R
Robert D. Dayton
Researcher at LSU Health Sciences Center Shreveport
Publications - 34
Citations - 1375
Robert D. Dayton is an academic researcher from LSU Health Sciences Center Shreveport. The author has contributed to research in topics: Neurodegeneration & Amyotrophic lateral sclerosis. The author has an hindex of 18, co-authored 33 publications receiving 1219 citations. Previous affiliations of Robert D. Dayton include Louisiana State University & Louisiana State University in Shreveport.
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Journal ArticleDOI
Efficient Neuronal Gene Transfer with AAV8 Leads to Neurotoxic Levels of Tau or Green Fluorescent Proteins
Ronald Klein,Robert D. Dayton,Nancy J. Leidenheimer,Karen Jansen,Todd E. Golde,Richard M. Zweig +5 more
TL;DR: The efficient AAV8 is promising for animal models of neurodegenerative diseases and potentially as well for gene therapy of brain diseases, although the toxicity observed with GFP expression warrants great caution.
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AAV8, 9, Rh10, Rh43 Vector Gene Transfer in the Rat Brain: Effects of Serotype, Promoter and Purification Method
TL;DR: At two doses of vectors optimized for serotype, promoter and purification, the AAV serotypes did not observe serotype differences among AAV8, AAV9, or AAV Rh10.
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The advent of AAV9 expands applications for brain and spinal cord gene delivery.
TL;DR: A peripheral-to-central gene delivery that can affect the entire CNS without having to inject the CNS is promising for basic functional experiments, and potentially for gene therapy, although other natural serotypes and recombineered vectors may also support or improve upon wide-scale expression.
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TDP43 nuclear export and neurodegeneration in models of amyotrophic lateral sclerosis and frontotemporal dementia
Hilary C. Archbold,Kasey L. Jackson,Ayush Arora,Kaitlin Weskamp,Elizabeth M. H. Tank,Xingli Li,Roberto Miguez,Robert D. Dayton,Sharon Tamir,Ronald Klein,Sami J. Barmada +10 more
TL;DR: SINE compounds modestly extend cellular survival in neuronal ALS/FTD models and mitigate motor symptoms in an in vivo rat ALS model, and overexpression of XPO1, XPO7 and NXF1 are each sufficient to promote nuclear TDP43 egress.
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Mimicking aspects of frontotemporal lobar degeneration and Lou Gehrig's disease in rats via TDP-43 overexpression.
Jason B Tatom,David B. Wang,Robert D. Dayton,Omar Skalli,Michael Hutton,Dennis W. Dickson,Ronald Klein +6 more
TL;DR: The cytoplasmic expression, ubiquitination, and neurodegeneration mimicked features of the TDP-43 diseases, and the gliosis, apoptosis, and motor impairment may also be relevant to T DP-43 disease forms involving nigrostriatal degeneration.