Publications associées (47)

Mimicking Phosphorylation at Serine 87 Inhibits the Aggregation of Human α-Synuclein and Protects against Its Toxicity in a Rat Model of Parkinson's Disease

Hilal Lashuel, Patrick Aebischer, Bernard Schneider, Abid Oueslati

Several lines of evidence suggest that phosphorylation of α-synuclein (α-syn) at S87 or S129 may play an important role in regulating its aggregation, fibrillogenesis, Lewy body formation, and neurotoxicity in vivo. However, whether phosphorylation at thes ...
2012

Parkin reinvents itself to regulate fatty acid metabolism by tagging CD36

Darren Moore

Parkinson disease (PD) is a relatively common neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra. About 5%-10% of PD cases are inherited. Mutations in the Parkin gene, which encodes a pr ...
American Society for Clinical Investigation2011

The anti-Parkinsonian drug selegiline delays the nucleation phase of α-synuclein aggregation leading to the formation of nontoxic species

Hilal Lashuel, Saviana Di Giovanni

Parkinson's disease (PD) is a movement disorder characterized by the loss of dopaminergic neurons in the substantia nigra and the formation of intraneuronal inclusions called Lewy bodies, which are composed mainly of α-synuclein (α-syn). Selegiline (Sel) i ...
2010

Motor Deficits upon Alpha-Synuclein Expression in the Nigrostriatal System Are Due to a Loss of Dopaminergic Vesicles and Reduced Dopamine Release at an early Stage of Neurodegeneration

Meret Gaugler

Alpha-synuclein is linked to both sporadic and familial forms of Parkinson's disease. The protein represents the major component of Lewy bodies – one of the hallmarks of the disease. Additionally, several point mutations and locus multiplications in the ge ...
EPFL2010

Embryonic substantia nigra grafts in the mesencephalon send neurites to the host striatum in non-human primate after overexpression of GDNF

Patrick Aebischer

In spite of partial success in treating Parkinson's disease by using ectopically placed grafts of dopamine-producing cells, restoration of the original neuroanatomical circuits, if possible, might work better. Previous evidence of normal anatomic projectio ...
2009

Assessment of metabolic changes in the striatum of a rat model of parkinsonism: An in vivo 1H MRS study

Degeneration of the dopaminergic neurons of the substantia nigra pars compacta in Parkinson's disease induces an abnormal activation of the glutamatergic neurotransmission system within the basal ganglia network and related structures. The aim of this stud ...
Wiley-Blackwell2009

Advanced phase-contrast imaging using a grating interferometer

Christian David, Marco Stampanoni

Phase-sensitive X-ray imaging methods can provide substantially increased contrast over conventional absorption-based imaging, and therefore new and otherwise inaccessible information. Differential phase-contrast (DPC) imaging, which uses a grating interfe ...
2009

Abnormal Localization of Leucine-Rich Repeat Kinase 2 to the Endosomal-Lysosomal Compartment in Lewy Body Disease

Darren Moore

Missense mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common causes of both familial and sporadic forms of Parkinson disease and are also associated with diverse pathological alterations. The mechanisms whereby LRRK2 mutations ca ...
2009

Inhibition of alpha-synuclein fibrillization by dopamine is mediated by interactions with five C-terminal residues and with E83 in the NAC region

Hilal Lashuel, Adrian Schmid, Paolo Carloni, Alessandra Chesi

The interplay between dopamine and alpha-synuclein (AS) plays a central role in Parkinson's disease (PD). PD results primarily from a severe and selective devastation of dopaminergic neurons in substantia nigra pars compacta. The neuropathological hallmark ...
Public Library of Science2008

Striatal and nigral pathology in a lentiviral rat model of Machado-Joseph disease

Nicole Déglon

Machado-Joseph disease (MJD) is a fatal, dominant neurodegenerative disorder. MJD results from polyglutamine repeat expansion in the MJD-1 gene, conferring a toxic gain of function to the ataxin-3 protein. In this study, we aimed at overexpressing ataxin-3 ...
Oxford University Press2008

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