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Mouse models of Alzheimer's disease: the long and filamentous road.
Neurol Res. 2003 Sep; 25(6):590-600.NR

Abstract

Alzheimer's disease (AD) is characterized by memory impairment leading to dementia, deposition of amyloid plaques and neurofibrillary tangles (NFTs), and neuronal loss. The major component of plaques is the amyloid beta peptide, A beta, whereas NFTs contain hyperphosphorylated forms of the microtubule-associated protein tau (tau). Familial AD (FAD) mutations either elevate A beta synthesis by favoring 'secretase' of the Alzheimer beta-amyloid precursor protein (APP) or enhance the fibrillogenic properties of this peptide. Mutations in the tau gene cause a different disease denoted FTPD-17, but suggest that the aberrant forms of tau seen in AD are unlikely to be benign. These findings imply a complex pathogenic cascade in AD and important goals of transgenic modeling are to capture and stratify this pathogenic process. Several laboratories have created APP transgenic (Tg) mice that exhibit AD-like amyloid pathology and A beta burdens. These Tg lines also exhibit deficits in spatial reference and/or working memory, with immunization against A beta attenuating both AD-associated phenotypes. Tangle-like pathologies are observed in mice expressing FTPD-17 mutant forms of tau, but florid tau pathologies based upon the wild type (wt) tau isoforms present in AD have proven more elusive. Creation of animal models with robust amyloid and tau pathologies, yet free of irrelevant confounding pathologies, remains a major objective in this field.

Authors+Show Affiliations

Phinney AL
Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Canada.
Horne P
No affiliation info available
Yang J
No affiliation info available
Janus C
No affiliation info available
Bergeron C
No affiliation info available
Westaway D
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalHumansMiceMice, TransgenicNeurofibrillary Tanglestau Proteins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

14503012

Citation

Phinney, Amie L., et al. "Mouse Models of Alzheimer's Disease: the Long and Filamentous Road." Neurological Research, vol. 25, no. 6, 2003, pp. 590-600.
Phinney AL, Horne P, Yang J, et al. Mouse models of Alzheimer's disease: the long and filamentous road. Neurol Res. 2003;25(6):590-600.
Phinney, A. L., Horne, P., Yang, J., Janus, C., Bergeron, C., & Westaway, D. (2003). Mouse models of Alzheimer's disease: the long and filamentous road. Neurological Research, 25(6), 590-600.
Phinney AL, et al. Mouse Models of Alzheimer's Disease: the Long and Filamentous Road. Neurol Res. 2003;25(6):590-600. PubMed PMID: 14503012.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mouse models of Alzheimer's disease: the long and filamentous road. AU - Phinney,Amie L, AU - Horne,Patrick, AU - Yang,Jing, AU - Janus,Chris, AU - Bergeron,Catherine, AU - Westaway,David, PY - 2003/9/25/pubmed PY - 2003/12/5/medline PY - 2003/9/25/entrez SP - 590 EP - 600 JF - Neurological research JO - Neurol Res VL - 25 IS - 6 N2 - Alzheimer's disease (AD) is characterized by memory impairment leading to dementia, deposition of amyloid plaques and neurofibrillary tangles (NFTs), and neuronal loss. The major component of plaques is the amyloid beta peptide, A beta, whereas NFTs contain hyperphosphorylated forms of the microtubule-associated protein tau (tau). Familial AD (FAD) mutations either elevate A beta synthesis by favoring 'secretase' of the Alzheimer beta-amyloid precursor protein (APP) or enhance the fibrillogenic properties of this peptide. Mutations in the tau gene cause a different disease denoted FTPD-17, but suggest that the aberrant forms of tau seen in AD are unlikely to be benign. These findings imply a complex pathogenic cascade in AD and important goals of transgenic modeling are to capture and stratify this pathogenic process. Several laboratories have created APP transgenic (Tg) mice that exhibit AD-like amyloid pathology and A beta burdens. These Tg lines also exhibit deficits in spatial reference and/or working memory, with immunization against A beta attenuating both AD-associated phenotypes. Tangle-like pathologies are observed in mice expressing FTPD-17 mutant forms of tau, but florid tau pathologies based upon the wild type (wt) tau isoforms present in AD have proven more elusive. Creation of animal models with robust amyloid and tau pathologies, yet free of irrelevant confounding pathologies, remains a major objective in this field. SN - 0161-6412 UR - https://www.unboundmedicine.com/medline/citation/14503012/Mouse_models_of_Alzheimer's_disease:_the_long_and_filamentous_road_ DB - PRIME DP - Unbound Medicine ER -