Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/43025
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Type: Journal article
Title: Alzheimer disease: amyloidogenesis, the presenilins and animal models
Author: Newman, M.
Musgrave, I.
Lardelli, M.
Citation: Biochimica et Biophysica Acta-Molecular Basis of Disease, 2007; 1772(3):285-297
Publisher: Elsevier Science BV
Issue Date: 2007
ISSN: 0925-4439
0167-4889
Organisation: Centre for the Molecular Genetics of Development
Abstract: Alzheimer’s disease is the most prevalent form of dementia. Neuropathogenesis is proposed to be a result of the accumulation of amyloid beta peptides in the brain together with oxidative stress mechanisms and neuroinflammation. The presenilin proteins are central to the gamma-secretase cleavage of the amyloid prescursor protein (APP), releasing the amyloid beta peptide. Point mutations in the presenilin genes lead to cases of familial Alzheimer’s disease by increasing APP cleavage resulting in excess amyloid beta formation. This review discusses the molecular mechanism of Alzheimer’s disease with a focus on the presenilin genes. Alternative splicing of transcripts from these genes and how these may function in several disease states is discussed. There is an emphasis on the importance of animal models in elucidating the molecular mechanisms behind the development of Alzheimer’s disease and how the zebrafish, Danio rerio, can be used as a model organism for analysis of presenilin function and Alzheimer’s disease pathogenesis.
Keywords: Alzheimer’s disease; Amyloid-beta; Animal models; Oxidative stress; Presenilin; Zebrafish
RMID: 0020070404
DOI: 10.1016/j.bbadis.2006.12.001
Appears in Collections:Pharmacology publications
Centre for the Molecular Genetics of Development publications

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