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人类突变淀粉样β蛋白前体(hAβPPSwInd)对小鼠嗅球的早期体内效应。

Early in vivo Effects of the Human Mutant Amyloid-β Protein Precursor (hAβPPSwInd) on the Mouse Olfactory Bulb.

作者信息

Rusznák Zoltán, Kim Woojin Scott, Hsiao Jen-Hsiang T, Halliday Glenda M, Paxinos George, Fu YuHong

机构信息

Neuroscience Research Australia, Sydney, NSW, Australia.

School of Medical Science, The University of New South Wales, Sydney, NSW, Australia.

出版信息

J Alzheimers Dis. 2016;49(2):443-57. doi: 10.3233/JAD-150368.

Abstract

The amyloid-β protein precursor (AβPP) has long been linked to Alzheimer's disease (AD). Using J20 mice, which express human AβPP with Swedish and Indiana mutations, we studied early pathological changes in the olfactory bulb. The presence of AβPP/amyloid-β (Aβ) was examined in mice aged 3 months (before the onset of hippocampal Aβ deposition) and over 5 months (when hippocampal Aβ deposits are present). The number of neurons, non-neurons, and proliferating cells was assessed using the isotropic fractionator method. Our results demonstrate that although AβPP is overexpressed in some of the mitral cells, widespread Aβ deposition and microglia aggregates are not prevalent in the olfactory bulb. The olfactory bulbs of the younger J20 group harbored significantly fewer neurons than those of the age-matched wild-type mice (5.57±0.13 million versus 6.59±0.36 million neurons; p = 0.011). In contrast, the number of proliferating cells was higher in the young J20 than in the wild-type group (i.e., 6617±425 versus 4455±623 cells; p = 0.011). A significant increase in neurogenic activity was also observed in the younger J20 olfactory bulb. In conclusion, our results indicate that (1) neurons participating in the mouse olfactory function overexpress AβPP; (2) the cellular composition of the young J20 olfactory bulb is different from that of wild-type littermates; (3) these differences may reflect altered neurogenic activity and/or delayed development of the J20 olfactory system; and (4) AβPP/Aβ-associated pathological changes that take place in the J20 hippocampus and olfactory bulb are not identical.

摘要

淀粉样β蛋白前体(AβPP)长期以来一直与阿尔茨海默病(AD)相关联。我们使用表达带有瑞典和印第安纳突变的人AβPP的J20小鼠,研究了嗅球的早期病理变化。在3个月龄(海马Aβ沉积开始之前)和5个月以上(海马存在Aβ沉积物时)的小鼠中检测了AβPP/淀粉样β(Aβ)的存在情况。使用各向同性分割法评估神经元、非神经元和增殖细胞的数量。我们的结果表明虽然AβPP在一些二尖瓣细胞中过表达,但广泛的Aβ沉积和小胶质细胞聚集在嗅球中并不普遍。较年轻的J20组的嗅球中神经元数量明显少于年龄匹配的野生型小鼠(55.7±1.3万与65.9±3.6万神经元;p = 0.011)。相比之下,年轻J20组中增殖细胞的数量高于野生型组(即6617±425与4455±623个细胞;p = 0.011)。在较年轻的J20嗅球中也观察到神经发生活动显著增加。总之,我们的结果表明:(1)参与小鼠嗅觉功能的神经元过表达AβPP;(2)年轻J20嗅球的细胞组成与野生型同窝小鼠不同;(3)这些差异可能反映了J20嗅觉系统神经发生活动改变和/或发育延迟;(4)J20海马体和嗅球中发生的AβPP/Aβ相关病理变化并不相同。

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