Gerardo A Morfini

Associate Profesor

College of Medicine at Chicago - Basic Sciences
Department of Anatomy and Cell Biology

Research Interests

  • The unique ability of neurons to receive, process, and transmit information depends upon the polarized distribution of cellular components within discrete subcellular compartments (i.e., axons and dendrites). Such distribution in turn depends upon intracellular trafficking events executed by motor proteins, a process collectively referred to as axonal transport. An illumination of molecular mechanisms regulating axonal transport is therefore critical for a comprehensive understanding of neuronal function.
  • Within this context above, our studies over the last years identified specific protein kinases that regulate AT by phosphorylating motor proteins. These findings bear significant implications for the pathogenesis of human neurodegenerative diseases including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and Amyotrophic Lateral Sclerosis, as all these diseases feature abnormal activation of protein kinases and deficits in axonal transport.
  • Our current research aims to evaluate the contribution of specific protein kinases to the progressive loss of neuronal connectivity that characterizes neurodegenerative diseases. Knowledge derived from this work will provide a conceptual framework for the development of novel therapeutic targeting based on kinase inhibitors to preserve axonal transport and neuronal function.
  • Selected publications
  • - Leo L, Weissmann C, Burns M, Kang M, Song Y, Qiang L, Brady ST, Baas PW, Morfini G. (2017) Mutant spastin proteins promote deficits in axonal transport through an isoform-specific mechanism involving casein kinase 2 activation. Hum Mol Genet. 15;26(12):2321-2334.
  • - Gatto et al (2015). Analysis of YFP(J16)-R6/2 reporter mice and postmortem brains reveals early pathology and increased vulnerability of callosal axons in Huntington's disease. Hum Mol Genet. 24(18):5285-98.
  • - Morfini et al (2013). Inhibition Of Fast Axonal Transport By Pathogenic SOD1 Involves Activation of P38 MAP Kinase. PLOS One 8(6):e65235.
  • - Bosco et al (2010) Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS. Nat. Neurosci. 13(11):1396-403.
  • - Pigino, et al. (2009) Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta. Proc. Natl. Acad. Sci. USA 106, 5907-5912.
  • - Morfini et al (2009) Axonal transport defects in neurodegenerative diseases. J. Neurosci. 29, 12776-12786.
  • - Morfini et al (2009) Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin. Nat. Neurosci. 12, 864-871.

At a Glance

  • Title Associate Profesor
  • College College of Medicine at Chicago - Basic Sciences
  • Department Department of Anatomy and Cell Biology
Contact the Researcher Back to Search

Contact the Researcher

The URE website is only for undergraduate student researchers.

Sign in with your UIC account to contact this researcher. Log in