VEGF significantly restores impaired memory behavior in Alzheimer's mice by improvement of vascular survival

The functional impact of amyloid peptides (Aβs) on the vascular system is less understood despite these pathologic peptides are substantially deposited in the brain vasculature of Alzheimer's patients. Here we show substantial accumulation of Aβs 40 and 42 in the brain arterioles of Alzheimer&#...

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Main Authors: Religa, Piotr (Author) , Cao, Renhai (Author) , Religa, Dorota (Author) , Xue, Yuan (Author) , Bogdanovic, Nenad (Author) , Westaway, David (Author) , Marti, Hugo (Author) , Winblad, Bengt (Author) , Cao, Yihai (Author)
Format: Article (Journal)
Language:English
Published: 24 June 2013
In: Scientific reports
Year: 2013, Volume: 3, Pages: 1-9
ISSN:2045-2322
DOI:10.1038/srep02053
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/srep02053
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/srep02053
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Author Notes:Piotr Religa, Renhai Cao, Dorota Religa, Yuan Xue, Nenad Bogdanovic, David Westaway, Hugo H. Marti, Bengt Winblad & Yihai Cao
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Summary:The functional impact of amyloid peptides (Aβs) on the vascular system is less understood despite these pathologic peptides are substantially deposited in the brain vasculature of Alzheimer's patients. Here we show substantial accumulation of Aβs 40 and 42 in the brain arterioles of Alzheimer's patients and of transgenic Alzheimer's mice. Purified Aβs 1-40 and 1-42 exhibited vascular regression activity in the in vivo animal models and vessel density was reversely correlated with numbers and sizes of amyloid plaques in human patients. A significant high number of vascular cells underwent cellular apoptosis in the brain vasculature of Alzheimer's patients. VEGF significantly prevented Aβ-induced endothelial apoptosis in vitro. Neuronal expression of VEGF in transgenic mice restored memory behavior of Alzheimer's. These findings provide conceptual implication of improvement of vascular functions as a novel therapeutic approach for the treatment of Alzheimer's disease.
Item Description:Gesehen am 21.12.2021
Physical Description:Online Resource
ISSN:2045-2322
DOI:10.1038/srep02053