Giuseppe P. Cortese

Assistant Professor

Contact Information:

2007 Weston Hall
Office Phone: (906) 227-2218
gcortese@nmu.edu

Personal web page

Education and Research Training:

  • 2017-2019 - Associate Research Scientist, Columbia University
  • 2015-2017 - Postdoctoral Research Associate, University of Wisconsin
  • 2013-2015 - Postdoctoral Research Scientist, Columbia University
  • 2008-2013 - Ph.D. in Neuroscience & Psychology, University of Colorado
  • 2008-2010 - M.A. in Neuroscience & Psychology, University of Colorado
  • 2006-2008 - Post-Baccalaureate (A.L.M.) in Biology, Harvard University
  • 2001-2005 - B.A. in Physiology, University of Minnesota

Research Interests:

The Cortese Lab is housed in the Department of Biology at Northern Michigan University, and is a member of the interdisciplinary Neuroscience Program here at NMU. Our goal is to uncover neurobiological mechanisms that may cause behavioral and physiological phenotypes associated with neurodegenerative and neurodevelopmental disorders, specifically Alzheimer's disease and Schizophrenia. Additionally, we are interested in identifying the influential role neuroinflammation and neuroinflammatory mediators may play in disease phenotype. In the lab, we employ a variety of scientific techniques and tools to explore behavior, physiology, and mechanism in rodent models of disease and neuronal cell lines. We hope that our work will identify novel disease mechanisms to further diagnostic and therapeutic efforts. 

Ongoing research projects in the lab

  1. Neurodegenerative Disorders: One of the earliest events in Alzheimer’s disease (AD) is synaptic dysfunction, which can lead to significant alterations in ion channel activity, neurotransmitter release, and neurotransmission as whole. In an effort 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 as 22q11.2 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. Thus, we are exploring neuro-immune mechanisms to determine the inflammatory contribution to phenotype in this genetic

Teaching:

  • BI 207 - Human Anatomy and Physiology I
  • BI 417 - Comparative Vertebrate Neuroanatomy

Selected Publications:

  1. de Jong JO, Llapashitca C, Genestine M, Strauss K, Provenzano F, Sun Y, Zhu J, Cortese GP, Brundu F, Brigatti KW, Corneo B, Migliori B, Tomer R, Kushner SA, Kellendonk C, Javitch JA, Xu B, Markx S. Cortical overgwoth in a preclinical forebrain organoid model of CNTNAP2-associated autism spectrum disorder. Nature Communications, 12(1):4087, 2021.
  2. Rigby MJ, Ding Y, Farrugia MA, Feig M, Cortese GP, Mitchell H, Burger C, Puglielli L.  The endoplasmic reticulum acetyltransferases ATase1/NAT8B and ATase2/NAT8 are differentially regulated to adjust engagement of the secretory pathway.  Journal of Neurochemistry, 16:e14958, 2020.
  3. Zu M, Cortese GP*, Waites C. Parkinson's disease-linked Parkin mutations impair glutamatergic synaptic transmission and plasticity. BMC Biology, 16(1):100, 2018. (*co-first author).
  4. Tanaka N, Cortese GP, Barrientos RM, Maier SF, Patterson SL.  Aging and an immune challenge interact to produce prolonged, but not permanent reductions in hippocampal L-LTP and mBDNF in a rodent model with features of delirium. eNeuro, 5(3), 2018.
  5. Cortese GP, Olin A, O’Riordan K, Hullinger R, Burger C.  Environmental enrichment improves hippocampal function in aged rats by enhancing learning and memory, and mGluR5-Homer1c activity.  Neurobiology of Aging, 63:1-11, 2018.
  6. Cortese GP, Zhu M, Williams D, Heath S, Waites C. Parkin deficiency reduces glutamatergic neurotransmission by impairing AMPA receptor endocytosis.  Journal of Neuroscience, 36(48):12243-12258, 2016. 
  7. Cortese GP & Burger C.  Neuroinflammatory challenges compromise neuronal function in the aging brain: Postoperative cognitive delirium and Alzheimer’s Disease.  Behavioural Brain Research, pii: S0166-4328(16):30539-3, 2016. 
  8. Johnson BN, Berger AK, Cortese GP, Lavoie MJ. The Ubiquitin E3 ligase Parkin regulates the proapoptotic function of Bax.  PNAS, 109(16):6283-8, 2012.
  9. Cortese GP, Barrientos RM, Maier SF, Patterson SL.  Aging and a peripheral immune challenge interact to reduce mature brain-derived neurotrophic factor and activation of TrkB, PLCγ1, and ERK in hippocampal synaptoneurosomes.  Journal of Neuroscience, 16;31(11):4274-9, 2011. 
  10. Berger AK, Cortese GP*, Amodeo KD, Weihofen A., Letai AG, LaVoie MJ.  Parkin selectively alters the intrinsic threshold for mitochondrial cytochrome c release.  Human Molecular Genetics, 18(22):4317-28, 2009. (*co-first author)
  11. LaVoie MJ, Cortese GP, Ostaszewski BL., Schlossmacher MG.  The effects of oxidative stress on parkin and other E3 ligases.  Journal of Neurochemistry, 103(6):2354-68, 2007.
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Giuseppe P. Cortese headshot