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Dr. Hersch's clinical and research interests are in neurodegenerative disorders and particularly Huntington's disease (HD). He was recruited to MGH/Harvard Medical School in 2001 to direct the HD clinical center and develop a laboratory devoted to translational research for HD. Dr. Hersch's work on HD has spanned basic, translational, and clinical and has included the neuropathology of HD, its pathogenesis, the development of therapeutics, and the development of clinical and biological measures of HD in humans to improve testing potential therapies.
His laboratory has examined the roles of huntingin protein in pathogenesis, the contributions of transcriptional dysfunction and cellular energetics to HD pathogenesis, and has extensively used HD mouse models to examine mechanisms of disease and explore potential therapies. Many of the compounds the Hersch lab has helped explore in HD mice are advancing through clinical trials. Dr. Hersch has been a principal investigator, steering committee member, or site investigator for many observational or therapeutic studies in HD patients. He has developed and holds INDs for potential disease modifying therapies for HD, which have gone to phase II and phase III clinical trials. He is leading a collaborative NIH supported program to develop neuroimaging, protein, small molecule, and genomic biomarkers of HD. He is also co-chair of the executive committee of the Huntington Study Group (HSG) and plays a major role in the planning and execution of multicenter clinical trials for HD. He also directs clinical care for HD provided by the New England Center of Excellence for Huntington's disease and sees patients in the Movement Disorders unit at MGH.
The first clinical trial of a drug intended to delay the onset of symptoms of Huntington disease reveals that high-dose treatment with the nutritional supplement creatine was safe and well tolerated by most study participants. In addition, neuroimaging provided evidence that creatine might slow the progression of presymptomatic disease.
An assay designed to measure normal and abnormal forms of the huntingtin protein – the mutated form of which causes Huntington's disease – was successful in detecting levels of the mutant protein in a large multicenter study of individuals at risk for the devastating neurological disorder.
In a new research paper BWH and MGH researchers identify a transcriptional biomarker that may assist in the monitoring of Huntington's disease activity and in the evaluation of new medications.
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