Associate Professor
Neurology and Molecular & Human Genetics
Baylor College of Medicine
Lead Physician
Neurogenetics Clinic
Baylor College of Medicine


MD from University of Padua School of Medicine
Fellowship at University of Padua School of Medicine
Molecular Biology
Post-Doctoral Fellowship at Columbia University
Molecular Genetics
Internship at Mount Sinai School of Medicine - Cabrini Medical Center
Internal Medicine
Residency at University of Michigan
Clinical Fellowship at Baylor College of Medicine
Clinical Genetics
Post-Doctoral Fellowship at Baylor College of Medicine


Board Certification in Neurology
American Board of Psychiatry and Neurology

Professional Interests

  • Neurogenetics
  • Movement Disorders
  • Neurodegenerative Diseases
  • Genetic and molecular studies of disease pathogenesis in Parkinson’s disease
  • Traumatic brain injury

Professional Statement

My laboratory uses a combination of clinical, genetic, and molecular approaches to study the pathogenesis of Parkinson’s disease, the second most common neurodegenerative disease, and traumatic brain injury.

Parkinson’s disease (PD) is a multifactorial neurological disorder. Several genes and pathways have been implicated in its pathogenesis and environmental factors have been shown to either cause parkinsonism or to be associated with an increased risk of PD. However, the relationships between these pathways remain to be elucidated. We have identified a number of novel protein-protein interactions with the products of known PD disease genes. We are currently characterizing the functional role of selected interactions, focusing on those shared between different PD genes.

Traumatic brain injury (TBI) is a major cause of death or life-long disability in people of all ages. Considerable variability exists in the clinical outcome after TBI, which is only partially explained by known factors. Clinical data suggest that one of these factors is the presence of individual differences in susceptibility to the effects of trauma. However, the cellular and molecular pathways underlying this heterogeneity remain largely unknown. We hypothesize that outcome from TBI correlates, at least in part, with differences in individual susceptibility to axonal injury. We have developed in vitro models of cellular and axonal injury relevant to the pathogenesis of TBI using induced pluripotent stem cell-derived neurons obtained from TBI patients. We are currently studying the responses of human glutamatergic cortical projection neurons to insults known to occur in TBI.

Selected Publications