Neuroimaging Spectrum at Pre-, Early, and Late Symptomatic Stages of SCA17 Mice-Reference-Cited by-同舟云学术

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Neuroimaging Spectrum at Pre-, Early, and Late Symptomatic Stages of SCA17 Mice

Published:2020-04-08 Issue:4 Volume:19 Page:487-500
ISSN:1473-4222
Container-title:The Cerebellum
language:en
Short-container-title:Cerebellum

Author:

Chen Chiao-Chi,Yao Nai-Wei,Lin Chia-Wei,Su Wei-Shuo,Wu Chin-Tien,Chang Chen,Hsieh-Li Hsiu Mei

Funder

Ministry of Science and Technology, Taiwan

Publisher

Springer Science and Business Media LLC

Subject

Clinical Neurology,Neurology

Link

http://link.springer.com/content/pdf/10.1007/s12311-020-01127-5.pdf

Reference33 articles.

1. Koide R, Kobayashi S, Shimohata T, Ikeuchi T, Maruyama M, Saito M, et al. A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene: a new polyglutamine disease? Hum Mol Genet. 1999;8:2047–53.

2. Rolfs A, Koeppen AH, Bauer I, Bauer P, Buhlmann S, Topka H, et al. Clinical features and neuropathology of autosomal dominant spinocerebellar ataxia (SCA17). Ann Neurol. 2003;54:367–75.

3. van Roon-Mom WM, Reid SJ, Faull RL, Snell RG. TATA-binding protein in neurodegenerative disease. Neuroscience. 2005;133:863–72.

4. Toyoshima Y, Yamada M, Onodera O, Shimohata M, Inenaga C, Fujita N, et al. SCA17 homozygote showing Huntington’s disease-like phenotype. Ann Neurol. 2004;55:281–6.

5. Bruni AC, Takahashi-Fujigasaki J, Maltecca F, Foncin JF, Servadio A, Casari G, et al. Behavioral disorder, dementia, ataxia, and rigidity in a large family with TATA box-binding protein mutation. Arch Neurol. 2004;61:1314–20.

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3. Polyglutamine Ataxias: Our Current Molecular Understanding and What the Future Holds for Antisense Therapies;Biomedicines;2021-10-20

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