PUBLICATION

Alzheimer disease: Amyloidogenesis, the presenilins and animal models

Authors
Newman, M., Musgrave, F.I., and Lardelli, M.
ID
ZDB-PUB-070122-25
Date
2007
Source
Biochimica et biophysica acta. Molecular basis of disease   1772(3): 285-297 (Review)
Registered Authors
Lardelli, Michael, Newman, Morgan
Keywords
Alzheimer’s disease, Amyloid-beta, Animal models, Oxidative stress, Presenilin, Zebrafish
MeSH Terms
  • Alzheimer Disease/etiology*
  • Alzheimer Disease/genetics
  • Amyloid beta-Protein Precursor/metabolism*
  • Animals
  • Disease Models, Animal*
  • Mice
  • Point Mutation
  • Presenilins/metabolism*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
PubMed
17208417 Full text @ BBA Molecular Basis of Disease
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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping