Virginie Buggia-Prevot
Affiliations: | Neurobiology | University of Chicago, Chicago, IL |
Area:
Alzheimer's disease, Secretases, neuronal transport, BACE1Google:
"Virginie Buggia-Prevot"Cross-listing: Neurotree
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Publications
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| Ray WJ, Buggia-Prevot V. (2020) Novel Targets for Alzheimer's Disease: A View Beyond Amyloid. Annual Review of Medicine |
| De Rossi P, Andrew RJ, Musial TF, et al. (2018) Aberrant accrual of BIN1 near Alzheimer's disease amyloid deposits in transgenic models. Brain Pathology (Zurich, Switzerland) |
| Buggia-Prevot V, Goodwani S, Fernandez C, et al. (2018) P2-167: Expression Of The Dual Leucine Zipper Kinase In Dystrophic Neurites And Axonal Beading During Pathology Progression In Alzheimer'S Disease Alzheimers & Dementia. 14 |
| Rossi PD, Andrew RJ, Musial TF, et al. (2018) P1-202: Myelin Breakdown Leads To Bin1 Accumulation In Amyloid Deposits Alzheimers & Dementia. 14 |
| De Rossi P, Buggia-Prevot V, Andrew RJ, et al. (2017) BIN1 localization is distinct from Tau tangles in Alzheimer's disease. Matters. 2017 |
| Andrew RJ, Fernandez CG, Stanley M, et al. (2017) Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. Proceedings of the National Academy of Sciences of the United States of America |
| De Rossi P, Buggia-Prévot V, Clayton BL, et al. (2016) Predominant expression of Alzheimer's disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts. Molecular Neurodegeneration. 11: 59 |
| Sadleir KR, Kandalepas PC, Buggia-Prévot V, et al. (2016) Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer's disease. Acta Neuropathologica |
| Buggia-Prévot V, Thinakaran G. (2015) Significance of transcytosis in Alzheimer's disease: BACE1 takes the scenic route to axons. Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology. 37: 888-98 |
| Wang Y, Buggia-Prévot V, Zavorka ME, et al. (2015) Overexpression of the Insulin-Like Growth Factor II Receptor Increases β-Amyloid Production and Affects Cell Viability. Molecular and Cellular Biology. 35: 2368-84 |