Young App Ps1
年輕的應用 Ps1

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10.1016/j.neuint.2021.105010

This might be owing to that in young APP/PS1 mice voluntary exercise reduced tau phosphorylation via inhibiting p-GSK3β activity, as well as reduced neuro-inflammation and elevated key proteins involved in synaptic plasticity.

這可能是由於在年輕的 APP/PS1 小鼠中，自願運動通過抑制 p-GSK3β 活性降低了 tau 磷酸化，以及減少了神經炎症和提高了與突觸可塑性有關的關鍵蛋白。

Voluntary wheel running is capable of improving cognitive function only in the young but not the middle-aged male APPSwe/PS1De9 mice

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10.29219/fnr.v65.5496

With regards to gut microbiota profiles, in the young APP/PS1 mice, lactoferrin elevated the α diversity index including ACE and Chao 1, and reduced the relative abundance of the genera Bacteroides and Alistipes and elevated Oscillibacter; in addition, Oscillibacter, Anaerotruncus, EF096579_g, EU454405_g, Mollicutes_RF39, EU474361_g, EU774448_g, and EF096976_g were specifically abundant via linear discriminant analysis with effect size (LEfSe) analysis.

在腸道微生物群方面，在年輕的 APP/PS1 小鼠中，乳鐵蛋白提高了包括 ACE 和 Chao 1 在內的 α 多樣性指數，降低了擬桿菌屬和 Alistipes 屬的相對豐度，並提高了 Oscillibacter；此外，通過線性判別分析和效應大小 (LEfSe) 分析，Oscillibacter、Anaerotruncus、EF096579_g、EU454405_g、Mollicutes_RF39、EU474361_g、EU774448_g 和 EF096976_g 特別豐富。

Dietary lactoferrin has differential effects on gut microbiota in young versus middle-aged APPswe/PS1dE9 transgenic mice but no effects on cognitive function

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10.1016/j.bbi.2021.07.016

We first evaluated the effects of early systemic ARA 290 administration on AD-like pathology in an early-onset model, represented by young APP/PS1 mice.

我們首先在以年輕 APP/PS1 小鼠為代表的早發模型中評估了早期全身 ARA 290 給藥對 AD 樣病理的影響。

Early monocyte modulation by the non-erythropoietic peptide ARA 290 decelerates AD-like pathology progression

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10.1038/s42003-021-02324-6

Using a combinatorial amino acid tagging approach to selectively label and enrich newly synthesized proteins, we found that the de novo proteome is disturbed in young APP/PS1 mice prior to symptom onset, affecting the synthesis of multiple components of the synaptic, lysosomal, and mitochondrial pathways.

使用組合氨基酸標記方法選擇性標記和富集新合成的蛋白質，我們發現年輕的 APP/PS1 小鼠在症狀出現之前從頭蛋白質組受到干擾，影響突觸、溶酶體和線粒體的多種成分的合成途徑。

Age-dependent shift in the de novo proteome accompanies pathogenesis in an Alzheimer’s disease mouse model

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Young App Ps1 年輕的應用 Ps1

Young App Ps1 年輕的應用 Ps1
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Young App Ps1 年輕的應用 Ps1 - This might be owing to that in young APP/PS1 mice voluntary exercise reduced tau phosphorylation via inhibiting p-GSK3β activity, as well as reduced neuro-inflammation and elevated key proteins involved in synaptic plasticity. [1] With regards to gut microbiota profiles, in the young APP/PS1 mice, lactoferrin elevated the α diversity index including ACE and Chao 1, and reduced the relative abundance of the genera Bacteroides and Alistipes and elevated Oscillibacter; in addition, Oscillibacter, Anaerotruncus, EF096579_g, EU454405_g, Mollicutes_RF39, EU474361_g, EU774448_g, and EF096976_g were specifically abundant via linear discriminant analysis with effect size (LEfSe) analysis. [2] We first evaluated the effects of early systemic ARA 290 administration on AD-like pathology in an early-onset model, represented by young APP/PS1 mice. [3] Using a combinatorial amino acid tagging approach to selectively label and enrich newly synthesized proteins, we found that the de novo proteome is disturbed in young APP/PS1 mice prior to symptom onset, affecting the synthesis of multiple components of the synaptic, lysosomal, and mitochondrial pathways. [4]
這可能是由於在年輕的 APP/PS1 小鼠中，自願運動通過抑制 p-GSK3β 活性降低了 tau 磷酸化，以及減少了神經炎症和提高了與突觸可塑性有關的關鍵蛋白。 [1] 在腸道微生物群方面，在年輕的 APP/PS1 小鼠中，乳鐵蛋白提高了包括 ACE 和 Chao 1 在內的 α 多樣性指數，降低了擬桿菌屬和 Alistipes 屬的相對豐度，並提高了 Oscillibacter；此外，通過線性判別分析和效應大小 (LEfSe) 分析，Oscillibacter、Anaerotruncus、EF096579_g、EU454405_g、Mollicutes_RF39、EU474361_g、EU774448_g 和 EF096976_g 特別豐富。 [2] 我們首先在以年輕 APP/PS1 小鼠為代表的早發模型中評估了早期全身 ARA 290 給藥對 AD 樣病理的影響。 [3] 使用組合氨基酸標記方法選擇性標記和富集新合成的蛋白質，我們發現年輕的 APP/PS1 小鼠在症狀出現之前從頭蛋白質組受到干擾，影響突觸、溶酶體和線粒體的多種成分的合成途徑。 [4]