PMC:6610326 / 61636-63096 JSONTXT

{"project":"2_test","denotations":[{"id":"31316328-1346630-38515691","span":{"begin":101,"end":105},"obj":"1346630"},{"id":"31316328-7826630-38515692","span":{"begin":125,"end":129},"obj":"7826630"},{"id":"31316328-14642280-38515693","span":{"begin":145,"end":149},"obj":"14642280"},{"id":"31316328-8360662-38515694","span":{"begin":311,"end":315},"obj":"8360662"},{"id":"31316328-19251638-38515695","span":{"begin":760,"end":764},"obj":"19251638"},{"id":"31316328-22668777-38515696","span":{"begin":1151,"end":1155},"obj":"22668777"},{"id":"31316328-18815246-38515697","span":{"begin":1278,"end":1282},"obj":"18815246"},{"id":"31316328-25892237-38515698","span":{"begin":1397,"end":1401},"obj":"25892237"}],"text":"Schwann cells are required for the long-term maintenance of synapses at the NMJ (Reynolds and Woolf, 1992; Son and Thompson, 1995; Reddy et al., 2003). Early studies demonstrated that myelin is altered along peripheral nerves in ALS patients, implying that Schwann cells are involved in disease (Perrie et al., 1993). However, unlike the other glial cell types, more recent studies on the role of Schwann cells in ALS have reached conflicting conclusions. Knockdown of SOD1G37R within Schwann cells significantly accelerates disease progression, concomitant with a specific reduction in insulin-like growth factor (IGF-I), which is protective to MNs (see section “Neuroprotective and Neurotoxic Factor Expression in MN Subpopulations” below) (Lobsiger et al., 2009). This surprising finding, implying that SOD1G37R is protective in Schwann cells, could be linked to the dismutase activity of SOD1. Whereas SOD1G37R retains its enzymatic activity, SOD1G85R does not, and similar experiments performed in SOD1G85R mice resulted in opposite findings; Schwann cell specific knock-down of SOD1G85R delayed disease onset and extended survival (Wang et al., 2012). Furthermore, TGF-β1 produced by Schwann cells promotes synaptogenesis by increasing nerve-muscle contacts (Feng and Ko, 2008), in contrast to TGF-β1 expression in astrocytes which accelerates disease progression in SOD1 mice (Endo et al., 2015). Hence, the role of Schwann cells in ALS remains unclear."}

{"project":"0_colil","denotations":[{"id":"31316328-1346630-631148","span":{"begin":101,"end":105},"obj":"1346630"},{"id":"31316328-7826630-631149","span":{"begin":125,"end":129},"obj":"7826630"},{"id":"31316328-14642280-631150","span":{"begin":145,"end":149},"obj":"14642280"},{"id":"31316328-8360662-631151","span":{"begin":311,"end":315},"obj":"8360662"},{"id":"31316328-19251638-631152","span":{"begin":760,"end":764},"obj":"19251638"},{"id":"31316328-22668777-631153","span":{"begin":1151,"end":1155},"obj":"22668777"},{"id":"31316328-18815246-631154","span":{"begin":1278,"end":1282},"obj":"18815246"},{"id":"31316328-25892237-631155","span":{"begin":1397,"end":1401},"obj":"25892237"}],"text":"Schwann cells are required for the long-term maintenance of synapses at the NMJ (Reynolds and Woolf, 1992; Son and Thompson, 1995; Reddy et al., 2003). Early studies demonstrated that myelin is altered along peripheral nerves in ALS patients, implying that Schwann cells are involved in disease (Perrie et al., 1993). However, unlike the other glial cell types, more recent studies on the role of Schwann cells in ALS have reached conflicting conclusions. Knockdown of SOD1G37R within Schwann cells significantly accelerates disease progression, concomitant with a specific reduction in insulin-like growth factor (IGF-I), which is protective to MNs (see section “Neuroprotective and Neurotoxic Factor Expression in MN Subpopulations” below) (Lobsiger et al., 2009). This surprising finding, implying that SOD1G37R is protective in Schwann cells, could be linked to the dismutase activity of SOD1. Whereas SOD1G37R retains its enzymatic activity, SOD1G85R does not, and similar experiments performed in SOD1G85R mice resulted in opposite findings; Schwann cell specific knock-down of SOD1G85R delayed disease onset and extended survival (Wang et al., 2012). Furthermore, TGF-β1 produced by Schwann cells promotes synaptogenesis by increasing nerve-muscle contacts (Feng and Ko, 2008), in contrast to TGF-β1 expression in astrocytes which accelerates disease progression in SOD1 mice (Endo et al., 2015). Hence, the role of Schwann cells in ALS remains unclear."}