Guilian Xu, Ph.D.

Affiliations: 
Neuroscience University of Florida, Gainesville, Gainesville, FL, United States 
Area:
transgenic mice, Alzheimer's disease, ALS,
Website:
http://neuroscience.ufl.edu/faculty-and-staff-directory/faculty/guilian-xu-ph-d/
Google:
"Guilian Xu"
Mean distance: 16.48 (cluster 31)
 
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Publications

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Ayers JI, Xu G, Lu Q, et al. (2023) Multiple Factors Influence the Incubation Period of ALS Prion-like Transmission in SOD1 Transgenic Mice. Viruses. 15
Xu G, Fromholt S, Borchelt DR. (2022) Modeling the Competition between Misfolded Aβ Conformers That Produce Distinct Types of Amyloid Pathology in Alzheimer's Disease. Biomolecules. 12
Xia Y, Prokop S, Bell BM, et al. (2022) Pathogenic tau recruits wild-type tau into brain inclusions and induces gut degeneration in transgenic SPAM mice. Communications Biology. 5: 446
Moore BD, Levites Y, Xu G, et al. (2022) Soluble brain homogenates from diverse human and mouse sources preferentially seed diffuse Aβ plaque pathology when injected into newborn mouse hosts. Free Neuropathology. 3
Williams T, Ruiz AJ, Ruiz AM, et al. (2022) Impact of APOE genotype on prion-type propagation of tauopathy. Acta Neuropathologica Communications. 10: 57
Xu G, Ulm BS, Howard J, et al. (2022) TAPPing into the potential of inducible tau/APP transgenic mice. Neuropathology and Applied Neurobiology
Koller EJ, Ibanez KR, Vo Q, et al. (2021) Combinatorial model of amyloid β and tau reveals synergy between amyloid deposits and tangle formation. Neuropathology and Applied Neurobiology
Ayers JI, Xu G, Dillon K, et al. (2021) Variation in the vulnerability of mice expressing human superoxide dismutase 1 to prion-like seeding: a study of the influence of primary amino acid sequence. Acta Neuropathologica Communications. 9: 92
Xia Y, Chen Z, Xu G, et al. (2021) Novel SOD1 monoclonal antibodies against the electrostatic loop preferentially detect misfolded SOD1 aggregates. Neuroscience Letters. 742: 135553
Xu G, Fromholt SE, Chakrabarty P, et al. (2020) Diversity in Aβ deposit morphology and secondary proteome insolubility across models of Alzheimer-type amyloidosis. Acta Neuropathologica Communications. 8: 43
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