Figure 2. Vitamin B₁₂ is the protective factor in the HB101 diet.

(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.