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Chronic effects of blast injury on the microvasculature in a transgenic mouse model of Alzheimer's disease related Aβ amyloidosis.

AT Clark | EE Abrahamson | MM Harper | MD Ikonomovic
Fluids and barriers of the CNS | 2022 Jan 10

Altered cerebrovascular function and accumulation of amyloid-β (Aβ) after traumatic brain injury (TBI) can contribute to chronic neuropathology and increase the risk for Alzheimer's disease (AD). TBI due to a blast-induced shock wave (bTBI) adversely affects the neurovascular unit (NVU) during the acute period after injury. However, the chronic effects of bTBI and Aβ on cellular components of the NVU and capillary network are not well understood.

Pubmed ID: 35012589

TBI Model

  • Blast model
  • Blast injury model

    • Animal Information

  • Species: mouse
  • Strain: C57BL/6-C3F1/J transgenic
  • Age (weeks): 11 - 15
  • Weight (grams): No weight reported

    • Assessments

    Amyloid burden, Astrocytic end feet contacts estimation, Capillary density estimation, Immunohistochemistry (IHC), Pericyte estimation, Histology

    TBI model parameters

  • Impact Depth (mm): No information available
  • Impact Duration (ms): No information available
  • Impact Velocity (m/s): No information available
  • Impactor Tip: No information available

    • Device Name

    No information available

    Associated Datasets

    No information available

    Associated Protocols

    No information available

    About

    The PRECISE-TBI toolbox are a collection tools and resources to increase rigor and reproducibility with Traumatic Brain Injury within the PRE Clinical Interagency reSearch resourcE - Traumatic Brain Injury (PRECISE-TBI). Please learn more about PRECISE-TBI at https://www.precise-tbi.org

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    Department of Neurosciences, School of Medicine

    University of California, San Diego





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