Dollars for Profs
Dig Into University Researchers' Outside Income and Conflicts of Interest
Published Dec. 6, 2019
This database was last updated in December 2019 and should only be used as a historical snapshot. There may be new or amended records not reflected here.
Conflict of Interest
Institutions must file significant disclosures to the National Institutes of Health if they determine financial relationships could affect the design, conduct or reporting of the NIH-funded research. The NIH provided us with their entire financial conflict of interest database, with filings from 2012 through 2019.
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Gusella James
Massachusetts General Hospital, Department: Na
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Triplet Therapeutics, Inc.
Equity Interest - Non-publicly traded entity ( e.g., stock, stock option, or other ownership interest)
Dr. Gusella is a consultant for Triplet Therapeutics, Inc. and owns equity in the private company. The company is developing new therapeutic approaches to address triplet repeat disorders such as Huntington’s Disease and Myotonic Dystrophy. The research project focuses on Huntington’s Disease (HD) and will result in knowledge of specific genes and pathways that can delay HD pathogenesis in human patients, of the degree to which they broadly affect both HD motor and other phenotypes and of the potential mechanisms by which they act. The research will provide critical cellular and mouse model resources necessary to rapidly drive the findings toward translation for the HD community. Disease modifying genes discovered in this project could later become targets for the company’s therapeutic development. The Partners Committee on Outside Activities review panel evaluated the financial interest in connection with this research project and determined that, based on the close connection between the company's interests and the research, the financial interest could directly and significantly affect the design, conduct, or reporting of the research.
Disease-Modifying Genes in Huntington's Diseae
Huntington's disease (HD), with its single genetic cause, expanded CAG tracts in the HTT gene, is an inherited neurodegenerative disorder that devastates entire families. This project uses genetic and genomic approaches to uncover other genes that significantly alter the timing with which diagnosable symptoms become manifest in Huntington's disease patients. We have discovered definitive chromosomal locations of several such modifier genes and have suggestive evidence for the locations of many more. Using a combination of human HD disease patient sample collections, induced pluripotent stem cell lines and neuronal cells derived from them, and lines of mice that precisely replicate the human mutation, we will home in on the precise genes and DNA variants and, therefore, the biological pathways that influence the HTT CAG-initiated disease process that leads to onset of motor symptoms, cognitive impairment and psychiatric symptoms and will evaluate their effects in accurate model systems. We will thereby generate the knowledge and experimental resources to support therapeutic development for the first time based upon targets already validated to alter the rate of HD in humans.
Filed on February 27, 2019.
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Notes: When a more specific filing date is not available for an individual financial disclosure or conflict of interest form, we use the year the form was filed. If the year was not disclosed, we report the range of years covered by our public records requests. In a few cases, a start date was provided instead of a filing date. In those cases, we use the start date instead.
Fewer than 10% of records from the University of Florida and fewer than 1% of records from the University of Texas system were removed because they did not contain enough information.
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