J
John B. Penney
Researcher at Harvard University
Publications - 68
Citations - 10083
John B. Penney is an academic researcher from Harvard University. The author has contributed to research in topics: Huntington's disease & AMPA receptor. The author has an hindex of 44, co-authored 68 publications receiving 9623 citations. Previous affiliations of John B. Penney include University of Michigan.
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Journal ArticleDOI
Unified huntington’s disease rating scale: Reliability and consistency
Karl Kieburtz,John B. Penney,Peter Corno,Neal G. Ranen,Ira Shoulson,Andrew Feigin,Davi Abwender,J. Timothy Greenarnyre,Donald S. Higgins,Frederick J. Marshall,Joshua L. Goldstein,Kimberly Steinberg,Charles Shih,Irene H. Richard,Charlyne Hickey,Carol Zimmerman,Constance Orme,Kathy Claude,David Oakes,Daniel S. Sax,Anthony Kim,Steven M. Hersch,Randi Jones,Alexander P. Auchus,David B. Olsen,Cheryl Bissey-Black,Allen Rubin,Rose Schwartz,Richard Dubinsky,William Mallonee,Carolyn Gray,Nan Godfrey,Greg Suter,Kathleen M. Shannon,Glenn T. Stebbins,Jean A. Jaglin,Karen Marder,Stuart Taylor,Elan D. Louis,Carol Moskowitz,Deborah Zeck Thorne,Naomi Zubin,Nancy S. Wexler,Michael R. Swenson,Jane S. Paulsen,Neal R. Swerdlow,Roger L. Albin,Christine Wernette,Francis O. Walker,Vicki Hunt +49 more
TL;DR: The limited longitudinal database indicates that the UHDRS may be useful for tracking changes in the clinical features of HD over time and there was an excellent degree of interrater reliability for the motor scores.
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Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease
Victor O. Ona,Mingwei Li,Jean Paul Vonsattel,L. John Andrews,Sohail Q. Khan,Woosik M. Chung,Ariel S. Frey,Anil Menon,Xiao-Jiang Li,Philip E. Stieg,Junying Yuan,John B. Penney,Anne B. Young,Jang-Ho J. Cha,Robert M. Friedlander +14 more
TL;DR: Evidence of caspase-1 activation in the brains of mice and humans with Huntington's disease is demonstrated and it is demonstrated that intracerebroventricular administration of a casp enzyme inhibitor delays disease progression and mortality in the mouse model of Huntington’s disease.
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CAG repeat number governs the development rate of pathology in Huntington's disease
John B. Penney,Jean-Paul Vonsattel,Marcy E. MacDonald,James F. Gusella,Richard H. Myers,Richard H. Myers +5 more
TL;DR: The results imply that striatal damage in Huntington's disease is almost entirely a lineaar function of the length of the polyglutamine stretch beyond 35.5 repeats, and it is predicted that the pathological process develops linearly from birth.
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Altered brain neurotransmitter receptors in transgenic mice expressing a portion of an abnormal human Huntington disease gene
Jang-Ho J. Cha,Christoph M. Kosinski,J A Kerner,Stephen A. Alsdorf,Laura Mangiarini,Stephen W. Davies,John B. Penney,Gillian P. Bates,Anne B. Young +8 more
TL;DR: Analysis of glutamate receptors in symptomatic 12-week-old R6/2 mice revealed decreases compared with age-matched littermate controls in the type 1 metabotropic GluR, and in situ hybridization indicated that mGluR and D1 dopamine receptor mRNA were altered as early as 4 weeks of age, long prior to the onset of clinical symptoms.
Journal ArticleDOI
Metabotropic glutamate receptor mRNA expression in the basal ganglia of the rat
TL;DR: MGluR1 was the only mGluR message prominently expressed in the dopaminergic neurons of the substantia nigra pars compacta, suggesting the involvement of this receptor in the regulation of dopamine release from nigrostriatal terminals.