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Abnormal platelet amyloid-β precursor protein metabolism in SAMP8 mice: Evidence for peripheral marker in Alzheimer's disease.

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收录情况： ◇ SCIE

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机构： [1]Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‐Sen University, Guangzhou, China [2]Department of Anatomy, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Southern Medical University, Guangzhou, China [3]Department of Ultrasound, The Third Affiliated Hospital of Sun Yat‐sen University, Guangzhou, China [4]Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat‐sen University, Guangzhou, China [5]Department of Anatomy, School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, China [6]Department of Anatomy, Guangdong Jiangmen Chinese Traditional Medicine College, Jiangmen, China

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关键词： aging amyloid precursor protein amyloid β platelets senescence‐accelerated mice

摘要：

Senescence-accelerated mouse strains have proved to be an accelerated-aging model, which mimics numerous features with Alzheimer's disease (AD). Three, six, and nine-month senescence-accelerated resistant 1 and senescence-accelerated prone 8 (SAMP8) mice were used in the current study, to unravel potential mechanisms for dementia and explore new diagnostic approaches for AD. The amyloid-β (Aβ40) and Aβ42 levels were elevated in hippocampi and platelets from SAMP8, along with a reduced α-secretase expression and an enhanced β-secretase expression extent with age, compared to control mice. Furthermore, hippocampal Aβ40 and Aβ42 of SAMP8 were positively correlated with platelet of these mice with aging progression. In addition, β-γ-secretase-modulated proteolytic proceeding of amyloid precursor protein in platelet might work through the PI3K/Akt/GSK3β pathway. These results indicate that platelet could be a potential early marker in the periphery to study the age-correlative aggregation of the amyloid-β peptide in patients with AD, while still requiring the considerable study. © 2019 Wiley Periodicals, Inc.

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出版当年[2018]版：

大类 | 2 区生物

小类 | 2 区生理学 3 区细胞生物学

最新[2025]版：

大类 | 3 区生物学

小类 | 3 区细胞生物学 3 区生理学

JCR分区：

出版当年[2017]版：

Q1 PHYSIOLOGY Q2 CELL BIOLOGY

最新[2023]版：

Q1 PHYSIOLOGY Q2 CELL BIOLOGY

影响因子： 4.5 最新[2023版] 5.3 最新五年平均 3.923 出版当年[2017版] 3.83 出版当年五年平均 4.08 出版前一年[2016版] 4.522 出版后一年[2018版]

第一作者：

第一作者机构： [1]Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‐Sen University, Guangzhou, China [2]Department of Anatomy, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Southern Medical University, Guangzhou, China

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通讯作者：

通讯机构： [1]Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‐Sen University, Guangzhou, China [4]Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat‐sen University, Guangzhou, China [*1]Department of Anatomy and Neurobiology, Zhongshan Medical College of Sun Yat‐Sen University, Guangzhou, 510080, China.

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Abnormal platelet amyloid-β precursor protein metabolism in SAMP8 mice: Evidence for peripheral marker in Alzheimer's disease.

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