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PDF Grant Programs

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2015 Investigator-Initiated Projects

Among PDF's research awards in 2015 are several novel investigator-initiated research projects. Abstracts of these projects appear below. 


International Research Grants

[+] Novel Insights into the Properties and Fate of Naturally Secreted Alpha-synuclein

Georgia Sotiropoulou, Ph.D., University of Patras

Scientists know that a protein called alpha-synuclein plays an important role in the death of certain brain cells, and that this cell death leads to Parkinson’s disease. It is also well known that alpha-synuclein forms toxic clumps inside of certain brain cells. But alpha-synuclein is also found outside of cells. One theory holds that the risk of PD increases when there is too much alpha-synuclein circulating outside of cells. This research project focuses on an enzyme, kallikrein-related peptidase 6 (KLK6), which may help break down and clear excess alpha-synuclein. We seek to understand, step-by-step, how levels of alpha-synuclein outside of cells are regulated. We are also looking for links between these levels and the development of PD. If the enzyme KLK6 is found to play a role in regulating alpha-synuclein levels, it provides a clue for developing new drugs. For example, it would demonstrate that drugs that increase the activity of KLK6 might have potential as PD therapies.


[+] Striatal CaV1.3 Calcium Channel Silencing as a Neuroprotective Target for Levodopa-induced Dyskinesias

Kathy Steece-Collier, Ph.D., and Frederic P. Manfredsson, Ph.D., Michigan State Universit

Levodopa is the gold-standard therapy for Parkinson’s disease. But after taking levodopa for several years most people develop dyskinesias – involuntary movements that are a side effect of the medication. Research has shown that when cellular calcium channels (the gateways that allow calcium into cells) are disrupted, the disruption plays a role in dyskinesias. In particular, one channel called CaV1.3 is implicated. Drugs already on the market for high blood pressure, called calcium channel blockers, are being investigated to treat dyskinesias. But they are not specific to CaV1.3, and thus only partially effective. This research, carried out in rats, investigates whether selectively blocking CaV1.3 might better protect against dyskinesias, and whether it can reverse dyskinesias after they have developed. The results will inform the development of calcium blocking therapies targeted at levodopa-induced dyskinesias.


[+] Neuroprotection by XPro1595 in a Chronic MPTP Monkey Model of Parkinson’s

Malú Tansey, Ph.D., and Yoland Smith, Ph.D., Emory University

Brain scans show that people with PD have more inflammation (the body’s response to injury or infection) in their brains than is normal. And studies suggest that drugs to treat inflammation may lower PD risk. We have already shown, in research on rodents with PD-like symptoms, that a new anti-inflammatory drug called XPro1595 penetrates into the brain and lessens and slows brain cell degeneration. Our new study will test the drug in monkeys that have been given MPTP, a substance that kills dopamine neurons and results in PD movement symptoms. If it is effective, XPro1595 will block or reduce the effects of the MPTP. This is an important step in moving this drug toward clinical trials in humans.


[+] Dysfunctional Signalling Mechanism of Neurotransmission in Parkinson’s Disease

Zhenyu Yue, Ph.D., Icahn School of Medicine at Mount Sinai

The neurons affected by PD use a chemical messenger called dopamine to help tell the body to move. Understanding how dopamine communicates is vital to developing new therapies for Parkinson’s disease. We recently identified a mutation in a gene that causes early-onset PD, which may help us to understand dopamine communication. This gene in which we found the mutation is responsible for a protein known as synaptojanin 1 (synj1), which plays a role in the transmission of dopamine from cell to cell. Our study uses novel laboratory methods to investigate the normal role of synj1 and what goes awry when it is mutated. In addition, we will study how synj1 interacts with another PD-causing gene, called LRRK2. A mutation in LRRK2 results in decreased dopamine transmission, which we think may because synj1 is impaired. Knowledge of how synaptojanin 1 mutations may cause PD could provide new targets for therapeutic intervention in PD.


Research Fellowship Grants

[+] Alpha Synuclein Aggregation Causes Toxicity by Decreasing Functional Forms of the Protein

Matthew Benskey, Ph.D., mentor: Fredric P. Manfredsson, Ph.D., Michigan State University

[+] Functional Analysis of Dopamine-dependent Circuits Activity in Parkinson’s Disease

Nan Li, Ph.D., mentor: Alan Jasanoff, Ph.D., Massachusetts Institute of Technology

[+] Mechanisms for the Modulation of Striatonigral and Striatopallidal Neuron Activity by Phosphodiesterase 10A Inhibition in L- DOPA-induced Dyskinesia

Fernando Padovan Neto, Ph.D., mentor: Anthony R. West, Ph.D., Rosalind Franklin University

[+] In Vivo Modulation of Alpha-Synuclein Phosphorylation: Tracking Aggregates in the Living Mouse Brain

Kateri Spinelli, Ph.D., mentor: Vivek Unni, M.D., Ph.D., Oregon Health & Science University

[+] Deciphering the Mechanism of Action of Parkin Using a Structure-Based FRET-Reporter System

Matthew Tang, Ph.D., mentor: Edward Fon, M.D., Montreal Neurological Institute, McGill University

[+] Novel Deep Brain Stimulation Paradigms on Treating Parkinsonian Non-human Primates and the Underlying Physiological Plasticity

Jing Wang, Ph.D., mentor: Jerrold Vitek, M.D., Ph.D., University of Minnesota

[+] Input- and Cell-type Specific Rewiring of Subcellular Connectivity in the Striatum in Parkinsonian Mice

Yu-Wei Wu, Ph.D., mentor: Jun Ding, Ph.D., Stanford University School of Medicine

[+] Phosphorylated Alpha-synuclein Peptides as Biomarkers of Parkinson’s Disease

Li Yang, Ph.D., mentor: Jing Zhang, M.D., Ph.D., University of Washington

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