Dr John Henry Stockley

Interests

Oligodendrocyte Precursor Cells (OPCs) are an abundant class of multipotent proliferating glia in the CNS. OPCs have the amazing capacity to not only generate oligodendrocytes that form the insulating myelin sheath surrounding axons, but also repair and replace lost myelin in the CNS in a process known as remyelination. We are developing compounds and identifying molecular targets to enhance CNS repair.

Live cell imaging of myelinating GFP labelled oligodendrocyte
Live cell imaging of myelinating ChR2 labelled oligodendrocyte
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Research Focus

Keywords

Stem Cells

Oligodendrocytes

Myelination

Drug Discovery

White matter plasticity

Clinical conditions

Autism

Cerebral Palsy

Multiple sclerosis

Schizophrenia

Traumatic brain injury

Equipment

Bioinformatics

Cell culture

Cloning

Confocal microscopy

Electrophysiological recording techniques

Fluorescence microscopy

Immunohistochemistry

In situ hybridisation

Media Formulation

Optogenetics

Western Blotting

Collaborators

No collaborators listed

Associated News Items


    Publications

    2013

    Lundgaard I, Luzhynskaya A, Stockley JH, Wang Z, Evans KA, Swire M, Volbracht K, Gautier HO, Franklin RJ, Ffrench-Constant C, Attwell D, Káradóttir RT (2013), “Neuregulin and BDNF Induce a Switch to NMDA Receptor-Dependent Myelination by Oligodendrocytes.” PLoS Biol 11(12):e1001743 Details

    2012

    Káradóttir RT, Stockley JH (2012), “Deconstructing myelination: it all comes down to size.” Nat Methods 9(9):883-4 Details

    2008

    Stockley JH, O'Neill C (2008), “Understanding BACE1: essential protease for amyloid-beta production in Alzheimer's disease.” Cell Mol Life Sci 65(20):3265-89 Details

    2007

    Stockley JH, O'Neill C (2007), “The proteins BACE1 and BACE2 and beta-secretase activity in normal and Alzheimer's disease brain.” Biochem Soc Trans 35(Pt 3):574-6 Details

    2006

    Stockley JH, Ravid R, O'Neill C (2006), “Altered beta-secretase enzyme kinetics and levels of both BACE1 and BACE2 in the Alzheimer's disease brain.” FEBS Lett 580(28-29):6550-60 Details