Experimental traumatic brain injury in rats stimulates the expression, production and activity of Alzheimer’s disease β-secretase (BACE-1) (original) (raw)
Summary.
Traumatic brain injury (TBI) is a risk factor for the development of Alzheimer’s disease (AD). After a traumatic brain injury depositions of amyloid beta (Aβ) in the brain parenchyma were found. In this study we investigated the expression pattern of β-secretase (BACE-1) in ipsi- or contralateral hippocampus and cortex following controlled cortical TBI in rats. BACE-1 mRNA levels, estimated by real time RT-PCR, were elevated 24 h post injury, and persisting up to 72 h, in the ipsi- and contralateral hippocampus and cerebral cortex as compared to the sham-treated animals (p<0.01). The TBI-induced changes in BACE-1 mRNA are due to enhanced hippocampal and cortical expression of BACE-1 mRNA in neurons and reactive astrocytes as revealed by in situ hybridization. The alterations in hippocampal BACE-1 mRNA levels are accompanied by corresponding increases in BACE-1 protein levels in ipsi- and contralateral hippocampus and ipsilateral cortex as demonstrated by Western blot analysis. In contrast, in the contralateral cortex only a weak increase of traumatically induced BACE-1 protein production was found. The activity of BACE-1 as measured by the formation of the cleavage product of amyloid beta precursor protein, transiently increased up to 48 h after injury, but returned to basal level 7 days post injury. This study demonstrates that the β-secretase is stimulated following TBI and may suggest a mechanism for the temporal increase of Aβ levels observed in patients with brain trauma.
Access this article
Subscribe and save
- Get 10 units per month
- Download Article/Chapter or eBook
- 1 Unit = 1 Article or 1 Chapter
- Cancel anytime Subscribe now
Buy Now
Price excludes VAT (USA)
Tax calculation will be finalised during checkout.
Instant access to the full article PDF.
Similar content being viewed by others
Author information
Authors and Affiliations
- Department of Psychiatry, University Hospital of Innsbruck, Innsbruck, Austria
I. Blasko & D. Rudzki - Department of Neurology, University Hospital of Innsbruck, Innsbruck, Austria
I. Blasko, R. Beer, G. Franz, G. Ransmayr & A. Kampfl - Paul Flechsig Institute of Brain Research, University of Leipzig, Germany
J. Apelt & R. Schliebs - Institute of Biochemistry, Medical Faculty, University of Leipzig, Germany
M. Bigl
Authors
- I. Blasko
You can also search for this author inPubMed Google Scholar - R. Beer
You can also search for this author inPubMed Google Scholar - M. Bigl
You can also search for this author inPubMed Google Scholar - J. Apelt
You can also search for this author inPubMed Google Scholar - G. Franz
You can also search for this author inPubMed Google Scholar - D. Rudzki
You can also search for this author inPubMed Google Scholar - G. Ransmayr
You can also search for this author inPubMed Google Scholar - A. Kampfl
You can also search for this author inPubMed Google Scholar - R. Schliebs
You can also search for this author inPubMed Google Scholar
Rights and permissions
About this article
Cite this article
Blasko, I., Beer, R., Bigl, M. et al. Experimental traumatic brain injury in rats stimulates the expression, production and activity of Alzheimer’s disease β-secretase (BACE-1).J Neural Transm 111, 523–536 (2004). https://doi.org/10.1007/s00702-003-0095-6
- Received: 06 June 2003
- Accepted: 20 October 2003
- Published: 04 February 2004
- Issue Date: April 2004
- DOI: https://doi.org/10.1007/s00702-003-0095-6