E
Eduardo A. Albornoz
Researcher at University of Queensland
Publications - 16
Citations - 799
Eduardo A. Albornoz is an academic researcher from University of Queensland. The author has contributed to research in topics: Inflammasome & Biology. The author has an hindex of 6, co-authored 10 publications receiving 454 citations. Previous affiliations of Eduardo A. Albornoz include Millennium Institute & Andrés Bello National University.
Papers
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Journal ArticleDOI
Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice
Richard D. Gordon,Eduardo A. Albornoz,Daniel C. Christie,Monica R. Langley,Vinod Kumar,Susanna Mantovani,Susanna Mantovani,Avril A. B. Robertson,Mark S. Butler,Dominic B. Rowe,Luke A. J. O'Neill,Anumantha G. Kanthasamy,Kate Schroder,Mark E. Cooper,Mark E. Cooper,Trent M. Woodruff +15 more
TL;DR: It is shown that activation of the microglial NLR family pyrin domain containing 3 (NLRP3) inflammasome is a common pathway triggered by both fibrillar α- synuclein and dopaminergic degeneration in the absence of α-synuclein aggregates.
Journal ArticleDOI
The microglial NLRP3 inflammasome is activated by amyotrophic lateral sclerosis proteins.
Vandana Deora,John D. Lee,Eduardo A. Albornoz,Luke McAlary,Cyril J. Jagaraj,Avril A. B. Robertson,Julie D. Atkin,Mark E. Cooper,Kate Schroder,Justin J. Yerbury,Richard D. Gordon,Trent M. Woodruff +11 more
TL;DR: It is demonstrated using Nlrp3‐GFP gene knock‐in mice that ALS microglia express NLRP3, and that pathological ALS proteins activate the microglial NL RP3 inflammasome, andNLRP3 inhibition may be a potential therapeutic approach to arrest microglian neuroinflammation and ALS disease progression.
Journal ArticleDOI
Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species.
Alejandro A. Arriagada,Alejandro A. Arriagada,Eduardo A. Albornoz,Eduardo A. Albornoz,M.C. Opazo,M.C. Opazo,Alvaro Becerra,Alvaro Becerra,Gonzalo Vidal,Gonzalo Vidal,Carlos E. Fardella,Luis Michea,Luis Michea,Nancy Carrasco,Felipe Simon,Alvaro A. Elorza,Susan M. Bueno,Susan M. Bueno,Alexis M. Kalergis,Claudia A. Riedel +19 more
TL;DR: The data shown here support the notion that excess I- inhibits NIS at the cell surface at early times by means of a posttranslational mechanism that involves reactive derived oxygen species.
Journal ArticleDOI
SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein.
Eduardo A. Albornoz,Alberto A. Amarilla,Naphak Modhiran,Sandra K. Parker,Xaria X. Li,Danushka K. Wijesundara,Julio Aguado,Adriana Pliego Zamora,Christopher L. D. McMillan,Benjamin Liang,Nias Y. G. Peng,Julian D. J. Sng,Fatema Tuj Saima,Jenny Nt Fung,John D. Lee,Devina Paramitha,Rhys Parry,Michael S. Avumegah,Ariel Isaacs,Martin W. Lo,Zaray Miranda-Chacon,Dan F Bradshaw,Constanza Salinas-Rebolledo,Niwanthi W. Rajapakse,Ernst J. Wolvetang,Trent P. Munro,Alejandro Rojas-Fernandez,Paul R. Young,Katryn J. Stacey,Alexander A. Khromykh,Keith J. Chappell,Daniel Watterson,Trent M. Woodruff +32 more
TL;DR: In this paper , SARS-CoV-2 infection of transgenic mice expressing human angiotensin-converting enzyme 2 (hACE2) as a COVID-19 pre-clinical model, established the presence of virus in the brain together with microglial activation and NLRP3 upregulation in comparison to uninfected mice.
Book ChapterDOI
Inflammasomes in CNS Diseases
TL;DR: Understanding of how inflammasomes are engaged in the pathogenesis of a variety of neurological diseases is crucial to develop effective therapeutic approaches for CNS pathologies that are propagated by chronic Inflammasome activation.