Advancing Scientific Breakthroughs and Empowering Parkinson’s Disease Research
Since 1961, APDA has been a funding partner in many major scientific breakthroughs and has awarded more than $60 million in research grants to date.
APDA awards individual research grants and fellowships to scientists performing innovative Parkinson’s disease (PD) research. Grantees are selected through a competitive application process, reviewed by APDA’s Scientific Advisory Board (SAB). The SAB is comprised of scientists with a wide array of backgrounds and expertise in all areas relevant to PD research.
To measure the continued success of APDA’s grants, we keep track of the researchers published work. In the past, we have introduced you to researchers who benefited from APDA grants – not only because the grants allowed them to perform their PD research and obtain results, but because it helped them get additional grants and solidify their careers in PD research.
Q&A with APDA research grant recipients
Today, we will introduce you to three more researchers and highlight how APDA funding was crucial in helping these scientists conduct their vital work and advance their commitment to PD research.
Dr. Xiaoxi Zhuang, PhD, Professor of Neurology and Neurobiology
University of Chicago
Post-doctoral fellowship, 2001
Research grant, 2005
Dr. Zhuang was awarded an APDA Post-doctoral fellowship in 2001 for a project entitled: Regulated Over-Expression of α-Synuclein in Dopamine Neurons. He also was awarded an APDA Research Grant in 2005 for a project entitled: Model PINK1-Linked Parkinson’s Disease Using PINK1 Null Mice.
Q: Can you give us a brief summary of the results of your APDA funded project and its potential implications for the PD community?
A: Using a tissue-specific gene amplification strategy, we generated a transgenic mouse line with human α-synuclein A53T overexpression specifically in dopamine (DA) neurons. These transgenic mice showed profound early-onset mitochondria abnormalities, characterized by autophagy marker-positive cytoplasmic inclusions containing mainly mitochondrial remnants, which preceded the degeneration of DA neurons. Genetic deletion of either parkin or PINK1 in these transgenic mice significantly worsened mitochondrial pathologies, including drastically enlarged inclusions and loss of total mitochondria contents. These data suggest that mitochondria are the main targets of α-synuclein and their defective autophagic clearance plays a significant role during pathogenesis. Moreover, endogenous PINK1 or parkin is indispensable for the proper autophagic removal of damaged mitochondria. Our data for the first time established an essential link between mitochondria autophagy impairments and DA neuron degeneration in an in vivo model based on known PD genetics. The mouse model, its well-defined pathologies, and the demonstration of a main pathogenesis pathway set the stage for many future studies.
Q: What would you say to donors who are considering giving to APDA? Why is their support of APDA research important?
A: I started my independent career as an addiction researcher. With the support from APDA and others, I was able to start PD research. PD research has become my main research focus since then.
Q: Is there anything else you’d like to share with us?
A: We made our A53T overexpression PD mouse model available to other labs. Over the years, it has helped many other labs conduct PD research.
Subajit Roy, Professor of Pathology
University of California, San Diego
Post-doctoral fellowship, 2006
Research grant, 2008
Dr. Roy was awarded an APDA Post-doctoral fellowship in 2006 when he was at University of Pennsylvania. His project was entitled: Axonal Transport and Synaptic Targeting of Normal and Mutant α-synuclein. He then was awarded an APDA Research Grant in 2008 for a project entitled Effects of α-Synuclein on Fast and Slow Axonal Transport when he was at the University of California, Los Angeles.
Q: Can you give us a brief summary of the results of your APDA funded project and its potential implications for the PD community?
A: This was one of the first grants we received when the lab started, and it jump-started our work on the normal function of α-synuclein that continues in our laboratory to this day. Our work showing that α-synuclein acts as a “brake” for neurotransmitter release is largely accepted today as the normal function of this protein. More recently, we have revealed several functional binding partners of α-synuclein and have found surprising physiologic roles for changes that are traditionally thought to be pathologic triggers. Understanding the normal function of α -synuclein is critical in revealing its ultimate transition to the pathologic state in PD.
Q: What would you say to donors who are considering giving to APDA? Why is their support of APDA research important?
A: Foundations like APDA support risky science that is difficult, or sometimes impossible, to get funded through traditional government funded agencies that tend to be risk-averse. Thank you, APDA and keep up the great work!
Yulan Xiong, PhD, Assistant Professor of Neuroscience
University of Connecticut School of Medicine
Post-doctoral fellowship, 2008
Research grant, 2017
Dr. Xiong was awarded an APDA Post-doctoral fellowship in 2008 when she was at Johns Hopkins University School of Medicine, for a project entitled: Modeling LRRK2-Induced Toxicity in Yeast. In 2017, as an Assistant Professor at Kansas State University, she was awarded an APDA Research Grant for a project entitled: Functional analysis of LRRK2 enzymatic activities with aging.
Q: Can you give us a brief summary of the results of your APDA funded project and its potential implications for the PD community?
A: I received an APDA research grant to investigate how aging affects LRRK2 enzymatic activity. To this end, we successfully developed a novel LRRK2 mouse aging model with progressive dopamine neuron degeneration and accompanying behavioral deficits with aging. Using this LRRK2 mouse model, we analyzed LRRK2 kinase and GTPase activities in vivo with aging. Mutations in LRRK2 are the most common genetic causes of PD. Understanding LRRK2 enzymatic function with aging provides novel insights into the development of PD.
Q: What has been the general trajectory of your research and your career since your APDA award?
A: I received an APDA Research grant in 2017 when I was an Assistant Professor at Kansas State University. It was the first grant that I received as an independent researcher, which set the stage for receiving many additional grants. Since my APDA Research grant, I successfully secured an NIH R01 grant and a Stanley Fahn Junior Faculty Award from the Parkinson’s Foundation.
Q: Did your APDA grant help shape the next steps of your research? If so, how?
A: Yes, stemming from my APDA-funded project, we further identified several key regulators of LRRK2. The APDA grant provided the seed money for us to dig further into LRRK2 biology.
Q: What would you say to donors who are considering giving to APDA? Why is their support of APDA research important?
A: I appreciate the APDA support very much. As Junior faculty, this grant was critical for me. It provided seed money for my research, helped with career development, and helped make important discoveries in our understanding of PD.
Read more about past successes in past blog posts:
Tips and Takeaways
- Drs. Zhuang, Roy, and Xiong are just three of the many researchers APDA has funded in the past.
- We are proud that our grants support new ideas in PD research and help shuttle these ideas into more involved research programs.
- Our research program is only possible due to the support and generosity of our donors. You can help us in this critical mission.
- We encourage you to learn more about all the research APDA has funded over the years.
- To learn more about some of the researchers APDA is currently supporting, you can read our recent interviews with Dr. Stephan Grimaldi and Dr. Enrico Opri.
- You can also view our recent Meet our APDA Researchers broadcast, where we learned about the work of Dr. James Liao and Dr. Ryan Roemmich.