ALS

Neurology
F JerusalemF Ries

Abstract

The cause of ALS is not known but there are four main hypotheses about its etiology. First, an excess of extracellular glutamate in the CNS of patients with ALS resulting from a defect in glutamate reuptake may have excitotoxic effects on motor neurons. Clinical trials suggest the antiglutamate agent riluzole improves survival of patients with the disease. Second, ALS may be an autoimmune disease, but immunologically-based treatments have been unsuccessful. The third hypothesis is that ALS results from a lack of neurotrophic growth factors. Preliminary results from clinical trials indicate recombinant human insulin-like growth factor I offers therapeutic promise. Finally, familial ALS is sometimes linked to a gene encoding a Cu/Zn-binding superoxide dismutase; the mutations in ALS are thought to result in gain of function of dismutase activity. The involvement of superoxide dismutase in sporadic ALS is unclear.

Citations

Oct 26, 2001·Journal of the Neurological Sciences·M Tavakoli, M Malek
Oct 8, 1997·Journal of Child Psychology and Psychiatry, and Allied Disciplines·J E Harrison, P F Bolton
Oct 20, 2007·The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry·David E Featherstone, Scott A Shippy
May 20, 2003·The European Journal of Neuroscience·Vincent LegayBruno Lina
Oct 29, 2008·Diabetes Research and Clinical Practice·Angelo AvogaroGianpaolo Fadini
Jun 20, 1998·Neuropathology and Applied Neurobiology·E M Fisher
Jun 26, 1998·Brain Research. Brain Research Reviews·B Connor, M Dragunow

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