Andrew Zimmerman

Andrew Zimmerman

Pediatric Neurologist, Associate Professor, Director of Medical Neuroscience, Center for Autism and Related Disorders, Kennedy Krieger Institute, Johns Hopkins Medicine, Broadway, Baltimore.
Phone: (443) 923-9150

Dr Zimmerman is a pediatric neurologist and research scientist at Kennedy Krieger Institute. He is also an associate professor of neurology and psychiatry at the Johns Hopkins University School of Medicine. Dr. Zimmerman is a diplomate of the American Board of Pediatrics, the American Board of Psychiatry and Neurology (special competence in child neurology), and has a continuing education recognition certificate from the American Board of Psychiatry and Neurology. He also holds memberships in the American Academy of Pediatrics, the American Academy of Neurology, the Child Neurology Society, the American Medical Association, and the Society for Neuroscience.

Dr. Zimmerman has been interested in research into possible relationships between nervous system disorders and the immune system. A variety of studies have shown that autistic patients have distinct abnormalities in their immune systems, including decreased immunoglobulins and T cells, as well as altered lymphocyte and natural killer cell functions. Dr. Zimmerman and colleagues recently found that rheumatoid arthritis and other autoimmune disorders are more common than expected in the families of children with autism. This leads to speculation that autoimmune disorders might be a sign of genetic susceptibility to autism.

Inflammatory Component in the Pathogenesis of Autism Spectrum Disorders.
Usually, autism disorders are described imprecisely and include the entire spectrum. However, it is important to separate subgroups, for instance Kanner in type, regressive or Asperger by virtue of the heterogeneity of clinical aspects. It has been demonstrated that autistic patients also have inflammation outside the CNS (in the bowel, for instance) and allergic inflammation. Recently, some studies have shown inflammation in the brain parenchyma involving reactive gliosis that can precede neuronal damage. Further research is needed to compare groups of patients and perhaps identify molecular targets in an attempt to offer new therapeutic approaches possibly including immunomodulation.