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US 11,298,409 B2Granted
Mutant huntingtin-mediated protein dysfunction
AssigneesUniversity of Pittsburgh—Of the Commonwealth System of Higher Education, Washington University
InventorsRobert Friedlander, Hiroko Yano
Life of this patent
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Abstract
The present invention relates to methods of inhibiting neurodegeneration in a subject suffering from or genetically at risk and/or destined to develop Huntington's Disease comprising increasing, in neurons of the subject, the activity of the TIM23 mitochondrial protein import complex.
Claims13
A method for attenuating a mitochondrial protein import defect in a subject, comprising administering to the subject an effective amount of an agent that comprises:
- (a) an exogenous TIM23 complex protein consisting essentially of the translocase of inner mitochondrial membrane 23 (Tim23) subunit, translocase of inner mitochondrial membrane 50 (Tim50) subunit, and translocase of inner mitochondrial membrane 17a (Tim17a) subunit;
- or
- (b) a nucleic acid molecule encoding the subunits Tim23, Tim50, and Tim17a.
A method for attenuating a mitochondrial protein import defect in a neuron, comprising:
- (a) contacting the neuron with an effective amount of an exogenous TIM23 complex protein that consists essentially of the translocase of inner mitochondrial membrane 23 (Tim23) subunit, translocase of inner mitochondrial membrane 50 (Tim50) subunit, and translocase of inner mitochondrial membrane 17a (Tim17a) subunit;
- or
- (b) introducing into the neuron a nucleic acid molecule encoding the subunits Tim23, Tim50, and Tim17a.
Dependencies are inferred from the claim text.