Steven M. LeVine, Ph.D.

Professional Background

Dr. Steven LeVine earned his BA in Biology from the University of California at Berkeley and his MA and PhD in Pathology from Albert Einstein College of Medicine. He did his Postdoctoral training at the University of California at Los Angeles. In 1990, he started an Assistant Professor in the Department of Physiology at the University of Kansas Medical Center and progressed through the ranks and is currently a full Professor. Dr. LeVine's research has focused largely on diseases of the central nervous system with an emphasis on demyelinating diseases (i.e., multiple sclerosis and Krabbe's disease) and Alzheimer's disease.

• BA, Biology, University of California at Berkeley
• MS, Pathology, Albert Einstein College of Medicine
• PhD, Pathology, Albert Einstein College of Medicine
• Post Doctoral Fellowship, Neuroscience, University of California at Los Angeles

Research

Overview

We perform translational research that is directed at identifying pathogenic mechanisms and investigating experimental interventions for Alzheimer’s disease, globoid cell leukodystrophy (Krabbe's disease), and multiple sclerosis. Earlier work included studies on mechanisms of toxin-induced vessel injury and method development.

• LeVine Steven M. 2026. Reexamining the Role of Amyloid β Clearance from the Brain: Exporting Labile Iron from the Interstitial Fluid Performs a Protective Function. Int J Mol Sci, 27 (3), 1485. https://pubmed.ncbi.nlm.nih.gov/41683906/
• LeVine SM. 2024. Exploring Potential Mechanisms Accounting for Iron Accumulation in the Central Nervous System of Patients with Alzheimer's Disease. Cells, 13 (6), 689. https://pubmed.ncbi.nlm.nih.gov/38667304/
• LeVine SM. 2024. The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration. Neuroscientist, 30 (5), 525-544. https://pubmed.ncbi.nlm.nih.gov/37599439/
• LeVine SM. 2023. Examining the Role of a Functional Deficiency of Iron in Lysosomal Storage Disorders with Translational Relevance to Alzheimer’s Disease. Cells, 12 (22), 2641. https://pubmed.ncbi.nlm.nih.gov/37998376/
• LeVine SM, Tsau S, Gunewardena S. 2023. Exploring whether iron sequestration within the CNS of patients with Alzheimer’s disease causes a functional iron deficiency that advances neurodegeneration. Brain Sciences, 13 (3), 511. https://pubmed.ncbi.nlm.nih.gov/36979320/
• LeVine SM, Tsau S. 2022. Substrate reduction therapy for Krabbe disease: Exploring the repurposing of the antibiotic D-cycloserine. Frontiers in Pediatrics, 9, 807973. https://pubmed.ncbi.nlm.nih.gov/35118033/
• Pan X, Sands SA, Yue Y, Zhang K, LeVine SM, Duan D. 2019. An engineered galactosylceramidase construct improves AAV gene therapy for Krabbe disease in twitcher mice. Human Gene Therapy, 30 (9), 1039-1051. https://pubmed.ncbi.nlm.nih.gov/31184217/
• LeVine SM. 2016. Albumin and multiple sclerosis. BMC Neurology, 16, 47. https://pubmed.ncbi.nlm.nih.gov/27067000/
• Tsau S, Emerson MR, Lynch SG, LeVine SM. 2015. Aspirin and multiple sclerosis. BMC Medicine, 13, 153. https://pubmed.ncbi.nlm.nih.gov/26123634/
• Biswas S, LeVine SM. 2002. Substrate-reduction therapy enhances the benefits of bone marrow transplantation in young mice with globoid cell leukodystrophy. Pediatric Research, 51 (1), 40-7. https://pubmed.ncbi.nlm.nih.gov/11756638/