Betty A. Diamond, M.D.
M.I.N.D. Institute Distinguished Lecturer Series – November 9, 2009
Biographical Information
Betty Diamond received an MD from Harvard Medical School in 1973. She completed a residency in
Internal Medicine at Columbia Presbyterian Medical Center, and then a post-doctoral fellowship in
Immunology with Dr. Matthew Scharff at the Albert Einstein College of Medicine. A former faculty
member at both Einstein and Columbia University, she was recently appointed Head of The Center for
Autoimmune and Musculoskeletal Disease at the Feinstein Institute for Medical Research. Dr. Diamond’s
primary interests are in the mechanisms of central and peripheral tolerance of autoreactive B cells, the
defects in these mechanisms that are present in autoimmune disease, and the role of antibodies in brain
disease.
Presentation Abstract
4:30 p.m.
Autoantibodies and the Brain: Lessons from Lupus
Systemic lupus erythematosus (SLE) is a disease characterized by the production of multiple
autoantibodies, most notably antibodies to double stranded DNA. A subset of these anti-DNA antibodies
cross-reacts with the NR2A and NR2B subunits of the NMDA receptor. This receptor is the primary
molecular mechanism for controlling synaptic plasticity and memory function. These antibodies are
present in serum of approximately 50% of patients. They can be found in cerebrospinal fluid of patients
with neuropsychiatric lupus, and their titers correlate with symptomatology. They can also be found in
brain tissue. In vivo in mice, they mediate memory loss if they access the hippocampus or impaired fear
conditioning if they access the amygdala. These antibodies modulate excitatory post synaptic potentials
at low concentration and induce mitochondrial transition permeability and apoptosis at high
concentration. When these antibodies are present in serum of pregnant mice, they alter fetal brain
development in a dose dependent fashion and can lead to permanent but isolated cognitive impairments.
Dr. Diamond will present information from studies that show that: 1) anti-brain antibodies may be
responsible for multiple instances of altered cognition and behavior in adults, and altered brain
development in fetuses, and 2) such antibodies may arise in susceptible individuals in response to
microbial challenge. She will also discuss studies of anti-pneumococcal antibodies that support this
hypothesis.