Jennifer Morgan, Marine Biological Laboratory
Friday, November 1, 2013 at 1:10pm
Thompson Biology, 112 59 Lab Campus Dr, Williamstown, MA 01267
Biology Department Colloquium
“Roles for Synuclein in Spinal Cord Injury and Parkinson’s Disease”
Spinal cord injury causes widespread death of neurons, thereby limiting regeneration and recovery. At present, little is known about how to improve the survival of damaged neurons after injury. To address this, our lab is taking advantage of the giant reticulospinal (RS) neurons in sea lampreys (Petromyzon marinus), which permit an examination of post-injury cellular and molecular responses at the level of individual neurons. In lampreys, some of the identified giant RS neurons reproducibly die after injury, while others survive the injury. By studying the molecular responses in these cells, we can identify specific molecular factors that govern cell death or survival after injury, which is difficult – if not impossible – in other vertebrate experimental models. We recently discovered some interesting parallels between neurodegeneration in spinal cord injury and that observed in Parkinson’s Disease. Specifically, we observed cell-specific accumulation of the neuronal protein, synuclein, into neurotoxic aggregates only in the subset of neurons that degenerate after injury. Using imaging and knockdown approaches, we have further shown that reducing the accumulation of synuclein consequently increases neuronal survival and improves axon sprouting and regeneration after spinal cord injury. Thus, synuclein accumulation is a risk factor for neurodegeneration after injury, as it is in Parkinson’s Disease, suggesting that this process may be a new therapeutic target for improving recovery from spinal cord injury.
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