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B cell-dependent EAE induces visual deficits in the mouse with similarities to human autoimmune demyelinating diseases. J Neuroinflammation. 2022;19(1):54..
The Lack of Amyloidogenic Activity Is Persistent in Old WT and APP/PS1ΔE9 Mouse Retinae. Int J Mol Sci. 2021;22(21)..
Nogo-A-targeting antibody promotes visual recovery and inhibits neuroinflammation after retinal injury. Cell Death Dis. 2020;11(2):101..
Corrigendum: Human Tau Expression Does Not Induce Mouse Retina Neurodegeneration, Suggesting Differential Toxicity of Tau in Brain vs. Retinal Neurons. Front Mol Neurosci. 2018;11:390..
Human Tau Expression Does Not Induce Mouse Retina Neurodegeneration, Suggesting Differential Toxicity of Tau in Brain vs. Retinal Neurons. Front Mol Neurosci. 2018;11:293..
Nogo-A inactivation improves visual plasticity and recovery after retinal injury. Cell Death Dis. 2018;9(7):727..
Nonamyloidogenic processing of amyloid beta precursor protein is associated with retinal function improvement in aging male APPswe/PS1ΔE9 mice. Neurobiol Aging. 2017;53:181-191..
Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System. Neural Plast. 2017;2017:6818970..
Nogo-A deletion increases the plasticity of the optokinetic response and changes retinal projection organization in the adult mouse visual system. Brain Struct Funct. 2016;221(1):317-29..
Reticulon 4A/Nogo-A influences the distribution of Kir4.1 but is not essential for potassium conductance in retinal Müller glia. Neurosci Lett. 2016;627:168-77..
Sphingosine 1-phosphate receptor 1 is required for retinal ganglion cell survival after optic nerve trauma. J Neurochem. 2016;138(4):571-86..