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Transgenic animal models of Alzheimer's disease and related disorders: histopathology, behavior and therapy


Götz, J; Streffer, J R; David, D; Schild, A; Hoerndli, F; Pennanen, L; Kurosinski, P; Chen, F (2004). Transgenic animal models of Alzheimer's disease and related disorders: histopathology, behavior and therapy. Molecular Psychiatry, 9(7):664-683.

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease that affects more than 15 million people worldwide. Within the next generation, these numbers will more than double. To assist in the elucidation of pathogenic mechanisms of AD and related disorders, such as frontotemporal dementia (FTDP-17), genetically modified mice, flies, fish and worms were developed, which reproduce aspects of the human histopathology, such as beta-amyloid-containing plaques and tau-containing neurofibrillary tangles (NFT). In mice, the tau pathology caused selective behavioral impairment, depending on the distribution of the tau aggregates in the brain. Beta-amyloid induced an increase in the numbers of NFT, whereas the opposite was not observed in mice. In beta-amyloid-producing transgenic mice, memory impairment was associated with increased levels of beta-amyloid. Active and passive beta-amyloid-directed immunization caused the removal of beta-amyloid plaques and restored memory functions. These findings have since been translated to human therapy. This review aims to discuss the suitability and limitations of the various animal models and their contribution to an understanding of the pathophysiology of AD and related disorders.

Alzheimer's disease (AD) is a devastating neurodegenerative disease that affects more than 15 million people worldwide. Within the next generation, these numbers will more than double. To assist in the elucidation of pathogenic mechanisms of AD and related disorders, such as frontotemporal dementia (FTDP-17), genetically modified mice, flies, fish and worms were developed, which reproduce aspects of the human histopathology, such as beta-amyloid-containing plaques and tau-containing neurofibrillary tangles (NFT). In mice, the tau pathology caused selective behavioral impairment, depending on the distribution of the tau aggregates in the brain. Beta-amyloid induced an increase in the numbers of NFT, whereas the opposite was not observed in mice. In beta-amyloid-producing transgenic mice, memory impairment was associated with increased levels of beta-amyloid. Active and passive beta-amyloid-directed immunization caused the removal of beta-amyloid plaques and restored memory functions. These findings have since been translated to human therapy. This review aims to discuss the suitability and limitations of the various animal models and their contribution to an understanding of the pathophysiology of AD and related disorders.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute for Regenerative Medicine (IREM)
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2004
Deposited On:05 Sep 2011 06:58
Last Modified:16 Aug 2016 10:14
Publisher:Nature Publishing Group
ISSN:1359-4184
Publisher DOI:https://doi.org/10.1038/sj.mp.4001508
PubMed ID:15052274

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