Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-9069
Wisniewski, T; Konietzko, U (2008). Amyloid-beta immunisation for Alzheimer's disease. Lancet Neurology, 7(9):805-811.
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Alzheimer's disease is the main cause of dementia in elderly people and is becoming an ever greater problem as societies worldwide age. Treatments that stop or at least effectively modify disease course do not yet exist. In Alzheimer's disease, the conversion of the amyloid-beta peptide (Abeta) from a physiological water-soluble monomeric form into neurotoxic oligomeric and fibrillar forms rich in stable beta-sheet conformations is an important event. The most toxic forms of Abeta are thought to be oligomers, and dimers might be the smallest neurotoxic species. Numerous immunological approaches that prevent the conversion of the normal precursor protein into pathological forms or that accelerate clearance are in development. More than ten new approaches to active and passive immunotherapy are under investigation in clinical trials with the aim of producing safe methods for immunological therapy and prevention. A delicate balance between immunological clearance of an endogenous protein with acquired toxic properties and the induction of an autoimmune reaction must be found.
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|Other titles:||Amyloid-β immunisation for Alzheimer’s disease|
|Item Type:||Journal Article, refereed, further contribution|
|Communities & Collections:||04 Faculty of Medicine > Psychiatric University Hospital Zurich > Division of Psychiatric Research and Clinic for Psychogeriatric Medicine|
|Dewey Decimal Classification:||610 Medicine & health|
|Date:||28 July 2008|
|Deposited On:||30 Dec 2008 18:37|
|Last Modified:||28 Oct 2014 16:00|
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