The Foundation supports research that can lead to the creation of better Parkinson's treatments. Here you can search previously awarded grants by keyword, program name, researcher name, institution or organization name and/or year.
FUNDED GRANTS ( 18)
Research Grant, 2016
The LRRK2 gene has been implicated in Parkinson's disease, but is too large to be expressed in viral vectors, a tool to modify cells. In order to study LRRK2 function, one needs a viral vector that permits expression of LRRK2. Helper dependent adenovirus (HdAd) can package large genes and so are an ideal viral vector system for LRRK2 expression.
Target Advancement Program, 2016
Abnormal build-up of the protein alpha-synuclein in Parkinson's disease (PD) has been linked to cell stress and death. These deficits can be rescued by expressing certain proteins that affect endoplasmic reticulum-golgi (production and sorting of proteins and lipids) trafficking (movement across the cell). Increasing evidence suggests that the Retention in endoplasmic reticulum 1 ...
Researchers: Nikolaus McFarland, MD, PhD
Improved Neuromodulation Approaches, 2014
Levodopa-resistant posture, gait and freezing symptoms are among the most disabling and difficult to treat in people with Parkinson's disease (PD). Recent findings from deep brain stimulation (DBS) trials have been promising for addressing many aspects of PD, but have failed to identify a therapeutic benefit for freezing and/or falling. We believe there are two c...
Researchers: Michael Okun, MD
Target Validation, 2013
One of the hallmark pathologies in the brains of patients with Parkinson's disease (PD) is an inflammatory response. We will test whether the cytokine interleukin-10 (IL-10), capable of dampening inflammatory responses, may prolong lifespan in pre-clinical models that recapitulate the major protein inclusion pathology in human PD. These transformative studies could...
Target Validation, 2013
Promising Outcomes of Original Grant:
Our original target validation grant was aimed at deciphering the role of the protein beta-arrestin2 in the manifestation of beneficial versus dyskinetic side-effects of levodopa. We hypothesized that altering beta-arrestin2 expression would alter both levodopa-induced dyskinesia and locomotion. Our hypotheses were proven correct, and we showed that over-expres...