Thomas H Gillingwater

Age-dependent synapse withdrawal at axotomised neuromuscular junctions in Wld(s) mutant and Ube4b/Nmnat transgenic mice.

Ultrastructural correlates of synapse withdrawal at axotomized neuromuscular junctions in mutant and transgenic mice expressing the Wld gene.

Neuroprotection after transient global cerebral ischemia in Wld(s) mutant mice.

The relationship of neuromuscular synapse elimination to synaptic degeneration and pathology: insights from WldS and other mutant mice.

Axotomy-dependent and -independent synapse elimination in organ cultures of Wld(s) mutant mouse skeletal muscle.

Myo-GDNF increases non-functional polyinnervation of reinnervated mouse muscle.

Progressive abnormalities in skeletal muscle and neuromuscular junctions of transgenic mice expressing the Huntington's disease mutation.

The slow Wallerian degeneration gene, WldS, inhibits axonal spheroid pathology in gracile axonal dystrophy mice.

A rat model of slow Wallerian degeneration (WldS) with improved preservation of neuromuscular synapses.

Progressive loss of motor neuron function in wasted mice: effects of a spontaneous null mutation in the gene for the eEF1 A2 translation factor.

The neuroprotective WldS gene regulates expression of PTTG1 and erythroid differentiation regulator 1-like gene in mice and human cells.

Synaptic Ras GTPase activating protein regulates pattern formation in the trigeminal system of mice.

Involvement of protein kinase A in patterning of the mouse somatosensory cortex.

Delayed synaptic degeneration in the CNS of Wlds mice after cortical lesion.

Synaptic vulnerability in neurodegenerative disease.

Differential proteomics analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wlds) gene.

Design of a novel quantitative PCR (QPCR)-based protocol for genotyping mice carrying the neuroprotective Wallerian degeneration slow (Wlds) gene.

Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy.

Synaptic changes in the thalamocortical system of cathepsin D-deficient mice: a model of human congenital neuronal ceroid-lipofuscinosis.

A neurological phenotype in mice with DNA repair gene Ercc1 deficiency.

VAPB interacts with and modulates the activity of ATF6.

VCP binding influences intracellular distribution of the slow Wallerian degeneration protein, Wld(S).

Rapid loss of motor nerve terminals following hypoxia-reperfusion injury occurs via mechanisms distinct from classic Wallerian degeneration.

Modified cell cycle status in a mouse model of altered neuronal vulnerability (slow Wallerian degeneration; Wlds).

Identity, developmental restriction and reactivity of extralaminar cells capping mammalian neuromuscular junctions.

mGluR5 regulates glutamate-dependent development of the mouse somatosensory cortex.

Loss of translation elongation factor (eEF1A2) expression in vivo differentiates between Wallerian degeneration and dying-back neuronal pathology.

The importance of exposure to human material in anatomical education: a philosophical perspective.

Protein product of CLN6 gene responsible for variant late-onset infantile neuronal ceroid lipofuscinosis interacts with CRMP-2.

Transcriptional regulation of the AP-1 and Nrf2 target gene sulfiredoxin.

Molecular correlates of axonal and synaptic pathology in mouse models of Batten disease.

Murine cathepsin D deficiency is associated with dysmyelination/myelin disruption and accumulation of cholesteryl esters in the brain.

Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy.

Expression of the neuroprotective slow Wallerian degeneration (WldS) gene in non-neuronal tissues.

Alternative splicing events are a late feature of pathology in a mouse model of spinal muscular atrophy.

Age-related motor neuron degeneration in DNA repair-deficient Ercc1 mice.

SMN deficiency disrupts brain development in a mouse model of severe spinal muscular atrophy.

Synaptic protection in the brain of WldS mice occurs independently of age but is sensitive to gene-dose.

The response of neuromuscular junctions to injury is developmentally regulated.

Induction of cell stress in neurons from transgenic mice expressing yellow fluorescent protein: implications for neurodegeneration research.

ApoE isoform-specific regulation of regeneration in the peripheral nervous system.

The contribution of mouse models to understanding the pathogenesis of spinal muscular atrophy.

Targeting synaptic pathology in multiple sclerosis: fingolimod to the rescue?

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy.

Morphologic and functional correlates of synaptic pathology in the cathepsin D knockout mouse model of congenital neuronal ceroid lipofuscinosis.

Using induced pluripotent stem cells (iPSC) to model human neuromuscular connectivity: promise or reality?

Development of a supported self-directed learning approach for anatomy education.

Altered maturation of the primary somatosensory cortex in a mouse model of fragile X syndrome.

WldS prevents axon degeneration through increased mitochondrial flux and enhanced mitochondrial Ca2+ buffering.

Combining comparative proteomics and molecular genetics uncovers regulators of synaptic and axonal stability and degeneration in vivo.

Spinal muscular atrophy: going beyond the motor neuron.

Morphological characteristics of motor neurons do not determine their relative susceptibility to degeneration in a mouse model of severe spinal muscular atrophy.

Quantitative tractography and tract shape modeling in amyotrophic lateral sclerosis.

Effect of limb lengthening on internodal length and conduction velocity of peripheral nerve.

Increasing SMN levels using the histone deacetylase inhibitor SAHA ameliorates defects in skeletal muscle microvasculature in a mouse model of severe spinal muscular atrophy.

Studying synapses in human brain with array tomography and electron microscopy.

Total protein analysis as a reliable loading control for quantitative fluorescent Western blotting.

Executive deficits, not processing speed relates to abnormalities in distinct prefrontal tracts in amyotrophic lateral sclerosis.

Label-free proteomics identifies Calreticulin and GRP75/Mortalin as peripherally accessible protein biomarkers for spinal muscular atrophy.

SMN-dependent intrinsic defects in Schwann cells in mouse models of spinal muscular atrophy.