Publications de Sarah Catherine Sonnay

Assessment of brain metabolite correlates of AAV-mediated overexpression of human alpha-synuclein in cortical neurons by in vivo(1) H-MR spectroscopy at 9.4 T

Sarah Catherine Sonnay

In this study, we used proton-localized spectroscopy ((1) H-MRS) for the acquisition of the neurochemical profile longitudinally in a novel rat model of human wild type alpha-synuclein (a-syn) overexpression. Our goal was to find out if the increased a-syn ...

Wiley-Blackwell2016

Imaging of prolonged BOLD response in the somatosensory cortex of the rat

Rolf Gruetter, João Miguel das Neves Duarte, Nathalie Just, Sarah Catherine Sonnay

Blood oxygenation level-dependent (BOLD) functional MRI is a widely employed methodology in experimental and clinical neuroscience, although its nature is not fully understood. To gain insights into BOLD mechanisms and take advantage of the new functional ...

Wiley-Blackwell2015

Common Pathogenic Effects of Missense Mutations in the P-Type ATPase ATP13A2 (PARK9) Associated with Early-Onset Parkinsonism

Liliane Glauser, Darren Moore, Sarah Catherine Sonnay, Klodjan Stafa, Alzbeta Trancikova, Alessandra Musso, Agata Podhajska

Mutations in the ATP13A2 gene (PARK9) cause autosomal recessive, juvenile-onset Kufor-Rakeb syndrome (KRS), a neurodegenerative disease characterized by parkinsonism. KRS mutations produce truncated forms of ATP13A2 with impaired protein stability resultin ...

Public Library of Science2012

PARK9-associated ATP13A2 localizes to intracellular acidic vesicles and regulates cation homeostasis and neuronal integrity

Liliane Glauser, Elpida Tsika, Darren Moore, Sarah Catherine Sonnay, Klodjan Stafa, Alzbeta Trancikova, David Ramonet Jimenez, Agata Podhajska

Mutations in the ATP13A2 gene (PARK9, OMIM 610513) cause autosomal recessive, juvenile-onset Kufor-Rakeb syndrome and early-onset parkinsonism. ATP13A2 is an uncharacterized protein belonging to the P-5-type ATPase subfamily that is predicted to regulate t ...

Oxford University Press2012

Parkin promotes the ubiquitination and degradation of the mitochondrial fusion factor mitofusin 1

Liliane Glauser, Darren Moore, Sarah Catherine Sonnay, Klodjan Stafa

Mutations in the parkin gene cause early-onset, autosomal recessive Parkinson's disease. Parkin functions as an E3 ubiquitin ligase to mediate the covalent attachment of ubiquitin monomers or linked chains to protein substrates. Substrate ubiquitination ca ...

2011

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