
BiographyAfter obtaining his undergraduate training in biochemistryat Princeton University, Dr. Schwarzschild went on to medical and graduateneuroscience training at Harvard Medical School. There he pursued his PhDthesis on the neurochemistry of tyrosine hydroxylase,the enzyme controlling dopamine biosynthesis. He undertook neurology residencyand then Parkinson's disease fellowship training at MGH.
Since 1996 Dr. Schwarzschild has directed the MolecularNeurobiology Laboratory at MGH, focusing on the role of three purines --adenosine, caffeine and urate -- in animal models of PD. His laboratorydiscovered the neuroprotective properties of adenosine A2A receptor blockers(including caffeine) in mouse models of the disease. His leadership of a seriesof international research conferences on A2A receptors in Parkinson's hashelped translate our understanding of this drug target into a promising newtherapy for Parkinson's patients.
Most recently, through a fruitful interdisciplinary collaborationwith epidemiologists at the Harvard School of Public Health, he and his colleagues have discovered a major clue towhy disease progression is mild in some and aggressive in others. Inpartnership with the Parkinson Study Group they showed that the purineantioxidant urate can serve as a predictor of not only the risk of PD, but alsothe rate at which it progresses. Their work identifies urate as a novelbiomarker of PD progression rate, as well as a candidate neuroprotective agent.
Dr. Schwarzschild has been the recipient of a Cotzias Fellowshipfrom the American Parkinson's Disease Association and a Paul Beeson PhysicianFaculty Scholar Award. Since 1997 he has been an activeclinical investigator in disease progression trials of the PSG. He serves as a staffphysician on the Neurology Service at MGH where he works with Parkinson'spatients and their families in his weekly movement disorders clinic.
Publications
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.
A Parkinson’s Disease Patient and Caregiver Symposium at Massachusetts General Hospital
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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