In SALS there is a progressive loss of motor neurons in the spinal cord and brain stem that results in muscle wasting and weakness, and ultimately death. The underlying pathological mechanism of the disease is yet to be elucidated. Indeed the pathogenesis may include several rather than one of these mechanisms.
Calcium regulation is crucial within the body.
Intracellular calcium serves as a second messenger, cell death mediator, and an aide in cell outgrowth. Improper regulation could lead to cell death. Several electrophysiological studies have shown multiple effects of SALS IgG on calcium currents in multiple cell types. Sporadic ALS IgG reduced peak calcium current and total charge movement in L-type skeletal muscle channels. However, SALS IgG enhanced calcium current in adrenal and Purkinje cells.