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Cited by 219Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease.

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Chesser, Adrianne S., Pritchard, Susanne M., Johnson, Gail V. W.·2013·Frontiers in Neurology
DOI 10.3389/fneur.2013.00122PMC PMC3759803
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Abstract

One of the defining pathological features of Alzheimer disease (AD) is the intraneuronal accumulation of tau. The tau that forms these accumulations is altered both posttranslationally and conformationally, and there is now significant evidence that soluble forms of these modified tau species are the toxic entities rather than the insoluble neurofibrillary tangles. However there is still noteworthy debate concerning which specific pathological forms of tau are the contributors to neuronal dysfunction and death in AD. Given that increases in aberrant forms of tau play a role in the neurodegeneration process in AD, there is growing interest in understanding the degradative pathways that remove tau from the cell, and the selectivity of these different pathways for various forms of tau. Indeed, one can speculate that deficits in a pathway that selectively removes certain pathological forms of tau could play a pivotal role in AD. In this review we will discuss the different proteolytic and degradative machineries that may be involved in removing tau from the cell. How deficits in these different degradative pathways may contribute to abnormal accumulation of tau in AD will also be considered. In addition, the issue of the selective targeting of specific tau species to a given degradative pathway for clearance from the cell will be addressed.

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Authors
Chesser, A. S., Pritchard, S. M., & Johnson, G. V. W.
Affiliations
University of Rochester Medicine (US)
Corresponding author
Johnson, Gail V. W.
ORCID
Johnson, Gail V. W.
Venue
Frontiers in Neurology
Publisher
Frontiers Media SA
Published
2013
Volume
4
Pages
122-122
ISSN
1664-2295 (ISSN-L)
DOI
10.3389/fneur.2013.00122
PMC
PMC3759803
OpenAlex
W2074059686
Cited by
219
References
116
Citations by year
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FWCI
1.73
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Neurology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (NS076789)
  • National Institute of Neurological Disorders and Stroke (R21NS076789)
  • National Institute of Environmental Health Sciences (F30ES020081)
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 clearance, Alzheimer's disease, tau pathology, neurofibrillary tangles, proteolysis, protein degradation pathways, tau conformation, selective degradation, neurodegeneration, neuronal cell death

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 ›

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