A
Aaron Lulla
Researcher at University of California, Los Angeles
Publications - 5
Citations - 344
Aaron Lulla is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Gene silencing & Dopaminergic. The author has an hindex of 4, co-authored 5 publications receiving 275 citations.
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Journal ArticleDOI
Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease
Arthur G. Fitzmaurice,Shannon L. Rhodes,Aaron Lulla,Niall P. Murphy,Hoa A. Lam,Kelley C. O’Donnell,Lisa M. Barnhill,John E. Casida,Myles Cockburn,Alvaro Sagasti,Mark Stahl,Nigel T. Maidment,Beate Ritz,Jeff M. Bronstein,Jeff M. Bronstein +14 more
TL;DR: It is proposed that benomyl, via its bioactivated thiocarbamate sulfoxide metabolite, inhibits aldehyde dehydrogenase (ALDH), leading to accumulation of the reactive dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL), preferential degeneration of dopamine neurons, and development of PD.
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Axon degeneration and PGC-1α-mediated protection in a zebrafish model of α-synuclein toxicity
Kelley C. O’Donnell,Aaron Lulla,Mark Stahl,Nickolas D. Wheat,Jeff M. Bronstein,Jeff M. Bronstein,Alvaro Sagasti +6 more
TL;DR: The rapid onset of axonal pathology in this system, and the relatively moderate degree of cell death, provide a new model for the study of aSyn toxicity and protection and might have utility in screening for novel disease-modifying compounds.
Journal ArticleDOI
Neurotoxicity of the Parkinson Disease-Associated Pesticide Ziram Is Synuclein-Dependent in Zebrafish Embryos
Aaron Lulla,Lisa M. Barnhill,Gal Bitan,Magdalena I. Ivanova,Binh Nguyen,Kelley C. O’Donnell,Mark Stahl,Chase Yamashiro,Frank-Gerrit Klärner,Thomas Schrader,Alvaro Sagasti,Jeff M. Bronstein,Jeff M. Bronstein +12 more
TL;DR: Data show that ziram is selectively toxic to DA neurons in vivo, and this toxicity is synuclein-dependent in zebrafish embryos, which has important implications for understanding the mechanisms by which pesticides may cause PD.
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Heme oxygenase-1 protects endothelial cells from the toxicity of air pollutant chemicals.
TL;DR: HO-1 expression protected HMECs from DEP-induced prooxidative and proinflammatory effects and could potentially serve as a therapeutic target in an attempt to inhibit the cardiovascular effects of ambient PM.