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<p>Epidemiologic study suggests that nicotine reduces the risk of Parkinson’s disease (PD) and thus could serve as a potential treatment. In this study, we aimed to investigate the effect of nicotine on the behavioral phenotypes and pathological characteristics of mice induced by human alpha-synuclein preformed fibers (α-syn-PFF). Mice were injected with 5&#xa0;µg of human α-syn-PFF in the hippocampus while administering nicotine-containing drinking water (200&#xa0;µg/mL). After 1&#xa0;month, the motor ability, mood, spatial learning, and memory ability of the PD phenotype-like model mice were detected using open field, rotarod, Y maze, and O maze tests. The expression of pathological α-syn and apoptotic proteins, as well as the number of glial and neural stem cells in the hippocampus of mice, was detected using western blot and immunofluorescence. The results demonstrated that nicotine significantly reduced pathological α-syn accumulation, α-syn serine 129 phosphorylation, and apoptosis induced by α-syn-PFF injection in the hippocampus of mice. Nicotine also inhibited the increase in the number of glia, microglia, and neuronal apoptotic cells, and it decreased the expression of PI3K and Akt while also exhibiting significant memory impairment, motor deficits, and anxiety-like behavior. In conclusion, our findings suggest that nicotine ameliorates behavioral deficits and pathological changes in mice by inhibiting human α-syn-PFF-induced neuroinflammation and apoptosis.</p>

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Nicotine Ameliorates α-Synuclein Preformed Fibril-Induced Behavioral Deficits and Pathological Features in Mice

  • 期刊论文

  • 发表日期：

    2025年1月16日

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  • Zhangqiong Huang,
  • Yue Pan,
  • Kaili Ma,
  • Haiyu Luo,
  • Qinglan Zong,
  • Zhengcun Wu,
  • Zhouhai Zhu,
  • Ying Guan

摘要

Epidemiologic study suggests that nicotine reduces the risk of Parkinson’s disease (PD) and thus could serve as a potential treatment. In this study, we aimed to investigate the effect of nicotine on the behavioral phenotypes and pathological characteristics of mice induced by human alpha-synuclein preformed fibers (α-syn-PFF). Mice were injected with 5 µg of human α-syn-PFF in the hippocampus while administering nicotine-containing drinking water (200 µg/mL). After 1 month, the motor ability, mood, spatial learning, and memory ability of the PD phenotype-like model mice were detected using open field, rotarod, Y maze, and O maze tests. The expression of pathological α-syn and apoptotic proteins, as well as the number of glial and neural stem cells in the hippocampus of mice, was detected using western blot and immunofluorescence. The results demonstrated that nicotine significantly reduced pathological α-syn accumulation, α-syn serine 129 phosphorylation, and apoptosis induced by α-syn-PFF injection in the hippocampus of mice. Nicotine also inhibited the increase in the number of glia, microglia, and neuronal apoptotic cells, and it decreased the expression of PI3K and Akt while also exhibiting significant memory impairment, motor deficits, and anxiety-like behavior. In conclusion, our findings suggest that nicotine ameliorates behavioral deficits and pathological changes in mice by inhibiting human α-syn-PFF-induced neuroinflammation and apoptosis.