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2015 Investigator Awards

2015 Clinical Research and Intervention Investigator Awards

The National Parkinson Foundation, under the direction of its Clinical and Scientific Advisory Board, has announced the 2015 Clinical Research and Intervention Investigator Awards for Parkinson's Disease. The four grants target key scientific questions about gender differences in Parkinson's, cognition and inflammation:

Determinants of sex differences in caregiving for Parkinson's disease
Nabila Dahodwala, MD, University of Pennsylvania, Philadelphia, PA

Dr. Dahodwala has been awarded a two-year grant to study issues that result in differences in caregiving and to explore whether there may be options to improve caregiving.  Starting with an analysis of data from NPF's Parkinson's Outcomes Project, Dr. Dahodwala will study barriers to effective caregiving, starting in a small-scale setting and expanding to understand a large and diverse group.  Drawing on outcomes data, she will design an approach to help clinicians to address issues of caregiving and to engage clinic social workers to improve the lives of both women and men affected by PD.

The relationship between microglial activation and β-amyloid deposition in PD-MCI and PD-dementia
Antonio Strafella, MD, PhD, University of Toronto, Toronto, Canada

In 2010, Dr. Strafella was awarded a grant from NPF to research how patients with mild cognitive impairment differed from those without, at the level of deep brain structures, using advanced imaging techniques. Dr. Strafella will follow up this work looking at inflammation, studying the impact of the Alzheimer's protein β-amyloid in Parkinson's.  This study will use an advanced imaging technique, positron emission tomography (PET) scans, to examine how a number of important factors interrelate in the brain.  First, they will look at how the brain's immune system, which is based on cells called microglia that respond to inflammation in the brain, are activated in patients experiencing cognitive change.  Second, they will look for deposition of β-amyloid to see if this Alzheimer's protein is linked to this inflammation.  Finally, they will look to see if the brain atrophies in regions where one or both of these signals are found.  A big question is which comes first: the bad proteins or the inflammation?  This study will be based around a new technology: an innovative PET scan tracer that shows where the brain's immune system is active.

Neuroinflammation via T-cell response in Parkinson's and Lewy body diseases
David Sulzer, PhD, Columbia University, New York, NY

In this study, Dr. Sulzer explores a radical new hypothesis: could Parkinson's disease be significantly characterized as an auto-immune disorder, where the cell damage in Parkinson's is caused more by immune system response than by accumulation of toxic proteins?  Dr. Sulzer's lab has identified two markers of immune response present in people with Parkinson's.  While this work is related to the current focus on the key Parkinson's protein called α-synuclein, it suggests that the greatest impact of this protein may actually be down-stream from its synthesis and misfolding.  By focusing on studying tissue from patients with Parkinson's and not models, Dr. Sulzer hopes to provide a greater understanding of Parkinson's.

Establishing the link between canonical TGFβ-superfamily signaling and Parkinson's disease pathophysiology
Paschalis Sideras, PhD, Biomedical Research Foundation Academy, Athens, Greece

Several processes in the brain, including some inflammatory reactions, are regulated using signaling proteins called transforming growth factor-beta (TGFβ) proteins.  Scientists know that several TGFβ proteins are linked to Parkinson's disease, but how they are linked is not yet known.  Dr. Sideras will study these regulatory proteins in several mouse models of Parkinson's, looking for common responses across models that could help inform treatment decisions and future research.  Dr. Sideras hopes that understanding TGFβ will guide strategies to make the dopamine-producing neurons more resistant to PD.