E. Camille Hanks receives analysis support from CDC and Shire Pharmaceuticals Inc. Eric A. Storch serves around the advisory board for the International Obsessive Compulsive Disorder Foundation. He serves as a consultant for Otsuka America Pharmaceutical, Inc. and ProPhase Inc. He receives grant support from Centers for Illness Control; National Institutes of Health; Ortho-McNeil Neurologics; and the Tourette Syndrome Association. He has intellectual home with Springer and Taylor Francis. He serves on the speakers bureau for the International Obsessive Compulsive Disorder Foundation. Erika F. Augustine has received grant assistance from the TSA, the FDA, the International Crucial Tremor Foundation, the New York State Division of Wellness, along with the National DYRK4 Inhibitor Source Institute of NeurologicalUTILITY Of the DISC FOR ASSESSING TS IN Kids Problems and Storke. She is on a Information Security Monitoring Board for Edison Pharmaceuticals and receives an iNOS Inhibitor review honorarium from the American Academy of Neurology. Heather R. Adams receives grant support in the Tourette Syndrome Association (TSA). Amy E. Vierhile has no monetary relationships to disclose. Alyssa R. Thatcher has no financial relationships to disclose. Tanya K. Murphy receives study funding from AstraZeneca Investigation Improvement, Brain and Behavior Analysis Foundation, the CDC, F. Hoffmann-La Roche Ltd., Indevus Pharmaceuticals, IOCDF, National Institutes of Health/National Institute of Mental Well being (NIH/NIMH), Ortho-McNeil Janssen Pharmaceuticals, Otsuka Pharmaceuticals, Pfizer, Inc., and Shire Pharmaceuticals. She has received travel support from the Tourette Syndrome Association and honoraria from grand rounds lectures.
Parkinson’s disease (PD) is really a progressive neurodegenerative disorder characterized by impaired motor functions, which are predominantly associated with degeneration of nigral dopaminergic neurons (TH, tyrosine hydroxylase good) and decreased striatal dopamine (DA) neurotransmission (Hornykiewicz 2008). Nevertheless, the complex pathophysiology of PD is extended significantly beyond the selective nigrostriatal degeneration to a number of extranigral and extrastriatal regions (Olanow et al. 2011, Giza et al. 2012). The spinal cord is 1 such site. Its involvement in PD pathology is implicated depending on the findings of significant degeneration of spinal neurons in human PD, postmortem PD spinal cord and animal models of experimental PD (Braak et al. 2007, Del Tredici Braak 2012, Knaryan et al. 2011, Samantaray et al. 2013a, Vivacqua et al. 2012, Vivacqua et al. 2011). We previously reported degeneration of cholinergic (ChAT, choline acetyltransferase constructive) spinal motoneurons in MPTP- and rotenone- induced experimental parkinsonism in mice and rats respectively (Chera et al. 2002, Chera et al. 2004, Ray et al. 2000, Samantaray et al. 2008a, Samantaray et al. 2007), and in postmortem spinal cord specimens of human PD (Samantaray et al. 2013a). On the other hand, the selective mechanisms of such degeneration usually are not well understood. In vitro research performed in hybrid VSC 4.1 cells differentiated into cholinergic spinal motoneurons and exposed to MPP+ or rotenone showed that mitochondrial toxins result in distinct intracellular damage in spinal motoneurons (Samantaray et al. 2011). The typical underlying mechanisms of spinal cord motoneuron degeneration found in vivo and in vitro involve aberrant Ca2+ homeostasis, up-regulation and activation of Ca2+-dependent cysteine proteases calpain and caspase-3, a.
