E
Edmund R. Hollis
Researcher at Cornell University
Publications - 25
Citations - 1434
Edmund R. Hollis is an academic researcher from Cornell University. The author has contributed to research in topics: Axon & Motor learning. The author has an hindex of 15, co-authored 23 publications receiving 1218 citations. Previous affiliations of Edmund R. Hollis include Columbia University & University of California, San Diego.
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Journal ArticleDOI
Guidance Molecules in Axon Regeneration
TL;DR: In experimental animal models of spinal cord injury (SCI), mono and combination therapies have been shown to promote neuronal growth and sprouting and challenges ahead include testing whether some of the most promising treatment strategies in animal models are also beneficial for human patients suffering from SCI.
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Chemotropic guidance facilitates axonal regeneration and synapse formation after spinal cord injury
Laura Taylor Alto,Leif A. Havton,James M. Conner,Edmund R. Hollis,Armin Blesch,Mark H. Tuszynski +5 more
TL;DR: The reinnervation of brainstem targets after SCI is reported for the first time and an essential role for chemotropic axon guidance in target selection is reported.
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Induction of corticospinal regeneration by lentiviral trkB-induced Erk activation
TL;DR: The hypothesis that the refractory regenerative state of adult corticospinal axons can be attributed at least in part to neuron-intrinsic mechanisms is supported, and activation of ERK signaling can elicit cortiospinal tract regeneration.
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Efficient Retrograde Neuronal Transduction Utilizing Self-complementary AAV1
Edmund R. Hollis,Ken Kadoya,Matthew L. Hirsch,Richard Jude Samulski,Mark H. Tuszynski,Mark H. Tuszynski +5 more
TL;DR: The data provide the basis for increased retrograde transduction efficiency using peripheral injections of scAAV1 vectors for therapeutic gene delivery to the spinal cord.
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IGF-I gene delivery promotes corticospinal neuronal survival but not regeneration after adult CNS injury.
TL;DR: Development patterns of growth factor responsiveness are not simply recapitulated after adult injury, potentially due to post-natal shifts in patterns of IGF-I receptor expression, and its application to sites of adult spinal cord injury or subcortical axotomy fails to promote corticospinal axonal regeneration.