T
Taiji Tsunemi
Researcher at University of California, San Diego
Publications - 18
Citations - 893
Taiji Tsunemi is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 7, co-authored 7 publications receiving 761 citations. Previous affiliations of Taiji Tsunemi include Tokyo Medical and Dental University.
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Journal ArticleDOI
PGC-1α Rescues Huntington’s Disease Proteotoxicity by Preventing Oxidative Stress and Promoting TFEB Function
Taiji Tsunemi,Travis D. Ashe,Bradley E. Morrison,Kathryn Soriano,Jonathan Au,Ruben A. Vázquez Roque,Eduardo R. Lazarowski,Vincent A. Damian,Eliezer Masliah,Albert R. La Spada,Albert R. La Spada,Albert R. La Spada +11 more
TL;DR: PGC-1α rescues Huntington’s disease neurodegeneration by reducing reactive oxygen species and inducing a master regulator of autophagy, and Regulation of TFEB by PGC-1 α underscores the importance of maintaining mitochondrial quality control under conditions of accelerated mitochondrial biogenesis and increased ATP generation.
Journal ArticleDOI
Muscle expression of mutant androgen receptor accounts for systemic and motor neuron disease phenotypes in spinal and bulbar muscular atrophy.
Constanza J. Cortes,Shuo-Chien Ling,Ling T. Guo,Gene Hung,Taiji Tsunemi,Linda Ly,Seiya Tokunaga,Edith Lopez,Bryce L. Sopher,C. Frank Bennett,G. Diane Shelton,Don W. Cleveland,Albert R. La Spada +12 more
TL;DR: A BAC mouse model featuring a floxed first exon to permit cell-type-specific excision of human AR121Q reveals a crucial role for muscle expression of polyQ-AR in SBMA and suggest muscle-directed therapies as effective treatments.
Journal ArticleDOI
PGC-1α at the intersection of bioenergetics regulation and neuron function: from Huntington's disease to Parkinson's disease and beyond
Taiji Tsunemi,Albert R. La Spada +1 more
TL;DR: The role of PGC-1α in normal nervous system function and potentially neurological disease has been investigated in this article, where the role of PPARγ co-activator was shown to contribute to the development of Parkinson's disease.
Journal ArticleDOI
S-nitrosylation of dynamin-related protein 1 mediates mutant huntingtin-induced mitochondrial fragmentation and neuronal injury in Huntington's disease.
Florian Haun,Tomohiro Nakamura,Alicia Shiu,Dong-Hyung Cho,Taiji Tsunemi,Emily A. Holland,Albert R. La Spada,Albert R. La Spada,Stuart A. Lipton,Stuart A. Lipton +9 more
TL;DR: The findings indicate that aberrant S-nitrosylation of Drp1 is a prominent pathological feature of neurodegenerative diseases such as AD and HD and the SNO-Drp1 signaling pathway links mutHTT neurotoxicity to a malfunction in mitochondrial dynamics, resulting in neuronal synaptic damage in HD.
Journal ArticleDOI
PPAR-δ is repressed in Huntington's disease, is required for normal neuronal function and can be targeted therapeutically.
Audrey S. Dickey,Victor V. Pineda,Taiji Tsunemi,Patrick Liu,Helen C. Miranda,Stephen K. Gilmore-Hall,Nicole S. Lomas,Kunal R. Sampat,Anne Buttgereit,Mark Joseph Manalang Torres,April L. Flores,Martin Arreola,Nicolas Arbez,Sergey S Akimov,Terry Gaasterland,Eduardo R. Lazarowski,Christopher A. Ross,Gene W. Yeo,Bryce L. Sopher,Gavin Magnuson,Anthony B. Pinkerton,Eliezer Masliah,Albert R. La Spada,Albert R. La Spada +23 more
TL;DR: In mouse models of HD, pharmacologic activation of PPAR-δ using the agonist KD3010 improved motor function, reduced neurodegeneration and increased survival, indicating that PPAR–δ activation may be beneficial in HD and related disorders.