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Anja Leona Biere
Researcher at Amgen
Publications - 11
Citations - 6052
Anja Leona Biere is an academic researcher from Amgen. The author has contributed to research in topics: Mutant & Fibrillogenesis. The author has an hindex of 8, co-authored 9 publications receiving 5732 citations.
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Journal ArticleDOI
Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE.
Robert Vassar,Brian D. Bennett,Safura Babu-Khan,Steve Kahn,Elizabeth A. Mendiaz,Paul Denis,David B. Teplow,Sandra Ross,Patricia Amarante,Richard Loeloff,Yi Luo,Seth Fisher,Janis Fuller,Steven P. Edenson,Jackson Lile,Mark A. Jarosinski,Anja Leona Biere,Eileen Curran,Teresa L. Burgess,Jean Claude Louis,Frank H. Collins,James J. S. Treanor,Gary Rogers,Martin Citron +23 more
TL;DR: Overexpression of a transmembrane aspartic protease, termed BACE (for beta-site APP-cleaving enzyme) increased the amount of beta-secretase cleavage products, and these were cleaved exactly and only at known beta- secretase positions.
Journal ArticleDOI
Both Familial Parkinson’s Disease Mutations Accelerate α-Synuclein Aggregation
Linda O. Narhi,Stephen J. Wood,Shirley Steavenson,Yijia Jiang,Dan Anafi,Stephen Kaufman,Francis Hall Martin,Karen C. Sitney,Paul Denis,Jean-Claude Louis,Jette Wypych,Anja Leona Biere,Martin Citron +12 more
TL;DR: It is shown that both wild type and mutant α-synuclein form insoluble fibrillar aggregates with antiparallel β-sheet structure upon incubation at physiological temperature in vitro, and that aggregate formation is accelerated by both PD-linked mutations.
Journal ArticleDOI
alpha-synuclein fibrillogenesis is nucleation-dependent. Implications for the pathogenesis of Parkinson's disease.
Stephen J. Wood,Jette Wypych,Shirley Steavenson,Jean-Claude Louis,Martin Citron,Anja Leona Biere +5 more
TL;DR: It is suggested that differences in aggregation kinetics of alpha-synucleins cannot be explained by differences in solubility but are due to different nucleation rates, and alpha- Synuclein nucleation may be the rate-limiting step for the formation of Lewy body alpha- synuclein fibrils in Parkinson's disease.
Journal ArticleDOI
Anti-Inflammatory Drug Therapy Alters β-Amyloid Processing and Deposition in an Animal Model of Alzheimer's Disease
Qiao Yan,Jianhua Zhang,Hantao Liu,Safura Babu-Khan,Robert Vassar,Anja Leona Biere,Martin Citron,Gary E. Landreth +7 more
TL;DR: Data show that chronic NSAID treatment can reduce brain Aβ levels, amyloid plaque burden, and microglial activation in an animal model of Alzheimer's disease.
Journal ArticleDOI
Parkinson's Disease-associated α-Synuclein Is More Fibrillogenic than β- and γ-Synuclein and Cannot Cross-seed Its Homologs
Anja Leona Biere,Stephen J. Wood,Jette Wypych,Shirley Steavenson,Yijia Jiang,Dan Anafi,Frederick W. Jacobsen,Mark A. Jarosinski,Gay-May Wu,Jean-Claude Louis,Francis Hall Martin,Linda O. Narhi,Martin Citron +12 more
TL;DR: β- and γ-synuclein are intrinsically less fibrillogenic than α- Synuclein and cannot form mixed fibrils with α- synuclein, which may explain why they do not appear in the pathological hallmarks of PD, although they are closely related to α-syn nuclein and are also abundant in brain.