Amyotrophic Lateral Sclerosis
Research News and Information

Monday, November 23, 2009

Reticulon-4A (Nogo-A) redistributes protein disulfide isomerase to protect mice from SOD1-dependent amyotrophic lateral sclerosis.

2 Nov 2009 Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease inherited in a small subset of patients. The SOD1(G93A) transgenic mouse models this subset of patients, and studies of this strain have suggested that endoplasmic reticulum (ER) ... Read more...

Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells.

17 Oct 2009 Activated protein C (APC) is a signaling protease with anticoagulant activity. Here, we have used mice expressing a mutation in superoxide dismutase-1 (SOD1) that is linked to amyotrophic lateral sclerosis (ALS) to show that administration of APC or ... Read more...

The APCs of neuroprotection.

17 Oct 2009 Mutations in the enzyme superoxide dismutase 1 (SOD1) have been linked to the neurodegenerative disease amyotrophic lateral sclerosis (ALS). In this issue of the JCI, Zhong et al. report that the endogenous anticoagulant activated protein C (APC) is ... Read more...

Latest indexed articles for 'Amyotrophic Lateral Sclerosis'

These are the very latest articles for this heading:

• Reticulon-4A (Nogo-A) redistributes protein disulfide isomerase to protect mice from SOD1-dependent amyotrophic lateral sclerosis. 2 Nov 2009
• [Prevalence of home ventilation therapy in Norway] 20 Oct 2009
• Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells. 17 Oct 2009
• The APCs of neuroprotection. 17 Oct 2009
• Subcutaneous IGF-1 is not beneficial in 2-year ALS trial. 11 Oct 2009
• Practice parameter update: The care of the patient with amyotrophic lateral sclerosis: multidisciplinary care, symptom management, and cognitive/behavioral impairment (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. 11 Oct 2009
• Practice parameter update: The care of the patient with amyotrophic lateral sclerosis: drug, nutritional, and respiratory therapies (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. 11 Oct 2009
• Lyme disease serology in amyotrophic lateral sclerosis. 29 Sep 2009
• DNA microarray analysis of transcriptional responses of mouse spinal cords to physical exercise. 29 Sep 2009
• Bone marrow-derived cells in the central nervous system of a mouse model of amyotrophic lateral sclerosis are associated with blood vessels and express CX(3)CR1. 29 Sep 2009
• Autophagy for the avoidance of neurodegeneration. 29 Sep 2009
• Prevalence of fatigue and depression in ALS patients and change over time. 29 Sep 2009
• The primary locus of motor neuron death in an ALS-PDC mouse model. 21 Sep 2009
• Trends and determinants of end-of-life practices in ALS in the Netherlands. 20 Sep 2009
• The ALS-associated mutation G93A in human copper-zinc superoxide dismutase selectively destabilizes the remote metal binding region. 20 Sep 2009
• XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy. 15 Sep 2009
• Structural changes to monomeric CuZn superoxide dismutase caused by the familial amyotrophic lateral sclerosis-associated mutation A4V. 14 Sep 2009
• TDP-43 is recruited to stress granules in conditions of oxidative insult. 14 Sep 2009
• A novel decoy that interrupts G93A-superoxide dismutase gain of interaction with malate dehydrogenase improves survival in an amyotrophic lateral sclerosis cell model. 8 Sep 2009
• Mutations in FUS cause FALS and SALS in French and French Canadian populations. 7 Sep 2009

See a longer list of these articles.

Technical information about 'Amyotrophic Lateral Sclerosis'

Definition: A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)

Descriptor UI: D000690

Alternative terms: Amyotrophic Lateral Sclerosis; Lateral Scleroses, Amyotrophic; Sclerosis, Amyotrophic Lateral; ALS (Amyotrophic Lateral Sclerosis); Lou Gehrig Disease; Gehrig's Disease; Gehrig Disease; Gehrigs Disease; Lou Gehrig's Disease; Lou Gehrigs Disease; Motor Neuron Disease, Amyotrophic Lateral Sclerosis; Amyotrophic Lateral Sclerosis, Guam Form; Guam Form of Amyotrophic Lateral Sclerosis; Amyotrophic Lateral Sclerosis With Dementia; Dementia With Amyotrophic Lateral Sclerosis;

Allowable Qualifiers: blood; cerebrospinal fluid; chemically induced; classification; complications; congenital; diagnosis; diet therapy; drug therapy; economics; embryology; enzymology; ethnology; etiology; genetics; history; immunology; metabolism; microbiology; mortality; nursing; epidemiology; parasitology; pathology; physiopathology; prevention & control; psychology; radiography; radionuclide imaging; radiotherapy; rehabilitation; surgery; therapy; urine; veterinary; ultrasonography; virology;

Tree Number: C10.228.854.139; C10.574.562.250; C10.668.460.250;