Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels.
Level 5 - mechanism / opinion, no new human data
Animal and in vitro laboratory study evaluating mechanisms in mice and cell culture
PubMed 28506637 · doi:10.1016/j.mcn.2017.05.005
What was done
C57BL6/J mice were exposed to predator stress for 5 consecutive nights and administered thiamine or benfotiamine (200 mg/kg/day in drinking water for 20 days). Proliferation (Ki67-positive cells) and survival (BrdU-positive cells) of newborn immature neurons were quantified in the subgranular zone of the dentate gyrus. The authors also evaluated body weight, anxiety-like behavior, brain free thiamine and thiamine diphosphate (ThDP) levels, and hippocampal protein carbonylation. In vitro protection against paraquat-induced oxidative stress was examined in cultured mouse neuroblastoma cells.
What was found
Predator stress reduced Ki67-positive and BrdU-positive cells in the dentate gyrus, caused body weight loss, induced anxiety-like behavior, and increased hippocampal protein carbonylation. Treatment with either thiamine or benfotiamine prevented the decrease in Ki67- and BrdU-positive cells, counteracted body weight loss, suppressed anxiety-like behavior, and antagonized protein carbonylation. Both treatments modestly increased brain free thiamine while brain ThDP levels remained unchanged. In cell culture, benfotiamine protected against paraquat-induced oxidative stress. No exact numerical counts, percentages, or effect sizes were reported in the abstract.
Why it matters
These findings suggest that thiamine and benfotiamine may preserve hippocampal neurogenesis and reduce stress-induced behavioral and oxidative changes via non-coenzyme antioxidant pathways rather than alterations in brain ThDP levels.
Limits
This is an animal and cell culture study with no human clinical data. The abstract does not provide sample sizes (n), baseline nutritional status, effect sizes, variance measures, or the specific cellular antioxidant signaling mechanisms.
Cited by
- supports Benfotiamine is a synthetic fat-soluble form of vitamin B1 that lacks substantial data showing it penetrates the brain.