Kathy Steece-Collier, PhD

• Professor of Translational Neuroscience

• Department of Translational Neuroscience
• Michigan State University College of Human Medicine
• Teaching Faculty, MSU Neuroscience Program

• Grand Rapids Research Center
• 400 Monroe Ave NW, Grand Rapids, MI 49503
• Phone: 616.234.0969
• Fax: 616.234.0991
• collie68@msu.edu

Biography

Dr. Kathy Steece-Collier is Professor of Translational Neuroscience in the College of Human Medicine at Michigan State University. For 30+ years, she has maintained dedication to development of improved therapeutics for individuals with Parkinson’s disease (PD). She was project leader for the MSU Udall PD Research Center of Excellence from 2009-2015, currently serves as Project Director for a SPARK-NS award (https://sparkns.org/programs/projects/; 01/2025-12/2026) and for a competitively funded NIH R01 award (2018-2029), and has had with continuous NIH funding since 2004. She is co-founder and Chief Scientific Officer at CavGene Therapeutics. Steece-Collier holds dual B.S. degrees in Biology and Chemistry, and a Doctorate in Physiology and Biophysics from University of Illinois. She did a post-doctoral fellowship in the department of Neuroanatomy at the University of Rochester.

A main research focus involves understanding the role of aberrant striatal plasticity, a characteristic of the parkinsonian brain, in therapy failure and symptom progression. She and her team employ preclinical models of PD and various precision medicine approaches including AAV-CaV1.3-shRNA targeted gene therapy and a CRISPR knock-in rat model of the human rs6265 SNP to understand the role of neurochemical and structural alterations, and circuit reorganization in therapy dysfunction in individuals with PD. Outside of her research life, she enjoys hanging out with friends, family and her horses.

• Steece-Collier Lab
• Dr. Steece-Collier's Pub Med publications

Education

Research Interests

Over the past 20+ years, I have maintained my dedication to the development of improved therapeutics for individuals with Parkinson’s disease (PD) with particular emphasis in understanding how striatal pathology impacts therapeutics for PD including levodopa (Sinemet) and regenerative dopamine terminal replacement strategies. Over the past 10+ years, our research has resulted in a series of studies examining the structural reorganization of cells and circuits in the basal ganglia associated with graft- and levodopa-induced dyskinesias, and molecular triggers that induce and/or maintain the dyskinetic state, and/or result in failure of DA treatment strategies. My current funding includes two R01 grants from NINDS to investigate: 1) the capacity and limitations of gene level silencing of a particular population of calcium channels, CaV1.3 channels, in the striatum using rAAV-CaV1.3-shRNA to prevent and reverse the devastating side-effect of the antiparkinsonian medication levodopa known as levodopa-induced dyskinesias (LID) using parkinsonian animal models (award period: 09/01/2018-08/31/2024); and 2) the impact of a common human single nucleotide polymorphism (SNP) on the on the ability to remodel the parkinsonian striatum with new DA terminals using neural grafting in a CRISPR knock-in rat model of the human SNP rs6265 BDNF as a model system (award period: 01/01/2019 – 12/31/2023).

Technical Expertise

• Stereotaxic surgery
• In vivo gene therapy
• Behavioral evaluations of motor performance in rodents
• Embryonic and adult brain microdissection
• Immunohistochemistry, immunofluorescence, immunoelectron microscopy
• Confocal and electron microscopy
• Stereological analyses
• Western blot
• In situ hybridization
• In vivo microdialysis
• Cell culture