Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 51, Issue 4, Pages 1023-1031Publisher
IOS PRESS
DOI: 10.3233/JAD-151102
Keywords
Alzheimer's disease; amyloid-beta protein precursor; beta-secretase; brain ischemia; dementia; temporal cortex
Categories
Funding
- Polish National Science Centre [DEC-2013/09/B/NZ7/01345-RP]
- Mossakowski Medical Research Centre, Polish Academy of Sciences, Poland [T3-RP]
- Medical University of Lublin, Poland [DS 475-SJC, DS 222/14-JK]
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Brain ischemia may be causally related with Alzheimer's disease. Presumably, beta-secretase and amyloid-beta protein precursor gene expression changes may be associated with Alzheimer's disease neuropathology. Consequently, we have examined quantitative changes in both beta-secretase and amyloid-beta protein precursor genes in the medial temporal lobe cortex with the use of quantitative rtPCR analysis following 10-min global brain ischemia in rats with survival of 2, 7, and 30 days. The greatest significant overexpression of beta-secretase gene was noted on the 2nd day, while on days 7-30 the expression of this gene was only modestly downregulated. Amyloid-beta protein precursor gene was downregulated on the 2nd day, but on days 7-30 postischemia, there was a significant reverse tendency. Thus, the demonstrated alterations indicate that the considerable changes of expression of beta-secretase and amyloid-beta protein precursor genes may be connected with a response of neurons in medial temporal lobe cortex to transient global brain ischemia. Finally, the ischemia-induced gene changes may play a key role in a late and slow onset of Alzheimer-type pathology.
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