Dr. Patrick Heilman holds a B.S. and a Ph.D. in biochemistry from Duquesne University of the Holy Spirit and Ohio State University, respectively. At OSU, his graduate studies focused on uncovering the consequences of peripheral neuropathy-associated mutations in heat shock protein B1 in a model of amyotrophic lateral sclerosis (ALS), a progressive, neurodegenerative disease marked by loss of movement and muscle control. In 2018, he joined the laboratory of Dr. Lena Brundin at Van Andel Research Institute as a postdoctoral fellow.
Increasing evidence suggests that inflammation plays an important role in the onset and progression of many neurological conditions, including depression and Parkinson’s disease. As a postdoctoral fellow in the lab of Dr. Lena Brundin, Dr. Heilman studies the role of an enzyme called ACMSD, which regulates the production of quinolinic acid (QUIN), a neurotoxin closely linked to inflammation. If ACMSD isn’t functioning properly, QUIN levels can spike, causing cellular damage and death. Dr. Heilman’s work focuses on better understanding ACMSD’s role in neurodegeneration, particularly through development and use of CRISPR-Cas9 knock-out models. His ultimate goal is to identify inflammatory biomarkers for Parkinson’s.
Ph.D. in biochemistry, Ohio State University (Advisor: Stephen J. Kolb, M.D., Ph.D.)
Thesis: Interrogating the functional consequences of peripheral neuropathy associated mutations in head shock protein B1
B.S. in biochemistry, Honors College of Duquesne University of the Holy Spirit (Advisor: Ellen Gawalt, Ph.D.)
Undergraduate Research Fellowship, Duquesne University of the Holy Spirit (2007–2009)
To view lists of Dr. Heilman’s selected publications, abstracts and oral presenations click below.
Keaton SA, Madaj ZB, Heilman P, Smart L, Grit J, Gibbons R, Postolache TT, Roaten K, Achtyes ED, Brundin L. 2019. An inflammatory profile linked to increased suicided risk. J Affect Disord 247:57 65.
Heilman PL, Song SW, Miranda C, Meyer K, Wier CG, Knapp AR, Kaspar BK, Kolb SJ. 2017. Hereditary neuropathy-associated HSPB1 mutations disrupt non-cell autonomous protection of motor neurons. Exp Neurol 7(297):101–109.