Research Investigator Profile

Michael A. Schwarzschild, MD, PhD

Michael A. Schwarzschild, MD, PhD


Research Description

The Molecular Neurobiology Laboratory at MGH/MIND, under the direction of Michael Schwarzschild, MD PhD, investigates molecular mechanisms in mouse models of Parkinson’s disease in an effort to develop improved therapies for Parkinson’s and related neurodegenerative diseases.  We focus on a natural class of compounds known as purines, in particular the role of three purines — adenosine, caffeine and urate — and how targeting them may prevent or slow the brain cell degeneration of Parkinson’s.

The lab is pursuing major epidemiological and clinical clues to the disease through fruitful inter-disciplinary collaborations with the research group of Professor Alberto Ascherio at the Harvard School of Public Health and with the Parkinson Study Group of North America. Caffeine and urate are linked to a lower risk of Parkinson’s and/or to a slower rate of disease progression in humans.

The lab explores how caffeine (and other blockers of the adenosine A2A receptor) and urate may be protecting brain cells in Parkinson’s. We employ complementary pharmacological and genetic (e.g., gene knockout) tools to dissect the role of adenosine and urate pathways in the brains of parkinsonian mice.  We are also studying the role of adenosine receptors in the disabling motor complications (abnormal involuntary movements known as dyiskinesia) that are sometimes triggered by standard anti-parkinsonian therapy. Read More.

Research interests Purines – caffeine, other adenosine A2A antagonists and urate – in Parkinson’s disease
Research techniques Neuropharmacology, transgenic/knockout models, dyskinesia models, toxin and genetic mouse models of Parkinson’s disease, neuroepidemiology
Diseases studied Parkinson’s disease and other neurodegenerative diseases
Selected publications 1.    Chen JF, Xu K, Petzer JP, Staal R, Xu YH, Beilstein M, Sonsalla PK, Castagnoli K, Castagnoli N Jr, & Schwarzschild MA (2001) Neuroprotection by caffeine and A2A adenosine receptor inactivation in a model of Parkinson's disease. J Neurosci 21:RC143:1-6.
2.    Kachroo A, Orlando LR, Grandy DK, Chen JF, Young AB, & Schwarzschild MA. (2005) Interactions between metabotropic glutamate 5 and adenosine A2A receptors in normal and parkinsonian mice. J Neurosci. 25:10414-10409.
3.    Xiao D, Bastia E, Xu YH, Benn CL, Cha JH, Peterson TS, Chen JF & Schwarzschild MA. (2006) Forebrain adenosine A2A receptors contribute to L-3,4-dihydroxyphenylalanine-induced dyskinesia in hemiparkinsonian mice. J Neurosci. 26:13548-13555.
4.    Xu K, Xu Y, Brown-Jermyn D, Chen JF, Ascherio A, Dluzen DE, & Schwarzschild MA. (2006) Estrogen prevents neuroprotection by caffeine in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease. J Neurosci. 26:535-41.
5.    Schwarzschild MA, Schwid SR, Marek K, Watts A, Lang AE, Oakes D, Shoulson I, & Ascherio A, and the Parkinson Study Group PRECEPT Investigators.  (2008) Serum urate as a predictor of clinical and radiographic progression in Parkinson’s disease. Arch Neurol 65(6):doi:10.1001/archneur.2008.65.6.nct70003.
NCBI PubMed link  NCBI PubMed Publications
E-mail address
Lab mailing address MassGeneral Institute for Neurodegenerative Disease
114 16th Street
Charlestown, MA 02129
Clinical interests Parkinson's disease
Clinical mailing address Massachusetts General Hospital
Neurology, Suite 835
Wang Ambulatory Care Center
55 Fruit Street
Boston, MA 02114 USA
Clinical website address Movement Disorders Unit
Parkinson's Disease and Movement Disorders Clinic

Back to Top