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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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Abstract

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.

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
DDC:610 Medicine & health
Language:English
Date:28 July 2008
Deposited On:30 Dec 2008 18:37
Last Modified:27 Nov 2013 17:43
Publisher:Elsevier
ISSN:1474-4422
Publisher DOI:10.1016/S1474-4422(08)70170-4
PubMed ID:18667360
Citations:Web of Science®. Times Cited: 94
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Scopus®. Citation Count: 103

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