Journal
NATURE MEDICINE
Volume 20, Issue 8, Pages 881-885Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3617
Keywords
-
Funding
- Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas (CiberNed-Instituto de Salud Carlos III)
- Ministerio de Ciencia e Innovacion (MICINN)
- Ministerio de Economia y Competitividad (MINECO)
- Comunidad Autonoma de Madrid
- Fundacion Ramon Areces
- European Commission [278486]
- CSIC
Ask authors/readers for more resources
An imbalance of tau isoforms containing either three or four microtubule-binding repeats causes frontotemporal dementia with parkinsonism linked to-chromosome 17 (FTDP-17) in families with intronic mutations in the MAPT gene. Here we report equivalent imbalances at the mRNA and protein levels and increased total tau levels in the brains of subjects with Huntington's disease (HD) together with rod-like tau deposits along neuronal nuclei. These tau nuclear rods show an ordered filamentous ultrastructure and can be found filling the neuronal nuclear indentations previously reported in HD brains. Finally, alterations in serine/arginine-rich splicing factor-6 coincide with tau missplicing, and a role of tau in HD pathogenesis is evidenced by the attenuation of motor abnormalities of mutant HTT transgenic mice in tau knockout backgrounds.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available