Zobrazeno 1 - 8
of 8
pro vyhledávání: '"R J, Ferrante"'
Publikováno v:
Journal of neurochemistry. 79(6)
Mitochondrial dysfunction and oxidative damage may play a role in the pathogenesis of Huntington's disease (HD). We examined concentrations of 8-hydroxy-2-deoxyguanosine (OH(8)dG), a well-established marker of oxidative damage to DNA, in a transgenic
Autor:
O A, Andreassen, R J, Ferrante, P, Klivenyi, A M, Klein, L A, Shinobu, C J, Epstein, M F, Beal
Publikováno v:
Annals of neurology. 47(4)
The pathogenesis of neuronal cell death as a consequence of mutations in copper/zinc superoxide dismutase (SOD1) associated with familial amyotrophic lateral sclerosis may involve oxidative damage and mitochondrial dysfunction. We examined whether cr
Autor:
S, Kuemmerle, C A, Gutekunst, A M, Klein, X J, Li, S H, Li, M F, Beal, S M, Hersch, R J, Ferrante
Publikováno v:
Annals of neurology. 46(6)
The mechanism by which polyglutamine expansion in Huntington's disease (HD) results in selective neuronal degeneration remains unclear. We previously reported that the immunohistochemical distribution of N-terminal huntingtin in HD does not correspon
Publikováno v:
Journal of neurochemistry. 73(5)
The polyglutamine-expanded N-terminal region of mutant huntingtin causes neurodegeneration in Huntington's disease (HD). Neuronal intranuclear and cytosolic inclusions composed of mutant huntingtin are found in brains of HD patients. Because tissue t
Autor:
E B, Hanlon, I, Itzkan, R R, Dasari, M S, Feld, R J, Ferrante, A C, McKee, D, Lathi, N W, Kowall
Publikováno v:
Photochemistry and photobiology. 70(2)
The purpose of this study was to investigate whether near-infrared (NIR) fluorescence spectroscopy could be used to detect Alzheimer's disease (AD) by brain tissue autofluorescence. Unfixed temporal cortex specimens from AD cases and age-matched, non
Publikováno v:
The Journal of biological chemistry. 273(30)
Huntington's disease (HD) is caused by the expansion of a glutamine repeat in the protein huntingtin. The expanded glutamine repeat is thought to mediate a gain of function by causing huntingtin to abnormally interact with other proteins. We previous
Publikováno v:
Agents and Actions. 39:C102-C103
Thromboembolic complications have been described in graft recipients receiving cyclosporine (CS). Whether these individuals have a hypercoagulable state when compared to healthy controls was evaluated. Recalcification times (RT) of saline-incubated c
Publikováno v:
Journal of Neuropathology and Experimental Neurology. 44:325