We are analyzing https://link.springer.com/article/10.1007/s00702-003-0095-6.

Title:
Experimental traumatic brain injury in rats stimulates the expression, production and activity of Alzheimer’s disease β-secretase (BACE-1) | Journal of Neural Transmission
Description:
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.
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Keywords {🔍}

bace, article, brain, injury, alzheimers, disease, access, privacy, cookies, content, journal, βsecretase, publish, research, search, traumatic, expression, activity, blasko, contralateral, cortex, mrna, levels, protein, university, innsbruck, data, information, log, neural, rats, production, beer, bigl, tbi, amyloid, ipsi, hippocampus, open, discover, springer, optional, analysis, personal, parties, policy, find, track, transmission, experimental,

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month download article/chapter real time rt-pcr post-translational mechanism involving traumatic brain injury neural transmission aims privacy choices/manage cookies full article pdf bace-1 protein levels disease β-secretase brain research disease protease bace1 european economic area scope submit manuscript sham-treated animals altered subcellular distribution transgenic mouse model related subjects 1007/s00702-003-0095-6 keywords conditions privacy policy western blot analysis bace1 sirna mediated aβ levels observed bace-1 mrna levels accepting optional cookies journal finder publish amyloid beta post injury controlled cortical tbi article journal brain parenchyma brain trauma check access schliebs institute aβpp access article log instant access neurology neural transm 111 β-secretase privacy policy article cite personal data books a article blasko bigl rights tbi-induced optional cookies manage preferences enhanced hippocampal bace-1 mrna

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         description: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.
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