Publications
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Filtres: Keyword is Amyotrophic Lateral Sclerosis [Enlever les filtres]
« Distinct Plasma Immune Profile in ALS Implicates sTNFR-II in pAMPK/Leptin Homeostasis. », Int J Mol Sci, vol. 24, nᵒ 6, 2023.
, « Transactive response DNA-binding protein 43 is enriched at the centrosome in human cells. », Brain, vol. 146, nᵒ 9, p. 3624-3633, 2023.
, « Ultrasensitive digital immunoassays for SOD1 conformation in amyotrophic lateral sclerosis. », Bioanalysis, vol. 15, nᵒ 15, p. 927-936, 2023.
, « A novel assessment of fine-motor function reveals early hindlimb and detectable forelimb deficits in an experimental model of ALS. », Sci Rep, vol. 12, nᵒ 1, p. 17010, 2022.
, « FUS contributes to mTOR-dependent inhibition of translation. », J Biol Chem, vol. 295, nᵒ 52, p. 18459-18473, 2020.
, « Adeno-associated virus-mediated delivery of a recombinant single-chain antibody against misfolded superoxide dismutase for treatment of amyotrophic lateral sclerosis. », Mol Ther, vol. 22, nᵒ 3, p. 498-510, 2014.
, « Mitochondrial damage revealed by immunoselection for ALS-linked misfolded SOD1. », Hum Mol Genet, vol. 22, nᵒ 19, p. 3947-59, 2013.
, « Neuroprotection through excitability and mTOR required in ALS motoneurons to delay disease and extend survival. », Neuron, vol. 80, nᵒ 1, p. 80-96, 2013.
, « Ablation of proliferating cells in the CNS exacerbates motor neuron disease caused by mutant superoxide dismutase. », PLoS One, vol. 7, nᵒ 4, p. e34932, 2012.
, « Abnormal regenerative responses and impaired axonal outgrowth after nerve crush in TDP-43 transgenic mouse models of amyotrophic lateral sclerosis. », J Neurosci, vol. 32, nᵒ 50, p. 18186-95, 2012.
, « Localization of a toxic form of superoxide dismutase 1 protein to pathologically affected tissues in familial ALS. », Proc Natl Acad Sci U S A, vol. 109, nᵒ 14, p. 5505-10, 2012.
, « Methylene blue administration fails to confer neuroprotection in two amyotrophic lateral sclerosis mouse models. », Neuroscience, vol. 209, p. 136-43, 2012.
, « TDP-43 aggregation in neurodegeneration: are stress granules the key? », Brain Res, vol. 1462, p. 16-25, 2012.
, « ALS pathogenesis: recent insights from genetics and mouse models. », Prog Neuropsychopharmacol Biol Psychiatry, vol. 35, nᵒ 2, p. 363-9, 2011.
, « Deregulation of TDP-43 in amyotrophic lateral sclerosis triggers nuclear factor κB-mediated pathogenic pathways. », J Exp Med, vol. 208, nᵒ 12, p. 2429-47, 2011.
, « Pathological hallmarks of amyotrophic lateral sclerosis/frontotemporal lobar degeneration in transgenic mice produced with TDP-43 genomic fragments. », Brain, vol. 134, nᵒ Pt 9, p. 2610-26, 2011.
, « TDP-43 is directed to stress granules by sorbitol, a novel physiological osmotic and oxidative stressor. », Mol Cell Biol, vol. 31, nᵒ 5, p. 1098-108, 2011.
, « Treatment with minocycline after disease onset alters astrocyte reactivity and increases microgliosis in SOD1 mutant mice. », Exp Neurol, vol. 228, nᵒ 1, p. 69-79, 2011.
, « Distinct biochemical signatures characterize peripherin isoform expression in both traumatic neuronal injury and motor neuron disease. », J Neurochem, vol. 114, nᵒ 4, p. 1177-92, 2010.
, « Induction of protective immunity by vaccination with wild-type apo superoxide dismutase 1 in mutant SOD1 transgenic mice. », J Neuropathol Exp Neurol, vol. 69, nᵒ 10, p. 1044-56, 2010.
, « Intracerebroventricular infusion of monoclonal antibody or its derived Fab fragment against misfolded forms of SOD1 mutant delays mortality in a mouse model of ALS. », J Neurochem, vol. 113, nᵒ 5, p. 1188-99, 2010.
, « Neuronal over-expression of chromogranin A accelerates disease onset in a mouse model of ALS. », J Neurochem, vol. 115, nᵒ 5, p. 1102-11, 2010.
, « Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS. », Nat Neurosci, vol. 13, nᵒ 11, p. 1396-403, 2010.
, « Chromogranin B P413L variant as risk factor and modifier of disease onset for amyotrophic lateral sclerosis. », Proc Natl Acad Sci U S A, vol. 106, nᵒ 51, p. 21777-82, 2009.
, « Live imaging of amyotrophic lateral sclerosis pathogenesis: disease onset is characterized by marked induction of GFAP in Schwann cells. », Glia, vol. 57, nᵒ 10, p. 1130-42, 2009.
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