Abstract
The use of natural compounds is an interesting stratagem in the search of drugs with therapeutic potential for the treatment of Alzheimers disease (AD). We report here the effect of the hyperforin derivative (IDN5706, tetrahydrohyperforin), a semi-synthetic derivative of the St. Johns Wort, on the brain neuropathology, learning and memory in a double transgenic (APPswe, PS-1dE9) mouse model of AD. Results indicate that, IDN5706 alleviates memory decline induced by amyloid-β (Aβ) deposits as indicated by the Morris water maze paradigm. Moreover, the analysis of Aβ deposits by immunodetection and thioflavin-S staining of brain sections, only reveals a decrease in the frequency of the largersize Aβ deposits, suggesting that IDN5706 affected the turnover of amyloid plaques. Immunohistochemical analysis, using GFAP and n-Tyrosine indicated that the hyperforin derivative prevents the inflammatory astrocytic reaction and the oxidative damage triggered by high Aβ deposit levels. We conclude that the hyperforin derivative, IDN5706, has therapeutic potential for prevention and treatment of AD.
Keywords: Hyperforin derivative, Alzheimer disease, spatial learning, neuropathological damage, amyloid-β-peptide, oxidative damage, transgenic mice, St. John's wort
Current Alzheimer Research
Title: The Hyperforin Derivative IDN5706 Occludes Spatial Memory Impairments and Neuropathological Changes in a Double Transgenic Alzheimers Mouse Model
Volume: 7 Issue: 2
Author(s): W. Cerpa, J. L. Hancke, P. Morazzoni, E. Bombardelli, A. Riva, P. P. Marin and N. C. Inestrosa
Affiliation:
Keywords: Hyperforin derivative, Alzheimer disease, spatial learning, neuropathological damage, amyloid-β-peptide, oxidative damage, transgenic mice, St. John's wort
Abstract: The use of natural compounds is an interesting stratagem in the search of drugs with therapeutic potential for the treatment of Alzheimers disease (AD). We report here the effect of the hyperforin derivative (IDN5706, tetrahydrohyperforin), a semi-synthetic derivative of the St. Johns Wort, on the brain neuropathology, learning and memory in a double transgenic (APPswe, PS-1dE9) mouse model of AD. Results indicate that, IDN5706 alleviates memory decline induced by amyloid-β (Aβ) deposits as indicated by the Morris water maze paradigm. Moreover, the analysis of Aβ deposits by immunodetection and thioflavin-S staining of brain sections, only reveals a decrease in the frequency of the largersize Aβ deposits, suggesting that IDN5706 affected the turnover of amyloid plaques. Immunohistochemical analysis, using GFAP and n-Tyrosine indicated that the hyperforin derivative prevents the inflammatory astrocytic reaction and the oxidative damage triggered by high Aβ deposit levels. We conclude that the hyperforin derivative, IDN5706, has therapeutic potential for prevention and treatment of AD.
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Cite this article as:
Cerpa W., Hancke L. J., Morazzoni P., Bombardelli E., Riva A., Marin P. P. and Inestrosa C. N., The Hyperforin Derivative IDN5706 Occludes Spatial Memory Impairments and Neuropathological Changes in a Double Transgenic Alzheimers Mouse Model, Current Alzheimer Research 2010; 7 (2) . https://dx.doi.org/10.2174/156720510790691218
DOI https://dx.doi.org/10.2174/156720510790691218 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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