R. Suzanne Zukin is an American neuroscientist and a professor of
neuroscience who directs a research lab as a F. M. Kirby Chair in Neural Repair and Protection and director of the Neuropsychopharmacology Center at
Albert Einstein College of Medicine.[1] Zukin's areas of research include
neurodegenerative disorders, Ischemia,
Epigenetics and
Autism and uses
molecular biology approaches to research these disorders. Zukin has made seminal contributions to the understanding of
NMDA and
AMPA receptor function and activity.[2][3][4][5][6]
Early career
After receiving a bachelor's degree from
Bryn Mawr College in 1970,[7] Zukin started her path as a molecular biologist with an understanding of protein structure-function relationships while working on her doctoral dissertation with Donald P. Hollis at
Johns Hopkins Medical School.[8] She subsequently pursued postdoctoral work with
Daniel E. Koshland Jr. at
UC Berkeley where she investigated ligand binding and conformational changes in sensory receptors.[citation needed]
Neuroscience career and research
In 1977 Suzanne Zukin joined the department of Biochemistry at Albert Einstein College of Medicine.[9]
Currently, the lab is part of the Neuroscience department at Albert Einstein, where Zukin presides as Director of the Neurophsycopharmacology Center[10] and F.M. Kirby Chair in Neural Repair and Protection.[9]
Currently, the lab is pursuing the following research questions related to molecular mechanisms of dysregulation of gene expression of synaptic proteins:[1]
Epigenetic control of synaptic proteins: The Zukin lab researches epigenetic mechanisms that underlie neuronal death in animal models of
stroke. They investigate the role of the gene silencing transcription factor
RE1-silencing transcription factor (REST) and REST-dependent epigenetic remodeling of genes encoding synaptic proteins. The lab also pursues
REST mediated experience-tuning expression of
NMDA receptors during development, demonstrating that maternal deprivation disrupts a REST mediated switch to mature NMDA receptor expression[11]
Molecular pathways leading to aberrations in
Autism and
fragile X syndrome: The Zukin lab aims to identify protein expression dysregulation that may result in the phenotypes observed in
autism spectrum disorders. The lab has found that the downstream targets of
mTORC2,
Rho GTPaseRac1 and
LIMK exhibit increased expression in a mouse model of autism.[12] Elevated expression of proteins in this pathway are causally related to reduced activity of the actin depolymerizing factor
Cofilin, a major determinant of
dendritic spine morphology.[12] Another marker of fragile X syndrome that the lab identified is an elevation of
GluA2 (
GluR2)
mRNA as a result of increased
CPEB3 protein expression. Elevated GluA2 mRNA increases the percent of AMPA receptors containing GluA2, thus potentially altering the transmission properties and excitation properties of neurons in the brains of individuals with
autism spectrum disorders.
Awards and honors
2009 McKnight Foundation Neuroscience of Brain Disorders Award[9]
F.M. Kirby Chair in Neural Repair and Protection[9]
Director of the Neurophsycopharmacology Center at Albert Einstein College of Medicine[10]
Standing member of the NIH Study Section on Neural Oxidative Metabolism and Death for the National Institute for Neurologic Disorders & Stroke[14]
2014 Brain and Behavior Research Foundation Distinguished Investigator award for "REST-dependent epigenetic remodeling of NMDA receptors as a risk factor in schizophrenia."[9]