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Ultrastructural Pathology of Neurofibrillary Tangles in Transgenic Mice Carrying Mutant (P301l) Human Tau Gene
Published online by Cambridge University Press: 02 July 2020
Extract
Tau is a microtubule-associated protein that promotes polymerization and stabilization of microtubules. It is the major component of fibrillary neuronal and glial inclusions in Alzheimer's disease (AD) and the tauopathies. An autosomal dominant familial tauopathy, frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), has been shown to be caused by pathogenic tau mutations. Neuropathologic features of FTDP-17 are filamentous tau aggregates in neurons and glia. Previous transgenic mice carrying the normal human tau gene developed motor neuron disease and had dystrophic axons, but no neurofibrillary tangles (NFT). In this report we describe ultrastructural features of NFT in transgenic mice carrying a mutant human tau gene. The mice were generated with a tau cDNA containing exon 1, 4, 5, 7, 9, 10, 11-13, intron 13 and exon 14, driven by the mouse prion promoter (MoPrP) and containing the most common FTDP-17 mutation, P301L. The transgenic construct was generated by ligating the P301L tau cDNA with the mouse prion promoter.
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- Pathology
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- Microscopy and Microanalysis , Volume 6 , Issue S2: Proceedings: Microscopy & Microanalysis 2000, Microscopy Society of America 58th Annual Meeting, Microbeam Analysis Society 34th Annual Meeting, Microscopical Society of Canada/Societe de Microscopie de Canada 27th Annual Meeting, Philadelphia, Pennsylvania August 13-17, 2000 , August 2000 , pp. 584 - 585
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- Copyright © Microscopy Society of America
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