Laboratory of Innovative Factor-based Therapies

Theo Hagg headshot                                                                 TheRunner animated gifo Hagg 



The Hagg lab investigates how novel neurotrophic mechanisms and endogenous stem cells might be used to develop CNS repair strategies.  We are currently investigating how small molecules that activate neuroprotective mechanisms might be used to reduce axon and myelin loss after a contusive spinal cord injury.  We currently investigate how vascular mechanisms could be utilized to reduce degeneration after such injuries.  Lastly, we are identifying molecular regulators of endogenous neural precursors in adult rodents which can be targeted for enhancing neurogenesis and redirect neuroblast migration towards stroke injuries.  The long term goal of these studies is to provide information that would lead to better treatment strategies for a variety of human neurological disorders, including spinal cord injury. Techniques used routinely include various refined microsurgical procedures in the brain and spinal cord of adult rats and mice, regular and confocal immunohistochemistry, Western blotting and real-time PCR.  We are members of the world-class Kentucky Spinal Cord Injury Research Center.


Journal of Neuroscience cover photo

Muradov JM, Ewan EE, Hagg T (2013) Dorsal column sensory axons degenerate due to impaired microvascular perfusion after spinal cord injury in rats. Experimental Neurology  [Epub ahead of print].

Keasey MP, Kang, SS, Lovins, C, Hagg T (2013) Inhibition of a novel specific neuroglial integrin signaling pathway increases STAT3-mediated CNTF expression.  Cell Communication and Signaling 11(1):35.

Kang SS, Keasey MP, Hagg T (2013) P2X7 receptor inhibition increases CNTF expression in the subventricular zone, but not neurogenesis of neuroprotection after stroke in adult mice.  Translational Stroke Research Published online before print, May 2013.

Muradov J, Hagg T (2013) Intravenous infusion of magnesium chloride improves epicenter blood flow during the acute stage of contusive spinal cord injury in rats.  Journal of Neurotrauma 30:840-52

Kang SS, Keasey MP, Arnold SA, Reid R, Geralds JT, Hagg T (2012)  Endogenous CNTF mediates stroke-induced adult CNS neurogenesis in mice. Neurobiology of Disease 49: 68-78.

Arnold SA, Hagg T (2012) Serotonin 1A receptor agonist increases species- and region-selective adult CNS proliferation, but not through CNTF.  Neuropharmacology 63: 1238-1247

Kang SS, Keasey MP, Cai J, Hagg T (2012) Loss of neuron-astrocyte interaction rapidly induces protective CNTF expression after stroke in mice.  Journal of Neuroscience 32:9277-87

Arnold SA, Hagg T (2011) Anti-inflammatory treatments during the chronic phase of spinal cord injury improve locomotor function in adult mice. J Neurotrauma 28:1995-2002

Benton RL, Hagg T (2011) Vascular pathology as potential therapeutic target in SCI. Translational Stroke Research 2: 556-572.

Fassbender JM, Whittemore SR, Hagg T. Targeting microvasculature for neuroprotection after SCI. Neurotherapeutics. 2011 8:240-51.

Han S, Arnold SA, Sithu SD, Mahoney ET, Geralds JT, Phuong V, Benton RL, Maddie MA, D’Sousa SE, Whittemore SR, Hagg T (2010) Rescuing vasculature with intravenous angiopoietin-1 and avb3 integrin peptide is protective after spinal cord injury. Brain 133: 1026-1042

antibody stained OligodendrocytesPEOPLE :

     Chiharu Lovins, Technician

     Yun Shi Long, Technician

     Seong Kang, Postdoctoral Fellow "Adult CNS neurogenesis, CNTF regulation and stroke"

     Eric Ewan, Postdoctoral Fellow "Treatments for spinal cord injury"



   Adam21 protein 3d image

            Lab pictures :
              Party Time 
              The dangers of learning Molecular Biology
              We DO get results



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