Hyperforin prevents β-amyloid neurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloid-β-deposits
The major protein constituent of amyloid deposits in Alzheimer's disease (AD) is the amyloid β -peptide (A β ). In the present work, we have determined the effect of hyperforin an acylphloroglucinol compound isolated from Hypericum perforatum (St John's Wort), on A β -induced spatial memor...
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Veröffentlicht in: | Molecular psychiatry 2006-11, Vol.11 (11), p.1032-1048 |
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Sprache: | eng |
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Zusammenfassung: | The major protein constituent of amyloid deposits in Alzheimer's disease (AD) is the amyloid
β
-peptide (A
β
). In the present work, we have determined the effect of hyperforin an acylphloroglucinol compound isolated from
Hypericum perforatum
(St John's Wort), on A
β
-induced spatial memory impairments and on A
β
neurotoxicity. We report here that hyperforin: (1) decreases amyloid deposit formation in rats injected with amyloid fibrils in the hippocampus; (2) decreases the neuropathological changes and behavioral impairments in a rat model of amyloidosis; (3) prevents A
β
-induced neurotoxicity in hippocampal neurons both from amyloid fibrils and A
β
oligomers, avoiding the increase in reactive oxidative species associated with amyloid toxicity. Both effects could be explained by the capacity of hyperforin to disaggregate amyloid deposits in a dose and time-dependent manner and to decrease A
β
aggregation and amyloid formation. Altogether these evidences suggest that hyperforin may be useful to decrease amyloid burden and toxicity in AD patients, and may be a putative therapeutic agent to fight the disease. |
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ISSN: | 1359-4184 1476-5578 |
DOI: | 10.1038/sj.mp.4001866 |