Cited by 722Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms

Andorfer, Cathy, Kress, Yvonne, Espinoza, Marisol, De Silva, Rohan, Tucker, Kerry L., Barde, Yves‐Alain, Duff, Karen, Davies, Peter·2003·Journal of Neurochemistry

Abstract

Neurofibrillary tangles are composed of insoluble aggregates of the microtubule-associated protein tau. In Alzheimer's disease the accumulation of neurofibrillary tangles occurs in the absence of tau mutations. Here we present mice that develop pathology from non-mutant human tau, in the absence of other exogenous factors, including beta-amyloid. The pathology in these mice is Alzheimer-like, with hyperphosphorylated tau accumulating as aggregated paired helical filaments. This pathologic tau accumulates in the cell bodies and dendrites of neurons in a spatiotemporally relevant distribution.

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Crossref · 10.1046/j.1471-4159.2003.01879.x

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Authors
Andorfer, C., Kress, Y., Espinoza, M., De Silva, R., Tucker, K. L., Barde, Y., Duff, K., & Davies, P.
Affiliations
  • Albert Einstein College of Medicine (US)
  • Friedrich Miescher Institute (CH)
  • Nathan Kline Institute for Psychiatric Research (US)
Corresponding author
Davies, Peter
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2003-06-27
Volume
86
Issue
3
Pages
582-590
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W2130723719
Cited by
722
References
2
Citations by year
2026: 19 · 2025: 32 · 2024: 27 · 2023: 39 · 2022: 40 · 2021: 47 · 2020: 41 · 2019: 37 · 2018: 49 · 2017: 51 · 2016: 37 · 2015: 36 · 2014: 32 · 2013: 28 · 2012: 26
FWCI
9.39
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
Funders
  • National Institute on Aging (R01AG022102)
  • National Institute of Mental Health (MH38623)
  • National Institute of Neurological Disorders and Stroke (T32NS007098, NS 07098)
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, hyperphosphorylation, tau aggregation, neurofibrillary tangles, Alzheimer's disease, transgenic mice, paired helical filaments, microtubule-associated proteins, neuronal pathology
MeSH terms
Age Factors, Alzheimer Disease, Animals, Brain, Brain Chemistry, Dendrites, Disease Models, Animal, Humans, Mice, Transgenic, Neurons, Phosphorylation, Neurofibrillary Tangles, tau Proteins, Alternative Splicing, Protein Isoforms, Reverse Transcriptase Polymerase Chain Reaction, Macromolecular Substances, Mice

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