Making Hope Possible: American Parkinson Disease Association Supports Researchers With $2.6 Million in New Funding

Exciting New Parkinson’s Disease Research is Underway

asian scientist team meeting

On September 5, 2024, APDA announced 20 new Parkinson’s disease (PD) research grants, for a total of $ 2.6 million in funding for the year ahead. Our grant recipients are working tirelessly to understand the complexities of Parkinson’s disease (PD) and to develop new treatments and eventually, a cure. We are honored to support these researchers and their innovative and inspiring work.

We know you are as eager as we are for PD research progress, which is why we are sharing this important news with you. Below, we present the individual research projects APDA will be funding and specify why they are important for the PD community. You can click on any of the researchers below to learn more about them and their exciting work.

These new grants have been awarded in the form of five Post-Doctoral Fellowships, eight Research Grants, three Diversity in Parkinson’s Disease Research grants, and one George C. Cotzias Memorial Fellowship. In addition, APDA is funding nine APDA Centers for Advanced Research.

The 2024-2025 APDA Parkinson’s Disease Research Grants and Fellowships:

The George C. Cotzias Fellowship

The George C. Cotzias Fellowship is APDA’s most prestigious award and is granted to a young physician-scientist with exceptional promise who is establishing a career in research, teaching, and clinical services relevant to PD. The award spans three years and is designed to fund a long-range project focused on PD.

This year’s awardee is:

William Zeiger, MD, PhD
The Regents of the University of California, Los Angeles 
Project Title:  
Neuronal microcircuit mechanisms of posterior cortical dysfunction and cognitive impairment in a mouse model of Parkinson’s disease 
Major question to be answered:
How does alpha-synuclein (a-syn) pathology contribute to thinking and memory problems and, specifically, problems with processing of visual information in Parkinson’s disease?
Why is this important?
Aggregation of the protein a-syn is a pathological hallmark of PD. This research will analyze the role of a-syn in the parts of the brain responsible for processing visual information, helping us understand the role that a-syn plays in the development and progression of thinking and memory problems in people with PD. The work will help with the design of treatment strategies to try to restore the function of these brain cells affected by a-syn.  
In addition to Dr. Zeiger, we continue to support two additional George C. Cotzias grantees,Krithi Irmady, MD, PhD andGary Ho, MD, PhD, who are in the second and third year of their three-year grants, respectively.

Diversity in Parkinson’s Disease Research Grants

This grant supports the study of the health inequities and/or differences among under-studied PD communities, across the spectrum of ethnicity, ancestry, geography, socioeconomic conditions, and gender.

This year’s awardees are:

Ignacio Mata, PhD
Cleveland Clinic Foundation, Cleveland, OH  
Project Title:                                                 
Machine-learning model for predicting levodopa-induced dyskinesias in a large cohort of Latinos with Parkinsons disease  
Major question to be answered:
Can a computer-based tool predict who might develop levodopa-induced dyskinesia (LID) among Latino individuals with PD?    
Why is this important?
Genetic data from more than 2,000 Latinos with PD from the Latin American Research consortium in the Genetics of Parkinson’s Disease (LARGE-PD) will be analyzed using algorithms to try to predict who might develop LIDs. These findings have the potential to offer personalized care for people with PD at high risk of developing LID, while focusing on the Latino PD community, a historically underrepresented population group.

Melissa Nirenberg, MD, PhD
Bronx Veterans Medical Research Foundation, New York, NY
Project Title: 
Parkinson’s disease phenotype in Black and Hispanic veterans 
Major question to be answered:
What are the clinical characteristics of Black and Hispanic veterans with PD? 
Why is this important?
This project seeks to determine the clinical features of PD specifically in Black and Hispanic veterans, a population which is under-represented and under-engaged in research. This information will therefore be useful in diagnosing PD, optimizing treatments, and identifying targeted therapies for people in these underrepresented groups.

Danielle Shpiner, MD 
Miller School of Medicine of the University of Miami, Miami, FL  
Project Title:                                                  
Improving access to advance care planning for Hispanic people with Parkinsons disease
Major question to be answered:
What are the reasons for barriers to advance care planning (ACP) engagement in the Hispanic, Miami-based Parkinson’s population?
Why is this important?
Focus groups and semi-structured interviews with Hispanic people with PD and their care partners will help to explore the reasons that people in this population have not been able to access ACP discussions. This will allow the implementation of appropriate interventions to overcome these barriers.  

Post-Doctoral Fellowships

This two-year fellowship is awarded to support post-doctoral scientists who recently completed their graduate degree work, and whose research holds promise to provide new insights into the pathophysiology, etiology, and treatment of PD.

This year’s awardees are:

Andrew Monaghan, PhD 
Emory University, Atlanta, GA
Project Title:
Electrophysiological characterization of neural circuit pathophysiology underlying freezing of gait 
Major question to be answered:
What are the electrophysiological biomarkers of freezing of gait (FoG) that can be identified using mobile electroencephalography (EEG)?
Why is this important?
This study will use mobile EEG to characterize irregular brain activity patterns that occur before and during episodes of FoG. Knowing the electrophysiological signals in the brain before these events can help with anticipating, monitoring, and prevention of FoG.  They could also provide neurophysiological input for adaptive interventions, such as deep brain stimulators or wearable cueing devices, to intervene during FoG episodes.

Yuxiao Ning, PhD
The Regents of the University of Minnesota, Twin Cities, Minneapolis-Saint Paul, MN
Project Title:
Multiregional neural population dynamics in PD and during directional deep brain stimulation (DBS) 
Major question to be answered:
How does PD disrupt the basal ganglia thalamocortical (BGTC) circuitry and how does DBS correct these disruptions? 
Why is this important?
PD impairs the brain’s BGTC network, which controls movement and cognition, whereas DBS in certain brain regions can improve PD symptoms. In this study, neuronal activity across multiple regions of the brain’s network will be recorded with and without DBS. The activity will be analyzed using advanced machine learning techniques to understand the role that DBS plays in correcting the disrupted circuitry.      

Brianne Rogers, PhD
HudsonAlpha Institute for Biotechnology, Huntsville, AL
Project Title: 
Mechanisms of SNCA regulation 
Major question to be answered:
What are the genetic regulatory elements controlling expression of the a-syn gene SNCA?
Why is this important?
This project will explore the genetic elements that drive the expression of a-syn. A comprehensive understanding of SNCA regulatory elements and the genetic variation that affects SNCA expression, can help expand potential therapeutic avenues for PD treatment. 

Carlos Soto-Faguás, PhD
Oregon Health & Science University, Portland, OR
Project Title:                                                                       
The effects of the ApoE Christchurch variant on Lewy body pathology development and spreading         
Major question to be answered:
What are the effects of the ApoE Christchurch mutation in the development and propagation of a-syn pathology using transgenic mouse models?
Why is this important?
Recently, a genetic mutation in the ApoE gene, called ApoE Christchurch, has been identified which appears to be protective against Alzheimer’s disease pathology and clinical dementia. This project will study whether the ApoE Christchurch mutation is also protective against the development and propagation of Lewy bodies, the pathological hallmark of PD.

Donghe Yang, PhD
Memorial Sloan Kettering Cancer Center , New York, NY
Project Title:                           
Characterizing and modeling the development of human A9 midbrain dopaminergic neurons with pluripotent stem cells
Major question to be answered:
What are the key processes that lead to the development of the specific type of dopamine neurons that is susceptible to neurodegeneration in PD? 
Why is this important?
This project will identify factors that influence the development of the specific subtype of dopamine neurons that degenerate in PD and assess the functional properties of these neurons. The project will also evaluate the therapeutic efficacy of these neurons as a cell-based therapy in animal models of PD, advancing the understanding of using such therapies to treat PD.

We also continue to support Abdulmunaim Eid, MD who is in the second year of his two-year post-doctoral fellowship.

Research Grants

The APDA Research Grant is awarded to investigators performing innovative research into the pathophysiology, etiology, and/or treatment of PD.

This year’s awardees are:

Patricia Aguilar Calvo, PhD  
University of Alabama at Birmingham, Birmingham, AL
Project Title:  
Heparan-sulfate mediated mechanisms of a-syn propagation in PD
Major question to be answered:
How do heparan sulfate proteoglycans modulate the propagation and clearance of a-syn aggregates in the nervous system?
Why is this important?
Heparan sulfate proteoglycans are found on the cell surface of many types of cells and are involved in a variety of biological activities. This project will investigate their role in cell-to-cell propagation, aggregation, and clearance of a-syn.

Athanasios Alexandris, MD              
Johns Hopkins University School of Medicine, Baltimore, MD
Project Title:  
Investigating the role of a-synucleinopathy in axonal protein homeostasis and viability 
Major question to be answered:
How does a-syn aggregation affect axons, the nerve cell extensions that transmit brain signals?
Why is this important?
Axonal degeneration is an early event in neurodegenerative disease, impairing brain connectivity before nerve cells die. This project will focus on how a-syn disrupts axonal localization and translation of mRNA, the template for producing proteins in axons which are crucial for their maintenance, plasticity, and repair. An understanding of the connection between abnormal a-syn and axonal survival and function will offer new ideas about why axons are vulnerable in neurodegeneration.

Saar Anis, MD                        
Cleveland Clinic Foundation, Cleveland, OH 
Project Title:  
Deep brain stimulation (DBS) neural recordings of varied stimulation during sleep in Parkinson’s disease (The DREAMS-PD Study) 
Major question to be answered:
What is the impact of DBS settings on sleep efficiency?
Why is this important?
This project will monitor 10 participants for six weeks in their home environment, with each participant alternating between three different DBS settings every two weeks. They will wear a device to track their sleep, with the goal of determining which setting best enhances sleep quality, a vital aspect of overall well-being for people with PD.

(Want to learn more about deep brain stimulation (DBS)? We covered Adaptive DBS – a new approach to improve PD symptoms in this article.)

Helen Hwang, MD, PhD                     
Washington University School of Medicine, St. Louis, MO
Project Title:  
Characterization of inhibitors of a-syn fibril growth 
Major question to be answered:
Can a cell-based platform test potential drug candidates for the ability to inhibit a-syn fibril growth?
Why is this important?
A cellular platform will be developed to test potential drug compounds that can have disease-modifying effects in people with PD. This platform can then be used to screen for small molecules capable of inhibiting a-syn fibril growth. This tool will hopefully bring the field closer to identifying potential neuroprotective agents for PD. 

Francesca Magrinelli, MD, PhD                                
University College London Institute of Neurology, London, UK 
Project Title:  
Dissecting PSMF1 as a new gene for early-onset Parkinson’s disease/parkinsonism 
Major question to be answered:
How do genetic defects in PSMF1 cause neuronal death?
Why is this important?
PSMF1 has recently been identified as a new gene associated with early-onset PD and parkinsonism in multiple families, but its function is unknown. This project will unveil the biological mechanisms underpinning this newly identified genetic form of PD which likely also contributes to sporadic forms of PD.

Franchino Porciuncula, PT, DScPT, EdD    
Trustees of Boston University, Boston, MA
Project Title:  
Does rhythmic auditory stimulus (RAS) reduce the cognitive demands of walking in PD? 
Major question to be answered:
What are the effects of RAS on cognitive demands as indexed by brain activation during walking?
Why is this important?
This study will enroll 30 people with PD and investigate walking automaticity and its response to rhythmic cueing via RAS. Functional Near-Infrared Spectroscopy (fNIRS), a non-invasive, mobile device will monitor where brain activity occurs during walking and wearable sensors will measure leg movements during walking. Together, these measurements will give a thorough examination of walking automaticity and its response to rhythmic cueing via RAS and determine whether RAS reduces cognitive demand. This study will elucidate processes related to walking automaticity in PD, thereby allowing gait rehabilitation in PD to be more effective. 

Emily Rocha,  PhD                 
University of Pittsburgh, Pittsburgh, PA
Project Title:  
Lysosomal dysfunction in PD 
Major question to be answered:
Could TRPML1 be a disease modifying therapy to slow neurodegeneration in PD?
Why is this important?
Accumulation of aggregated proteins is a pathological hallmark of PD and could be due to dysfunctional lysosomes, the garbage collectors of the cell. TRPML1 transports positively charged molecules such as calcium from inside the lysosome to the rest of the cell, a process which regulates lysosomal function and may promote lysosomal health.  This project seeks to determine if targeting TRPML1 could be a disease modifying strategy to improve lysosomal health and halt the progression of PD. 

Mariangela Scarduzio, PhD            
University of Alabama at Birmingham, Birmingham, AL 
Project Title:  
Striatal acetylcholine dynamics in L-DOPA-induced dyskinesia 
Major question to be answered:
How do fluctuating levels of the neurotransmitter dopamine (DA) affect the levels of acetylcholine (ACh), another neurotransmitter involved in movement regulation, to contribute to levodopa induced dyskinesia (LID)?  
Why is this important?
Previous research has suggested that the loss of DA in PD is accompanied by an opposite increase in Ach signaling. Treatment with L-DOPA, while replacing DA and ameliorating motor symptoms, does not fix ACh transmission, which rather becomes more dysfunctional, possibly contributing to the development of the involuntary movements of LID. This project will focus on how striatal ACh spontaneous oscillations evolve as DA levels decrease, and LID develops in a mouse model of PD. Understanding the interplay between DA and Ach will contribute to new ways of controlling LID.

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