The olfactory molecular snapshot of Tg2576 mice at early stages of amyloid pathology. The olfactory molecular snapshot of Tg2576 mice at early stages of amyloid pathology

Olfaction is often deregulated in Alzheimer's disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from Tg2576 mice (2, and 6 months of age) respect to age-matched wild-type (WT) littermates. Overall design: Olfactory bulbs from 3 WT mice vs. olfactory bulbs from 3 Tg2576 transgenic mice in each time point.

阿尔茨海默病（Alzheimer's disease, AD）患者常出现嗅觉功能失调，而过表达人源淀粉样前体蛋白（amyloid precursor protein, APP）瑞典突变体的转基因Tg2576 AD小鼠模型同样存在嗅觉损伤。然而，目前学界对Tg2576小鼠嗅觉结构神经退行性变伴随的分子机制仍缺乏深入了解。为此，本研究采用蛋白质组学与转录组学全基因组分析策略，对2月龄、6月龄Tg2576小鼠及其同月龄野生型（wild-type, WT）同窝对照小鼠的嗅球（olfactory bulb, OB）样本进行分子扰动检测。实验整体设计：在每个时间节点下，分别选取3只野生型小鼠的嗅球与3只Tg2576转基因小鼠的嗅球进行对照实验。