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Recent insights into cerebral B-amyloidosis| old_uid | 12029 |
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| title | Recent insights into cerebral B-amyloidosis |
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| start_date | 2013/01/28 |
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| schedule | 11h |
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| online | no |
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| details | Invité par Alexis Brice |
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| summary | Many neurodegenerative disorders are characterized by a predictable temporal progression of specific aggregated proteins in the brain. The hallmark proteopathy is Alzheimer’s disease in which multimerized and misfolded amyloid-Beta peptide (ABeta) is deposited in form of parenchymal amyloid plaques and vascular amyloid. Emerging evidence suggests that -amyloidosis can be exogenously induced by the application of brain extracts containing aggregated ABeta. The amyloid-inducing agent is likely A itself, although in a conformation generated most effectively in the living brain. Once induced, -amyloid lesions spread within and among brain regions. The induced amyloid is dependent on the structural and biochemical nature of the -amyloid seed and of the host, an observation reminiscent of prion strains. I will summarize the most recent developments in this emerging field and how these novel results can be exploited in search of biomarkers and novel therapeutic strategies. |
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| responsibles | Miles |
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