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<p>Brain-derived neurotrophic factor (BDNF) plays a pivotal role in learning and memory, and reductions in BDNF levels are closely associated with cognitive decline and psychiatric disorders. Dietary factors that maintain or restore brain BDNF expression may therefore contribute to brain health. In this study, we evaluated the effects of heat-killed lactic acid bacteria (LAB) on scopolamine-induced BDNF reduction using <i>Bdnf-Luciferase</i> (<i>Bdnf-Luc</i>) transgenic mice, which allow noninvasive monitoring of BDNF expression in the living brain by in vivo bioluminescence imaging. Administration of scopolamine induced a significant reduction in brain BDNF expression, which was successfully visualized by bioluminescence imaging. Oral administration of heat-killed <i>Bifidobacterium longum</i> KABP-042 markedly prevented this reduction, while heat-killed <i>Lactiplantibacillus plantarum</i> KABP-051 showed partial protective effects. Furthermore, both LAB strains significantly ameliorated scopolamine-induced impairment of hippocampus-dependent memory in contextual fear conditioning. These results demonstrate that specific heat-killed LAB exert protective effects against BDNF reduction and cognitive dysfunction in vivo. In addition, our findings highlight the utility of <i>Bdnf-Luc</i>-based in vivo bioluminescence imaging as a practical tool for evaluating dietary factors with potential benefits for brain health.</p>

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Heat-Killed Bifidobacterium longum KABP-042 and Lactiplantibacillus Plantarum KABP-051 Prevent Scopolamine-Induced BDNF Reduction and Memory Impairment in Mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月14日

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  • Mamoru Fukuchi,
  • Naoki Arai,
  • Shinichi Honda,
  • Yuji Tominaga

摘要

Brain-derived neurotrophic factor (BDNF) plays a pivotal role in learning and memory, and reductions in BDNF levels are closely associated with cognitive decline and psychiatric disorders. Dietary factors that maintain or restore brain BDNF expression may therefore contribute to brain health. In this study, we evaluated the effects of heat-killed lactic acid bacteria (LAB) on scopolamine-induced BDNF reduction using Bdnf-Luciferase (Bdnf-Luc) transgenic mice, which allow noninvasive monitoring of BDNF expression in the living brain by in vivo bioluminescence imaging. Administration of scopolamine induced a significant reduction in brain BDNF expression, which was successfully visualized by bioluminescence imaging. Oral administration of heat-killed Bifidobacterium longum KABP-042 markedly prevented this reduction, while heat-killed Lactiplantibacillus plantarum KABP-051 showed partial protective effects. Furthermore, both LAB strains significantly ameliorated scopolamine-induced impairment of hippocampus-dependent memory in contextual fear conditioning. These results demonstrate that specific heat-killed LAB exert protective effects against BDNF reduction and cognitive dysfunction in vivo. In addition, our findings highlight the utility of Bdnf-Luc-based in vivo bioluminescence imaging as a practical tool for evaluating dietary factors with potential benefits for brain health.