An agonist antibody to MuSK, delivered after disease onset, decreases the loss of neuromuscular synapses, improves motor function and extends the lifespan of ALS mice.

Proteins implicated in Alzheimer’s disease, including amyloid precursor protein and ApoE receptors, interact with each other and with a signalling molecule called agrin to influence the development of the neuromuscular junction.

Depending upon the parameters used, neuromuscular stimulation can have beneficial or deleterious impacts on muscle structure and function in an animal model of Duchenne muscular dystrophy.

Human skeletal muscle progenitors and motor neurons self-organize in three-dimensional co-culture to form functional neuromuscular junctions that developmentally mature from the embryonic to the adult state.

A liver-specific depletion of the survival motor neuron protein in a mouse model unveils a compelling and intricate connection between liver function and pancreatic abnormalities in spinal muscular atrophy.

Skeletal muscle stem cells play important roles in the regeneration of neuromuscular junctions, and so present new targets for therapies to treat neuromuscular decline observed in the context of aging and various neuromuscular diseases.

Motor axons undergo dynamic branch-specific changes for weeks before complete neuronal degeneration in a model of amyotrophic lateral sclerosis, highlighting the importance of peripheral factors, intrinsic and extrinsic to motoneurons.

Nemo-like kinase is a key protein promoting the pathogenesis of spinal and bulbar muscular atrophy.

Muscle stem cells locally respond to perturbations of motor neurons and the neuromuscular junction.

The discovery of markers specific to perisynaptic Schwann cells will accelerate the discovery of mechanisms important for their differentiation and function.