Maria Traka, Ph.D.Profile page
Associate Professor
Anatomy
BIO
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.
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.
MIDWESTERN UNIVERSITY APPOINTMENTS
- Associate ProfessorCollege of Dental Medicine-Illinois
- Associate ProfessorCollege of Graduate Studies - Illinois
DEGREES
- Ph.D.University of Crete, Heraklion, Greece2002
- M.S.University of Crete, Heraklion, Greece1997
- B.S.University of Crete, Heraklion, Greece1993
LANGUAGES
- EnglishCan read, write, speak, understand and peer review
- Greek, Modern (1453-)Can read, write, speak, understand and peer review
- FrenchCan read, write, speak and understand
AVAILABILITY
- IL-MABS Student Research
- IL-MBS Student Research
- CCOM Student Research
ACADEMIC DEGREE PROGRAM
- Doctor of Dental Medicine (D.M.D.)
- Doctor of Osteopathic Medicine (D.O.)
- Master of Arts in Biomedical Sciences (M.A.)
- Master of Biomedical Sciences (M.B.S.)
- Doctor of Optometry (O.D.)
- Master of Medical Sciences in Physician Assistant Studies (M.M.S.)
CAMPUS
- Downers Grove