Altered Expression of Amyloid Precursor Proteins After Traumatic Brain Injury in Rats: In Situ Hybridization and Immunohistochemical Study
Abstract
The expression of alternatively spliced mRNAs for amyloid precursor protein (APP) isoforms and their translation products were examined in the rat cerebral cortex 1, 3, 6, and 12 h and 1, 3, and 7 days (n = 4-5 in each group) after fluid-percussion brain injury. In situ hybridization studies demonstrated that the expression of APP695 mRNA decreased in and around the damaged area of the cerebral cortex exposed to fluid-percussion injury 1 h after the insult. On the other hand, APP751/770 mRNAs were increased in the regions surrounding the damaged cortical areas 1 day after the injury. An increase of immunoreactive APP was detected in the regions around the damaged cortical areas 3 h after traumatic injury and maintained for the following 3 days. The APP immunoreactivity in the damaged cortices declined to the level of sham-operated animals by post-experimental day 7. Using an anti-amyloid beta (Abeta) protein (17-24) antibody, no deposits of immunoreactive Abeta (17-24) were observed in any of the samples examined in these experiments. These results suggest that the induction of Kunitz-type protease inhibitor (KPI) domain-containing APP mRNAs and the increased accumulation of APP are involved in the physiological and neuropathological responses of brains under various neurodegenerative conditions, including head trauma.
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APP expression increase after TBI has been replicated in multiple follow-up studies using CCI as well as midline and lateral FPI.
“which has been replicated in multiple follow-up studies using CCI as well as midline and lateral FPI (124–126).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [125]
A majority of rodent studies fail to show Aβ deposition after TBI in non-transgenic animals using CCI, FPI, and weight drop models.
“a majority of rodent studies fail to show this association in non-transgenic animals using CCI, FPI, and weight drop models (121, 122, 124, 125, 135).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [125]
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References 52 · Cited by 34
- Authors
- MASUMURA, M., HATA, R., URAMOTO, H., MURAYAMA, N., OHNO, T., & SAWADA, T.
- Affiliations
- National Cerebral and Cardiovascular Center (JP)
- ORCID
- MURAYAMA, NORIHITO
- Venue
- Journal of Neurotrauma
- Publisher
- SAGE Publications
- Published
- 2000-02
- Volume
- 17
- Issue
- 2
- Pages
- 123-134
- ISSN
- 0897-7151 (ISSN-L)
- 1557-9042
- OpenAlex
- W1992607163
- Cited by
- 34
- References
- 52
- Citations by year
- 2026: 1 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 1 · 2015: 1 · 2013: 2
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurotrauma (publishedVersion)
- PubMed (publishedVersion)
- 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
- amyloid precursor protein, traumatic brain injury, fluid percussion injury, APP isoforms, APP695, cerebral cortex, amyloid-beta, APP mRNA expression
- MeSH terms
- Animals, Brain Injuries, Cerebral Cortex, Gene Expression Regulation, Immunohistochemistry, Male, RNA, Messenger, Time Factors, Transcription, Genetic, Protein Biosynthesis, Amyloid beta-Protein Precursor, Rats, Sprague-Dawley, Alternative Splicing, In Situ Hybridization, Protein Isoforms, Rats
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