cached image

Robert P. Bowser, PhD, Yale University

Affiliations: 
Pathology University of Pittsburgh, Pittsburgh, PA, United States 
Area:
molecular and cellular basis of neurodegenerative diseases
Website:
http://neuro.pathology.pitt.edu/webstuff/Bowser.html
Google:
"Robert Bowser"
Bio:

http://path.upmc.edu/cmp/fac05.htm
http://www.mirm.pitt.edu/people/bios/Bowser1.asp

Mean distance: 17.17 (cluster 11)
 
Cross-listing: Neuropathology Tree - Computational Biology Tree

BETA: Related publications

Publications

You can help our author matching system! If you notice any publications incorrectly attributed to this author, please sign in and mark matches as correct or incorrect.

Lorenzini I, Alsop E, Levy J, et al. (2023) Moderate intrinsic phenotypic alterations in ALS/FTD iPSC-microglia despite the presence of C9orf72 pathological features. Frontiers in Cellular Neuroscience. 17: 1179796
Lehmkuhl EM, Loganathan S, Alsop E, et al. (2021) TDP-43 proteinopathy alters the ribosome association of multiple mRNAs including the glypican Dally-like protein (Dlp)/GPC6. Acta Neuropathologica Communications. 9: 52
Saul J, Hutchins E, Reiman R, et al. (2020) Global alterations to the choroid plexus blood-CSF barrier in amyotrophic lateral sclerosis. Acta Neuropathologica Communications. 8: 92
Collins M, Li Y, Bowser R. (2020) RBM45 associates with nuclear stress bodies and forms nuclear inclusions during chronic cellular stress and in neurodegenerative diseases. Acta Neuropathologica Communications. 8: 91
Huang F, Zhu Y, Hsiao-Nakamoto J, et al. (2020) Longitudinal biomarkers in amyotrophic lateral sclerosis. Annals of Clinical and Translational Neurology
Vu L, An J, Kovalik T, et al. (2020) Cross-sectional and longitudinal measures of chitinase proteins in amyotrophic lateral sclerosis and expression of CHI3L1 in activated astrocytes. Journal of Neurology, Neurosurgery, and Psychiatry
Benatar M, Wuu J, Lombardi V, et al. (2019) Neurofilaments in pre-symptomatic ALS and the impact of genotype. Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration. 1-11
Manzo E, Lorenzini I, Barrameda D, et al. (2019) Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS. Elife. 8
Manzo E, Lorenzini I, Barrameda D, et al. (2019) Author response: Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS Elife
Boehringer A, Bowser R. (2018) RNA Nucleocytoplasmic Transport Defects in Neurodegenerative Diseases. Advances in Neurobiology. 20: 85-101
See more...