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Immune Cell Dysfunction in PINK1 Parkinson’s Models

This grant builds upon the research from a prior grant: Advancing PINK1 Knockout Models of Parkinson’s

Promising Outcomes of Original Grant:
In our previous project, we significantly advanced the characterization of PINK1 knockout (KO) models. We found evidence of innate and adaptive immune cell dysfunction in PINK1 KO models that coincides with the robust age-dependent locomotor phenotype of these models. We hypothesize that the axon terminal degeneration we observe in PINK1-deficient models is caused by aberrant over-activation of immune cells that can release reactive oxygen species and damage axon terminals.

Objectives for Supplemental Investigation:
In this project, we will determine more specifically which cells are altered by PINK1 deficiency and how that relates to axon terminal degeneration in PINK1 KO models. We will use flow cytometry to examine immune cell populations and phenotypes. We will also map which immune signaling pathways are most altered by PINK1 deficiency.

Importance of This Research for the Development of a New PD Therapy:
The mechanisms by which loss-of-function mutations in the PINK1 and PRKN genes cause recessively inherited forms of PD remain uncertain. The results of our previous project, together with recent publications, indicate that PINK1 functions to limit immune responses that could damage cells. Our studies will pinpoint more specifically which immune cells and which signaling pathways are most altered due to PINK1-deficiency. These studies are important to determine the most promising targets for PD therapeutic development.


  • Matthew S. Goldberg, PhD

    Birmingham, AL United States

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