About   Help   FAQ
References
Query Results -- Details

MGI Accession ID: MGI:1354277
J Number: J:61052
Other Accession IDs: Title: Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform.
Authors: Ishihara T; Hong M; Zhang B; Nakagawa Y; Lee MK; Trojanowski JQ; Lee VM
Journal: Neuron
Volume: 24
Issue: 3
Date: 1999 Nov
Year: 1999
Pages: 751-62
Review Status: Peer Reviewed

Abstract:

Filamentous tau aggregates are hallmarks of tauopathies, e.g., frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) and amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC). Since FTDP-17 tau gene mutations alter levels/functions of tau, we overexpressed the smallest human tau isoform in the CNS of transgenic (Tg) mice to model tauopathies. These mice acquired age-dependent CNS pathology similarto FTDP-17 and ALS/PDC, including insoluble, hyperphosphorylated tau and argyrophilic intraneuronal inclusions formed by tau-immunoreactive filaments. Inclusions were present in cortical and brainstem neurons but were most abundant in spinal cord neurons, where they were associated with axon degeneration, diminished microtubules (MTs), and reduced axonal transport in ventral roots, as well as spinal cord gliosis and motor weakness. These Tg mice recapitulate key features of tauopathies and provide models for elucidating mechanisms underlying diverse tauopathies, including Alzheimer's disease (AD).

Additional Information:

Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
11/20/2009
MGI_4.31
Web browser compatibility
The Jackson Laboratory