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PMID: 19337449 Published · ppublish English Journal Article

An update on the toxicity of Abeta in Alzheimer's disease.

Neuropsychiatric disease and treatment ·Vol. 4 ·No. 6 ·2008-12-00 ·Pages 1033-42

Götz J, Ittner LM, Schonrock N, Cappai R

Abstract

Alzheimer's disease is characterized histopathologically by deposition of insoluble forms of the peptide Abeta and the protein tau in brain. Abeta is the principal component of amyloid plaques and tau of neurofibrillary tangles. Familial cases of AD are associated with causal mutations in the gene encoding the amyloid precursor protein, APP, from which the amyloidogenic Abeta peptide is derived, and this supports a role for Abeta in disease. Abeta can promote tau pathology and at the same time its toxicity is also tau-dependent. Abeta can adopt different conformations including soluble oligomers and insoluble fibrillar species present in plaques. We discuss which of these conformations exert toxicity, highlight molecular pathways involved and discuss what has been learned by applying functional genomics.

Keywords
amyloid mitochondria oligomer proteomic tau transgenic
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Götz Jürgen
Alzheimer's and Parkinson's Disease Laboratory, Brain and Mind Research Institute, University of Sydney, 100 Mallett St, Camperdown, NSW 2050, Australia. jgoetz@med.usyd.edu.au
Ittner Lars M
Schonrock Nicole
Cappai Roberto
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Article Info
Journal
Neuropsychiatric disease and treatment
Abbr.
Neuropsychiatr Dis Treat
ISSN
1176-6328
DOI
10.2147/ndt.s3016
Email
jgoetz@med.usyd.edu.au
Published
2008-12-00
Pages
1033-42
Language
English
Region
New Zealand
NLM ID
101240304
PMCID
PMC2646638
External Links
PubMed source DOI: 10.2147/ndt.s3016 PMC Full Text
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