Carlos A. Pardo, M.D.

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Carlos A. Pardo, M.D.
M.I.N.D. Institute Distinguished Lecturer Series – January 9, 2008
Biographical Information
Carlos A. Pardo, M.D., is an associate professor of neurology and pathology (neuropathology) in the
Division of Neuroimmunology and Neuroinfectious Disorders at Johns Hopkins University School of
Medicine. He also serves as co-director of the Transverse Myelitis Center, staff neurologist of the
Multiple Sclerosis Center and a member of the HIV Neurosciences Research Group at Johns Hopkins
Hospital. His medical specialization and clinical focus is on neuroimmunological and infectious disorders
of the nervous system, with particular focus on multiple sclerosis, transverse myelitis and neurological
complications of autoimmune disorders. Dr. Pardo’s research interests focus on neuroimmunology and
neuropathology and his laboratory research includes studies of immunopathological mechanisms in
neurodevelopmental disorders such as autism, epilepsy and Rasmussen’s syndrome; the role of cytokines,
chemokines and chemokines receptors in neurological disorders; animal models of neurological disorders;
and immunopathological and molecular mechanisms of disease in HIV neurological disorders. His
research has been funded through the National Institutes of Health, The Epilepsy Foundation of America,
Cure Autism Now, The Peter Emch Fund for Autism Research and The Bart Mclean Fund for
Neuroimmunology Research.
Presentation Abstracts
Is Neuroimmunity Involved in the Pathogenesis of Autism?(4 pm)
Autism is a complex neurodevelopmental disorder of early onset that is highly variable in its clinical
presentation. Although the causes of autism in most patients remain unknown, several lines of research
support the view that both polygenic and environmental factors influence the development of abnormal
cortical circuitry that underlies autistic cognitive processes and behaviors. The role of the immune system
in the development of autism is controversial. Several studies showing peripheral immune abnormalities
support immune hypotheses, however until recently there have been no demonstration of immune
abnormalities within the central nervous system (CNS). Our laboratory recently demonstrated the
presence of neuroglial and innate neuroimmune system activation in brain tissues and cerebrospinal fluid
of patients with autism, findings that support the view that neuroimmune abnormalities occur in the CNS
of autistic patients and may contribute to the diversity of the autistic phenotypes. The role of neuroglial
activation and neuroinflammation is still uncertain but could be critical in maintaining, if not also in
initiating, some of the CNS abnormalities present in autism. A better understanding of the role of
neuroinflammation in the pathogenesis of autism may have important clinical and therapeutic
implications. Future studies should focus on the interaction of neuroimmune factors and brain
development as a factor involved in the pathogenesis of autism.
Is There Brain Inflammation in Autism? (6 pm)
Autism is a complex neurodevelopmental disorder of early onset that is highly variable in its clinical
presentation. The role of the immune system in the development of autism is controversial. Several
studies showing peripheral immune abnormalities support immune hypotheses. However, until recently
there have been no demonstration of immune abnormalities within the central nervous system (CNS). Our
laboratory recently demonstrated the presence of neuroglial and innate neuroimmune system activation in
brain tissues and cerebrospinal fluid of patients with autism, findings that support the view that
neuroimmune abnormalities occur in the CNS of autistic patients and may contribute to the diversity of
the autistic phenotypes. The role of neuroglial activation and neuroinflammation is still uncertain but
could be critical in maintaining, if not also in initiating, some of the CNS abnormalities present in autism.
A better understanding of the role of neuroinflammation in the pathogenesis of autism may have
important clinical and therapeutic implications.
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