Rochester, Minnesota




In the Translational Neuroimmunology Lab of Charles L. Howe, Ph.D., Benjamin (Ben) D. Clarkson, Ph.D., studies how inflammatory cells and cytokines cause neuronal dysfunction in epilepsy, central nervous system autoimmune disease and neurodegenerative diseases. This includes studying changes in the balance of excitatory and inhibitory neurotransmission, trafficking and replacement of injured axonal mitochondria, as well as changes in neuronal transcription or translation induced by retrograde signals arising from inflamed axonal segments.

Dr. Clarkson and colleagues in the Translational Neuroimmunology Lab also investigate how acute systemic inflammation promotes seizure onset. The lab is currently working to develop a cell-based assay that may help determine diagnosis and prognosis for patients with idiopathic neurological symptoms or suspected novel autoimmune epilepsy.

Focus areas

  • Mitochondrial injury after axonal insult. Dr. Clarkson studies how axonal insults alter turnover of mitochondria and how failure of mitochondrial repair and replacement perpetuate axonal injury. He is also working to identify therapies that effectively prevent mitochondrial dysfunction or promote repair and test whether these therapies are effective distally when administered to neuronal cell bodies.
  • Multiple sclerosis. Dr. Clarkson is working to determine how myelin loss alters neuronal susceptibility to immune clearance. This involves measuring changes in neuronal expression of antigen processing and presentation genes following myelin loss or cytokine exposure and whether these changes make neurons more susceptible to attack by neuroantigen-specific cytotoxic T cells.
  • Immune-mediated synaptic dysfunction. Dr. Clarkson has developed a cell-based assay to measure changes in the patterns of spontaneous calcium transients arising in cultured neurons after exposure to specific inflammatory cytokines. He uses this assay to study how cytokines produced by glia and leukocytes alter synaptic transmission and cause cognitive impairment either acutely or insidiously in neurological diseases.
  • Autoimmune epilepsy. In collaboration with the Neuroimmunology Lab, Dr. Clarkson is working to determine how distinct auto-antibodies from patients with limbic encephalitis or other autoimmune epilepsies alter neuronal electrophysiology and synaptic transmission.

Significance to patient care

The goal of Dr. Clarkson's research is to prevent long-term neuronal dysfunction in patients with neuroinflammatory diseases. This includes testing drugs and gene therapy approaches for their ability to promote repair and replacement of injured axonal mitochondria, identifying druggable checkpoints along pathways of immune-mediated synaptic dysfunction, and determining the mechanisms by which cytotoxic T cells directly cause neuron loss.


See my publications



  1. Ph.D. - Cellular and Molecular Pathology University of Wisconsin
  2. BA - Physics Chemistry Biochemistry Biology Wartburg College

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