(A) Supplementation with 10 mM glucose accelerated paralysis of Aβ animals fed OP50 but did not eliminate the dietary shift (n ≥ 102).
(B) Supplementation with 0.3 mM oleic acid did not affect Aβ-induced paralysis (n ≥ 174).
(C) Pacdh-1∷GFP expression was induced in animals fed OP50 and DA837, but not OP50+B12, HB101, HB101+B12, and HT115.
(D) Supplementation with 148 nM vitamin B12 eliminated the impact of bacterial diet on paralysis of Aβ animals (n ≥ 139).
(E) Supplementation with 740 nM B12 had no added protective effect compared to 148 nM B12 (n = 3); *p < 0.05 compared to the no-supplementation control.
(F) B12 supplementation enhanced motility in C. elegans models of amyotrophic lateral sclerosis (ALS) and Huntington’s disease but did not affect the WT (n = 15).
(G) Vitamin B12 increased ATP levels in Aβ animals fed OP50 compared to those without B12 supplementation (no sup.; n = 6).
(H) Vitamin B12 increased average mitochondrial length in Aβ animals fed OP50 (n = 30).
(I) Vitamin B12 reduced H2O2, measured with H2DCFDA, in Aβ animals fed OP50 (n = 9).
(J) Vitamin B12 decreased O2−, measured with MitoSox, in Aβ animals fed OP50 (n ≥ 6).
(K) Transfer of Aβ animals from OP50 plus vitamin B12 plates to B12-free OP50 plates at the end of L4 eliminated the B12 protective effect (n ≥ 132).
(L) Transfer of Aβ animals fed OP50 to OP50 plates supplemented with B12 at the end of L4 delayed paralysis (n ≥ 54).
Error bars show SEM; *p < 0.05, **p < 0.01, and ***p < 0.001 one-way ANOVA with Dunnett’s post-test. See also Figures S2 and S3.