Cited by 43Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury and Neurovascular Disturbances

The effect of focal brain injury on beta-amyloid plaque deposition, inflammation and synapses in the APP/PS1 mouse model of Alzheimer’s disease

Collins, Jessica M., King, Anna E., Woodhouse, Adele, Kirkcaldie, Matthew T.K., Vickers, James C.·2015·Experimental Neurology

Abstract

Traumatic brain injury is a risk factor for Alzheimer's disease (AD), however the effect of such neural damage on the onset and progression of beta-amyloid (Aβ) plaque pathology is not well understood. This study utilized an in vivo model of focal brain injury to examine how localized damage may acutely affect the onset and progression of Aβ plaque deposition as well as inflammatory and synaptic changes, in the APP/PS1 (APPSWE, PSEN1dE9) transgenic model of AD relative to wild-type (Wt) mice. Acute focal brain injury in 3- and 9-month-old APP/PS1 and Wt mice was induced by insertion of a needle into the somatosensory neocortex, as compared to sham surgery, and examined at 24h and 7d post-injury (PI). Focal brain injury did not induce thioflavine-S stained or (pan-Aβ antibody) MOAB-2-labeled plaques at either 24h or 7d PI in 3-month-old APP/PS1 mice or Wt mice. Nine-month-old APP/PS1 mice demonstrate cortical Aβ plaques but focal injury had no statistically significant (p>0.05) effect on thioflavine-S or MOAB-2 plaque load surrounding the injury site at 24h PI or 7d PI. There was a significant (p 0.05). For both Wt and APP/PS1 mice alike, synaptophysin puncta near the injury site were significantly reduced 24h PI (compared to sites distant to the injury and the corresponding area in sham mice; p 0.05). There was no significant effect of genotype on this response (p>0.05). These results indicate that focal brain injury and the associated microglial response do not acutely alter…

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Crossref · 10.1016/j.expneurol.2015.02.034

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  • Several experimental studies have failed to show that TBI induces or worsens AD-related pathology, with some even reporting a reduction in post-injury Aβ accumulation in transgenic mice.

    “Finally, several experimental studies have failed to show that TBI induces or worsens AD-related pathology (38, 39) with some even reporting a reduction in post-injury Aβ accumulation in transgenic mice (40, 41).”

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Authors
Collins, J. M., King, A. E., Woodhouse, A., Kirkcaldie, M. T. K., & Vickers, J. C.
Affiliations
University of Tasmania (AU)
Corresponding author
Collins, Jessica M.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2015-05
Volume
267
Pages
219-229
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2066097200
Cited by
43
References
57
Citations by year
2025: 2 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 9 · 2019: 7 · 2018: 6 · 2017: 4 · 2016: 6 · 2015: 1
FWCI
4.17
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • eCite Digital Repository (University of Tasmania) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
Alzheimer's disease, traumatic brain injury, amyloid plaques, APP/PS1 mice, microglial activation, synaptic loss, synaptophysin, neuroinflammation, cortical injury, synaptic recovery, thioflavine S
MeSH terms
Age Factors, Alzheimer Disease, Animals, Brain Injuries, Calcium-Binding Proteins, Disease Models, Animal, Encephalitis, Gene Expression Regulation, Humans, Macrophages, Mice, Inbred C57BL, Mice, Transgenic, Microfilament Proteins, Nerve Tissue Proteins, Synapses, Time Factors, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Mice, Presenilin-1, Plaque, Amyloid

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