopathy, neurofibrillary tangles, tau hyperphosphorylation, pathological tau
MeSH terms
Alzheimer Disease, Animals, Humans, Models, Biological, Nerve Degeneration, tau Proteins, Tauopathies

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review