Grahame J. Kidd

Proteolipid promoter activity distinguishes two populations of NG2-positive cells throughout neonatal cortical development.

RNA trafficking and stabilization elements associate with multiple brain proteins.

Dysmyelinated lower motor neurons retract and regenerate dysfunctional synaptic terminals.

Beta IV tubulin is selectively expressed by oligodendrocytes in the central nervous system.

A dual tyrosine-leucine motif mediates myelin protein P0 targeting in MDCK cells.

Evidence for synaptic stripping by cortical microglia.

NG2-positive cells generate A2B5-positive oligodendrocyte precursor cells.

Activation of the ciliary neurotrophic factor (CNTF) signalling pathway in cortical neurons of multiple sclerosis patients.

Genetic deletion of BACE1 in mice affects remyelination of sciatic nerves.

Imaging correlates of decreased axonal Na+/K+ ATPase in chronic multiple sclerosis lesions.

Antisense suppression of tau in cultured rat oligodendrocytes inhibits process formation.

P0 protein is required for and can induce formation of schmidt-lantermann incisures in myelin internodes.

Beta4 tubulin identifies a primitive cell source for oligodendrocytes in the mammalian brain.

Demyelination increases axonal stationary mitochondrial size and the speed of axonal mitochondrial transport.

Demyelination causes synaptic alterations in hippocampi from multiple sclerosis patients.

Myelination and axonal electrical activity modulate the distribution and motility of mitochondria at CNS nodes of Ranvier.

Lipopolysaccharide-induced microglial activation and neuroprotection against experimental brain injury is independent of hematogenous TLR4.

Cortical remyelination: a new target for repair therapies in multiple sclerosis.

Clinically feasible MTR is sensitive to cortical demyelination in MS.

WDR81 is necessary for purkinje and photoreceptor cell survival.

Biology of Schwann cells.

Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons.

Microglial displacement of inhibitory synapses provides neuroprotection in the adult brain.

Proteolipid protein cannot replace P0 protein as the major structural protein of peripheral nervous system myelin.

Mapping and morphometric analysis of synapses and spines on fusiform cells in the dorsal cochlear nucleus.

Nuclear export inhibitors avert progression in preclinical models of inflammatory demyelination.