[HTML][HTML] Amyotrophic lateral sclerosis

MC Kiernan, S Vucic, BC Cheah, MR Turner, A Eisen… - The lancet, 2011 - thelancet.com
Amyotrophic lateral sclerosis (ALS) is an idiopathic, fatal neurodegenerative disease of the
human motor system. In this Seminar, we summarise current concepts about the origin of the …

Energy metabolism in amyotrophic lateral sclerosis

L Dupuis, PF Pradat, AC Ludolph… - The Lancet Neurology, 2011 - thelancet.com
Amyotrophic lateral sclerosis (ALS) is characterised by the progressive degeneration of
upper and lower motor neurons. Besides motor neuron degeneration, ALS is associated …

Motor unit and neuromuscular junction remodeling with aging

MR Deschenes - Current aging science, 2011 - ingentaconnect.com
The neuromuscular system is one of the largest and most vital organ systems of the body.
The function and mass of the neuromuscular system gradually deteriorate during the natural …

Optimised and Rapid Pre-clinical Screening in the SOD1G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis (ALS)

RJ Mead, EJ Bennett, AJ Kennerley, P Sharp… - PloS one, 2011 - journals.plos.org
The human SOD1G93A transgenic mouse has been used extensively since its development
in 1994 as a model for amyotrophic lateral sclerosis (ALS). In that time, a great many insights …

Abnormalities of satellite cells function in amyotrophic lateral sclerosis

PF Pradat, A Barani, J Wanschitz… - Amyotrophic Lateral …, 2011 - Taylor & Francis
Amyotrophic lateral sclerosis (ALS) is characterized by progressive denervation leading to
muscle atrophy prevented, during the early phase, by compensatory reinnervation. Little is …

Motor neuron trophic factors: therapeutic use in ALS?

TW Gould, RW Oppenheim - Brain research reviews, 2011 - Elsevier
The modest effects of neurotrophic factor (NTF) treatment on lifespan in both animal models
and clinical studies of Amyotropic Lateral Sclerosis (ALS) may result from any one or …

Neuroprotection by gene therapy targeting mutant SOD1 in individual pools of motor neurons does not translate into therapeutic benefit in fALS mice

C Towne, V Setola, BL Schneider, P Aebischer - Molecular Therapy, 2011 - cell.com
A major challenge in neurological gene therapy is delivery of the transgene to sufficient cell
numbers in an atraumatic manner. This is particularly difficult for motor neuron (MN) …

Altered expression of myogenic regulatory factors in the mouse model of amyotrophic lateral sclerosis

R Manzano, JM Toivonen, S Oliván, AC Calvo… - Neurodegenerative …, 2011 - karger.com
Background: In the superoxide dismutase 1 (SOD1)-G93A mouse model of amyotrophic
lateral sclerosis (ALS), skeletal muscle is a key target of mutant SOD1 toxicity. However, the …

Respiration and ROS production in brain and spinal cord mitochondria of transgenic rats with mutant G93a Cu/Zn-superoxide dismutase gene

A Panov, N Kubalik, N Zinchenko, R Hemendinger… - Neurobiology of …, 2011 - Elsevier
Mitochondrial dysfunction is involved in the pathogenesis of motor neuron degeneration in
the G93A mutant transgenic (tgmSOD1) animal model of ALS. However, it is unknown …

Comparison of muscle ultrastructure in myasthenia gravis with anti-MuSK and anti-AChR antibodies

G Cenacchi, P Valentina, F Marina, P Elena… - Journal of …, 2011 - Springer
Patients with myasthenia gravis (MG) with antibodies to muscle-specific receptor tyrosine
kinase (MuSK) differ from acetylcholine receptor (AChR)-positive MG patients, as they …