Dr. Schwarzschild completed undergraduate training in biochemistry at Princeton University. He went on to medical, and graduate neuroscience training at Harvard Medical School to write his PhD thesis on the neurochemistry of tyrosine hydroxylase, the enzyme controlling dopamine biosynthesis. His neurology residency and Parkinson's disease (PD) fellowship training were at MGH.
Since 1996 Dr. Schwarzschild has directed the Molecular Neurobiology Laboratory at MGH, focusing on the role of three purines, adenosine, caffeine, and urate, in PD. His laboratory discovered the neuroprotective properties of adenosine A2A receptor blockers (including caffeine). His leadership of a series of international research conferences on A2A receptors in Parkinson's has helped translate our understanding of this drug target into a promising new therapy for Parkinson's patients.
Most recently, through an interdisciplinary collaboration with epidemiologists at the Harvard School of Public Health, he and his colleagues, in partnership with the Parkinson Study Group (PSG), have shown that the purine antioxidant urate is a novel biomarker that can help predict the risk of PD and its progression rate as well as being a neuroprotective agent candidate.
Dr. Schwarzschild has been the recipient of a Cotzias Fellowship from the American Parkinson's Disease Association and a Paul Beeson Physician Faculty Scholar Award. He has led disease progression studies of the PSG, a consortium of North American clinical trial sites and investigators dedicated to finding improved treatments for PD. In 2012 Dr. Schwarzschild was elected to chair the Executive Committee of the PSG, now headquartered in the MGH Neurology Department. He is a staff neurologist at MGH, working with Parkinson's patients and their families in his weekly movement disorders clinic.
ResearchDr. Schwarzschild is the principal investigator at the Molecular Neurobiology Laboratory at the MassGeneral Institute for Neurodegenerative Disease. His team of researchers investigates molecular mechanisms in Parkinson's disease in an effort to develop improved therapies for Parkinson's and related neurodegenerative diseases.
Visit Dr. Schwarzschild's Molecular Neurobiology Laboratory to read about current research.
What do Gaucher’s disease, gout, and amyloid plaques have in common? For researchers at the MGH, each of them may shed light on the causes and treatment of Parkinson’s disease.
By examining data from a 20-year-old clinical trial, a research team based at the MassGeneral Institute for Neurodegenerative Diseases and Harvard School of Public Health, has found evidence supporting the findings of their 2008 study – that elevated levels of the antioxidant urate may slow the progression of Parkinson’s disease.
Researchers at Massachusetts General Hospital are seeking recently diagnosed Parkinson's disease (PD) patients to participate in a clinical trial investigating whether inosine taken to raise the body’s level of urate — a naturally occurring antioxidant — can be used to slow the progress of PD.
Use of the antioxidant urate to protect against the neurodegeneration caused by Parkinson's disease appears to rely on more than urate's ability to protect against oxidative damage.
A study by MGH researchers adds further support to the possibility that increasing levels of urate may protect against Parkinson's disease. The investigators report that mice with a genetic mutation increasing urate levels were protected against Parkinson's-like neurodegeneration, while the damage was worse in animals with abnormally low urate.
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