Faculty
Maria Traka, Ph.D.
Mechanisms of demyelination and remyelination in adult-onset CNS and PNS demyelinating diseases. Role of N-Acetylaspartate (NAA) in the CNS and in Canavan disease pathogenesis Demyelinating diseases of the central and the peripheral nervous system I am interested in the biology of myelinating glial cells i.e. oligodendrocytes in the CNS and Schwann cells in the PNS that produce the myelin sheath, which is the lipid-rich membrane that wraps around the axons and ensures the saltatory propagation of the neuronal action potential. In demyelinating diseases of the central nervous system (CNS) such as multiple sclerosis (MS) and leukodystrophies i.e. the genetic disorders affecting the white matter in the CNS, as well as in demyelinating diseases of the peripheral nervous system (PNS) such as demyelinating Charcot-Marie-Tooth (CMT) diseases the myelin sheath is significantly damaged, leading to motor and sensory dysfunction causing serious neurological deficits. In my lab, we are using genetic mouse models and primary neural cell culture systems to investigate the cellular and molecular mechanisms of myelin and neuronal damage that occurs in CNS and PNS demyelinating diseases as well as to identify new molecular targets to promote myelin repair and restore neuronal function in these devastating neurological diseases. We have developed several mouse models for CNS neurodegenerative diseases: the Aspanur7 mouse, which is an authentic model for the fatal childhood leukodystrophy Canavan disease and has helped uncover critical information regarding the pathogenesis of this disease ( Traka et al., J Neurosci. 2008 ); the Wdr81nur5 mouse model for cerebellar ataxia, mental retardation and quadrupedal locomotion syndrome (CAMRQ2; Traka et al., J Neurosci. 2013 ); the diphtheria-toxin A chain (DTA) mouse model that allows for the tamoxifen-induced ablation of oligodendrocytes throughout the CNS. Our studies on the DTA mouse have revealed that the CNS has a robust innate capacity to repair myelin damage and restore neuronal function upon inducing oligodendrocyte cell loss ( Traka et al., Brain 2010 ). Moreover, we recently used the DTA mouse to show that oligodendrocyte death might be the primary trigger of MS ( Traka et al., Nat Neurosci. 2016 ; Nature Reviews Neuroscience 17, 76, 2016 ). This finding is of fundamental importance to our understanding of the origins of the autoimmunity that characterizes MS and it might lead to the development of new therapeutic approaches to the treatment of this devastating disease in the future.
Faculty
Hilal Arnouk, M.D., Ph.D.
Hilal Arnouk, MD, PhD is an Associate Professor at the Department of Pathology at Midwestern University. Dr. Arnouk has received his education and post-doctorates training at Roswell Park Cancer Institute , the State University of New York at Buffalo , the Medical College of Georgia and the University of Alabama at Birmingham . He has directed research studies in academia and biotech industry settings. His major areas of expertise include Cancer Immunotherapy, Biomarker Discovery and Precision Medicine. Dr. Arnouk also enjoys being an educator for professional students in the medical and biomedical sciences.
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