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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: J Neurochem. 2012 Jan 4;120(4):598–610. doi: 10.1111/j.1471-4159.2011.07601.x

Fig. 4. D-serine treatment of G93A mSOD1 mice presymptomatically and at symptom onset.

Fig. 4

(a) D-serine administered in chow (1 gram/kg chow = 160 mg/kg/day) from postnatal day 65 hastens symptom onset by approximately 15 days. Bars represent mean onset day ± S.E.M. (b) Values for untreated G93A mice (Fig. 4c, top bar) represent the means for two groups (controls for SR deletion and controls for D-serine treatment), which were very similar. Initiation of D-serine treatment at the time of normal symptom onset (90 days) demonstrates that it can slow disease progression, independently of any effect on time of onset. Bars represent mean S.I. ± S.E.M. n values = 7 (4 M/3 F), 10 (4 M/6 F), and 9 (4 M/5 F) for controls, presymptomatic D-serine treatment, and D-serine treatment at onset, respectively. * P < 0.001, # P < 0.05. (c) Summary of survival interval effects of SR mutation and D-serine treatment in G93A mSOD1 mice (from figures 3 and 4), illustrating combined effects on symptom onset and ultimate survival.