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. 2006 Sep 20;26(38):9794–9804. doi: 10.1523/JNEUROSCI.2116-06.2006

Figure 6.

Figure 6.

Profound protective effects of NAm on the behavioral defects of the EAE model. A, Behavioral scores (mean ± SEM) of different groups of EAE mice. Differences between each treated group and untreated controls were significant as determined by two-tailed Student's t test: p < 0.05, from 7 d p.i. in the low-dose NAm-treated wild-type group (125 mg/kg); p < 0.001, from 6 d p.i. in the high-dose NAm-treated wild-type and Wlds groups (500 mg/kg). B, Clinical features of the EAE model in NAm-treated groups and untreated controls. Symptom onset was significantly delayed in each treated group when compared with untreated wild-type EAE mice (*p < 0.05; **p < 0.001; Student's t test). C, NAD levels (mean ± SEM) in cervical spinal cords from different groups of EAE mice as analyzed by HPLC. At both 2 and 4 weeks p.i., the NAD levels in each treated group were significantly higher than those from untreated controls (**p < 0.001; Student's t test).