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Cited by 86Alzheimer's disease research and treatmentsTraumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury Research

Distinct temporal and anatomical distributions of amyloid-β and tau abnormalities following controlled cortical impact in transgenic mice

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Tran, Hien T., Sanchez, Laura, Esparza, Thomas J., Brody, David L.·2011·PLoS ONE
DOI 10.1371/journal.pone.0025475PMC PMC3183029
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Abstract

Traumatic brain injury (TBI) is a major environmental risk factor for Alzheimer's disease. Intracellular accumulations of amyloid-β and tau proteins have been observed within hours following severe TBI in humans. Similar abnormalities have been recapitulated in young 3xTg-AD mice subjected to the controlled cortical impact model (CCI) of TBI and sacrificed at 24 h and 7 days post injury. This study investigated the temporal and anatomical distributions of amyloid-β and tau abnormalities from 1 h to 24 h post injury in the same model. Intra-axonal amyloid-β accumulation in the fimbria was detected as early as 1 hour and increased monotonically over 24 hours following injury. Tau immunoreactivity in the fimbria and amygdala had a biphasic time course with peaks at 1 hour and 24 hours, while tau immunoreactivity in the contralateral CA1 rose in a delayed fashion starting at 12 hours after injury. Furthermore, rapid intra-axonal amyloid-β accumulation was similarly observed post controlled cortical injury in APP/PS1 mice, another transgenic Alzheimer's disease mouse model. Acute increases in total and phospho-tau immunoreactivity were also evident in single transgenic Tau(P301L) mice subjected to controlled cortical injury. These data provide further evidence for the causal effects of moderately severe contusional TBI on acceleration of acute Alzheimer-related abnormalities and the independent relationship between amyloid-β and tau in this setting.

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  • Many animal studies show increased production and accumulation of amyloid precursor protein (APP), Aβ, and pathological tau following TBI.

    “Second, many animal studies show increased production and accumulation of amyloid precursor protein (APP), Aβ, and pathological tau following TBI (16, 21–28).”

    From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [25]

    The Discussion reports post-injury APP accumulation in injured axons and this study’s Aβ accumulation and tau abnormalities in transgenic mice (pages not provided). It does not establish increased APP production after TBI, and its findings are limited to particular transgenic models rather than animal studies generally. (LLM, conf=0.83)

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Authors
Tran, H. T., Sanchez, L., Esparza, T. J., & Brody, D. L.
Affiliations
Washington University in St. Louis (US)
Corresponding author
Brody, David L.
ORCID
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2011-09-29
Volume
6
Issue
9
Pages
e25475
ISSN
1932-6203 (ISSN-L)
DOI
10.1371/journal.pone.0025475
PMC
PMC3183029
OpenAlex
W2048063971
Cited by
86
References
10
Citations by year
2026: 2 · 2025: 2 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 11 · 2018: 8 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 8 · 2013: 12 · 2012: 5
FWCI
5.67
Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS ONE (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
  • Thrasher Research Fund
  • National Institutes of Health (5k08ns049237-05, NIH-R01)
  • National Institute of Neurological Disorders and Stroke (R01NS065069, K08-NS049237)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
Keywords
traumatic brain injury, amyloid-beta, tau protein, Alzheimer's disease, controlled cortical impact, 3xTg-AD mice, APP/PS1 mice, fimbria, amygdala, CA1, phosphorylated tau, temporal distribution, anatomical distribution, bruising
MeSH terms
Alzheimer Disease, Animals, Axons, Brain Injuries, Disease Models, Animal, Humans, Mice, Transgenic, Mutation, Risk Factors, Time Factors, Amyloid beta-Peptides, tau Proteins, Mice, Presenilin-1

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