Dr. Giuseppe Cortese, Associate Professor, Joins the Weissman Hood Institute at Touro University (aka MRI) (Copy)

We are very glad to welcome Dr. Giuseppe Cortese to the MRI/WHIT.  Giuseppe joins us from Montana State University – Northern where he served as an Associate Professor.  Prior to that he was on the faculty of Northern Michigan University and a Research Scientist at Columbia University.  He received his BA degree in physiology from the University of Minnesota, his doctoral degree in Neuroscience and Psychology from the University of Colorado, and postdoctoral work at Columbia University and the University of Wisconsin.  Giuseppe’s areas of research focus are based in neuroscience where he has investigated:

1. Neurodegenerative Disorders: Synaptic dysfunction associated with Alzheimer’s disease (AD) and Parkinson’s disease (PD). To better understand mechanism, our lab is using in vitro neuronal cell models to investigate synaptic mechanisms (both ion channel proteins and synaptic vesicle proteins) that may be targeted early in the course of AD pathology.

2. Psychiatric Disorders: A chromosomal microdeletion at region q11.2 of human chromosome 22, clinically referred to as22q11.2 Deletion Syndrome, presents the highest risk for developing Schizophrenia to date. In our lab, we are using a mouse model of the 22q11.2 microdeletion to uncover the neurobiology that may underlie behavioral and neurophysiological deficits observed in 22q11.2DS, which has greater implications for understanding general schizophrenia. Additionally, ~77% of patients with 22q11.2DS have some form of immune dysfunction. We are exploring neuro-immune mechanisms to determine the inflammatory contribution to phenotype in this genetic model.

3. Inflammation: Immune challenges that result in an exaggerated inflammatory response in the brain are known to be associated with several neurodegenerative, psychiatric, and neurodevelopmental disorders. Our lab seeks to understand the interactions between elevated levels of pro-inflammatory cytokines (like IL-1b and TNFa) and neuronal function.

4. Apoptosis: Mitochondrial dysfunction seems to be strongly associated with neurological disorders. More specifically, mitochondrial-dependent cell death via excessive cytochrome c release results from the loss-of-function mutations in the Park2 gene (second most common cause of familial Parkinson’s disease)20. Our lab seeks to determine if mitochondrial-dependent aberrations and cell death mechanism underlie neuron loss in other neurological disorders.

Welcome to MRI/WHIT, Giuseppe.  We know you will be very successful here.