Scientific Review Committee
The Brain Research Foundation Scientific Review Committee was established to review our research grant applications. This committee is a combination of researchers from several institutions throughout greater Chicago and nationwide. Their scientific expertise is invaluable when reviewing the Brain Research Foundation research grant proposals. Following is a brief description of each reviewer's research interests:
Chair
Sangram S. Sisodia, Ph.D.
The University of Chicago
Dr. Sangram Sisodia’s laboratory studies the molecular and cellular basis of Alzheimer's disease (AD), the most common cause of senile dementia. AD affects neurons in the neocortex, hippocampus and basal forebrain. Affected brain regions contain abundant levels of senile plaques composed of ß amyloid, derived from amyloid precursor proteins (APP). Early-onset, familial forms of AD (FAD) are caused by inheritance of genes encoding mutant variants of presenilin 1 (PS1), presenilin 2 (PS2), and APP. Research in his laboratory has focused on understanding the normal biology of PS1 and PS2, and the molecular and cellular mechanisms by which mutant PS and APP cause AD. To explore these issues, his laboratory has employed cellular and biochemical approaches, as well as transgenic and gene-targeted mouse models. The mouse models have offered important insights into disease pathogenesis and his laboratory has discovered critical genetic and environmental factors that influence these processes.
Members
Scott T. Brady, Ph.D.
University of Illinois at Chicago
The size and complex shapes of many neurons present unique challenges
in delivering essential components to the right places in the right
amounts. An efficient set of intracellular transport processes known as
axonal transport are required to generate and maintain the functional
architecture of neurons. Recent evidence suggests that many late onset
neurodegenerative diseases, including Alzheimer’s, Huntington’s, and
Parkinson’s disease, as well as ALS, are the result of disruptions in
this trafficking of proteins essential for neuronal function.
Remarkably, these often involve changes in the regulation of motor
proteins and targeting of cargoes carried by axonal transport. Based on
these approaches, Dr. Scott Brady’s lab is identifying novel pathogenic
mechanisms and new therapeutic targets by studying these changes in
neuronal transport mechanisms.
Judy L. Cameron, Ph.D
University of Pittsburgh
Dr. Judy Cameron, a renowned researcher of stress and resilience, has devoted her career to understanding how everyday life experiences, including stress exposure, and changes in diet and exercise affect brain function. Her research examines how an individual’s genetic predisposition interacts with exposure to different life events to lead to differences in the incidence of stress-related disease processes including the mental health problems of anxiety and depression, reproductive dysfunction and immune problems. She has tracked the developmental course of monkeys to uncover what makes some individuals more sensitive and others more resilient to stress—work that has profound implications for the development of prevention and early intervention programs for human physical and mental health. A major figure in the field of behavioral neuroscience, she continues to lead research that may one day enable clinicians to identify which individuals are most vulnerable to stress-sensitive diseases.
John F. Disterhoft, Ph.D.
Northwestern University
Dr. John Disterhoft is the Magerstadt Memorial Research Professor of Physiology at Northwestern University. Dr. Disterhoft studies the neurobiology of associative learning in the mammalian brain at the molecular, cellular and systems levels using both in vivo and in vitro techniques. His laboratory focuses on characterizing how neurons store new information during associative learning. An important component of his research program is identifying mechanisms for altered learning in aging. He uses a combination of behavioral, biophysical and molecular biological approaches to address these questions. Although most of his experiments are done with animals, he also studies learning in humans using behavioral and imaging techniques. Disterhoft’s laboratory is in a unique position to translate the findings from animal research to humans to better understand learning in the young and aging brain.
Jeffrey H. Kordower, Ph.D.
Rush University Medical Center
Dr. Jeffrey Kordower is a leading researcher in the fields of gene
therapy, neural transplantation, nonhuman primate models of
neurodegenerative disease and experimental therapeutic strategies for
Parkinson’s and Huntington’s disease. In 1995, he made the pioneering
demonstration that fetal transplants can survive in patients with
Parkinson’s disease; a paper that was published in
The New England Journal of Medicine. In 2000, he published the lead article in
Science,
demonstrating for the first time that gene delivery of a trophic factor
called GDNF can prevent degeneration and restore function in nonhuman
primate models of Parkinson’s disease. Dr. Kordower is a Scientific
Advisory Board (SAB) Member for numerous biotechnology companies and
foundations, including a founding member of the SAB for the Michael J.
Fox Foundation. Currently his main interests involve gene therapy and
cell replacement strategies using stem cells in rodent and nonhuman
primate models of Parkinson’s and Huntington’s disease.
A. Kimberley McAllister, Ph.D.
University of California
Research in McAllister's laboratory focuses on understanding the cellular and molecular mechanisms of synapse formation, competition, and elimination in the developing visual cortex. The lab studies the formation, persistence, and elimination of individual synapses between dissociated, cultured visual cortical neurons using time-lapse imaging. In addition to studying the cellular and molecular mechanisms of synapse formation and plasticity, her lab is also interested in elucidating the role for immune molecules in early postnatal cortical development. McAllister's lab is working to identify the role for cytokines and synaptic activity in regulating MHCI expression as well as detemrining the mechanisms that MHCI uses to negatively regulate cortical connectivity. Since these immune molecules are implicated in several neurodevelopmental disorders, including autism and schizophrenia, MHCI molecules could mediate the effects of the environment on cortical connectivity both during normal development and in neurodevelopmental disorders.
John L.R. Rubenstein, M.D., Ph.D.
University of California San Francisco
John Rubenstein, MD, PhD is a Professor in the Department of Psychiatry at the University of California San Francisco. He also serves as a Nina Ireland Distinguished Professor in Child Psychiatry at the Nina Ireland Laboratory of Developmental Neurobiology. His research focuses on the regulatory genes that orchestrate development of the forebrain. In the mammalian embryo, the forebrain is the portion of the neural tube where primitive cells are organized to form the cerebral cortex, the basal ganglia and other components of the adult brain -- the structures of the human brain most involved in key functions such as speech, language, cognition and fine motor skills.
Rubenstein's lab has demonstrated the role of specific genes in regulating neuronal specification, differentiation, migration and axon growth during embryonic development and on through adult life. His work may help to explain some of the mechanisms underlying human neurodevelopmental disorders such as autism.