PARK14-dependent SOCE and Sporadic Parkinsonís Disease
Research Grant, 2014
This grant builds upon the research from a prior grant:
Objective/Rationale: † † † † † ††
Mutations in the PARK14 gene are associated with Parkinsonís disease (PD), but its role in idiopathic PD is presently unknown. Recently we identified a role of PARK14 as a master regulator of calcium ion (Ca2+) signaling and found that its impairment initiates events that are detrimental to dopamine neurons. The objective of this project is to translate our discoveries from pre-clinical models to human idiopathic PD to determine if dysfunction of PARK14-dependent Ca2+ signaling could be found in the cells of idiopathic PD patients.
Project Description: † † † † † ††
PARK14-dependent Ca2+ signaling will be studied using advanced imaging and molecular techniques in skin fibroblasts from idiopathic PD and control donors, as well as in induced pluripotent stem cell-derived dopaminergic neurons.
Relevance to Diagnosis/Treatment of Parkinsonís Disease: † † † † † † † † † ††
Successful translation of our findings and validation of the novel role of PARK14-dependent Ca2+ signaling in PD will unveil new targets for development of novel disease-modifying treatments.†
Anticipated Outcome: † † † † †
This study will establish a new cascade of pathological PARK14-dependent Ca2+ signaling events as a trigger of PD.
Professor of Medicine, Physiology and Biophysics at Boston University School of Medicine
Location: Boston, Massachusetts, United States