Walker S Jackson, Ph.D.

Affiliations: 
German Center for Neurodegenerative Diseases, Bonn 
Area:
prion diseases, FFI, CJD, transgenic mice
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"Walker Jackson"
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Publications

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Jackson WS, Bauer S, Kaczmarczyk L, et al. (2024) Selective Vulnerability to Neurodegenerative Disease: Insights from Cell Type-Specific Translatome Studies. Biology. 13
Walsh DJ, Rees JR, Mehra S, et al. (2023) Anti-prion drugs do not improve survival in knock-in models of inherited prion disease. Biorxiv : the Preprint Server For Biology
Jackson WS. (2023) Etiology matters: genetic and acquired prion diseases engage different mechanisms at a presymptomatic stage. Neural Regeneration Research. 18: 2707-2708
Arifin MI, Kaczmarczyk L, Zeng D, et al. (2023) Heterozygosity for cervid S138N polymorphism results in subclinical CWD in gene-targeted mice and progressive inhibition of prion conversion. Proceedings of the National Academy of Sciences of the United States of America. 120: e2221060120
Bauer S, Chen CY, Jonson M, et al. (2023) Cerebellar granule neurons induce Cyclin D1 before the onset of motor symptoms in Huntington's disease mice. Acta Neuropathologica Communications. 11: 17
Vallabh SM, Zou D, Pitstick R, et al. (2023) Therapeutic Trial of anle138b in Mouse Models of Genetic Prion Disease. Journal of Virology. e0167222
Bauer S, Dittrich L, Kaczmarczyk L, et al. (2022) Translatome profiling in fatal familial insomnia implicates TOR signaling in somatostatin neurons. Life Science Alliance. 5
Kaczmarczyk L, Schleif M, Dittrich L, et al. (2022) Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice. Plos Pathogens. 18: e1010747
Thackray AM, Lam B, McNulty EE, et al. (2022) Clearance of variant Creutzfeldt-Jakob disease prions in vivo by the Hsp70 disaggregase system. Brain : a Journal of Neurology
Kaczmarczyk L, Reichenbach N, Blank N, et al. (2021) Slc1a3-2A-CreERT2 mice reveal unique features of Bergmann glia and augment a growing collection of Cre drivers and effectors in the 129S4 genetic background. Scientific Reports. 11: 5412
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