Age-related olfactory dysfunction: cellular and molecular analyses

1.热量限制可加重小鼠嗅粘膜神经上皮的老化性变性，并使损伤后的嗅神经上皮再生恶化。通过热量限制下调神经上皮细胞的增殖活性似乎在发病机制中起重要作用。2.使用Poly（I：C）（病毒双链RNA的合成类似物）在小鼠中建立病毒后嗅觉障碍（PVOD）的免疫模型。提示嗜中性粒细胞介导的天然免疫反应所引起的继发性损伤在PVOD的发病中起重要作用。3.对雌激素受体β（ER β）缺陷小鼠的分析表明，雌激素通过ER β在嗅粘膜的稳态中起作用。4. FAT-1小鼠在损伤后表现出更好的神经上皮再生，表明组织脂肪酸与嗅神经上皮的再生有关。

1. Caloric restriction exacerbated the age-related neuroepithelial degeneration in the mouse olfactory mucosa and also worsened the regeneration of the olfactory neuroepithelium after injury. The downregulation of proliferative activity in neuroepithelium by caloric restriction appeared to play an important role in the pathogenesis. 2. The immune model of postviral olfactory disorder (PVOD) was developed in mice using Poly(I:C), a synthetic analog of viral double-stranded RNA. The analyses suggested that the secondary damage caused by the neutrophil-mediated innate immune response plays an important role in the pathogenesis of PVOD. 3. The analyses of estrogen receptor beta (ERbeta) -deficient mice suggested that estrogen plays a role in the homeostasis of the olfactory mucosa through ERbeta. 4. FAT-1 mice demonstrated better neuroepithelical regeneration after injury, suggesting that the tissue fatty acid is associated with the regeneration of the olfactory neuroepithelium.