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高血压导致脑实质中的实质β-淀粉样蛋白积累。

Hypertension drives parenchymal β-amyloid accumulation in the brain parenchyma.

机构信息

Department of Neurology, Otto-von-Guericke University Magdeburg, Germany ; German Center for Neurodegenerative Diseases (DZNE) Magdeburg, Germany.

Faculty of Medicine, University of Southampton Southampton, United Kingdom.

出版信息

Ann Clin Transl Neurol. 2014 Feb;1(2):124-9. doi: 10.1002/acn3.27. Epub 2014 Jan 9.

Abstract

There is substantial controversy regarding the causative role of amyloid β (Aβ) deposition in Alzheimer's disease (AD). The cerebrovasculature plays an important role in the elimination of Aβ from the brain and hypertension is a well-known risk factor for AD. In spontaneously hypertensive stroke-prone rats (SHRSP), an animal model of chronic arterial hypertension, cerebral small vessel disease (CSVD) leads to age-dependent parenchymal Aβ accumulation similar to that observed in AD. These data approve the neuropathological link between CSVD and AD, confirm the challenge that parenchymal Aβ deposition is a specific marker for AD and disclose the meaning of SHRSP as valid experimental model to investigate the association between hypertension, CSVD, and Aβ plaques.

摘要

关于淀粉样蛋白 β(Aβ)沉积在阿尔茨海默病(AD)中的因果作用存在很大争议。脑血管在 Aβ从大脑中清除方面起着重要作用,高血压是 AD 的已知危险因素。在自发性高血压脑卒中易发性大鼠(SHRSP)中,一种慢性动脉高血压动物模型,脑小血管疾病(CSVD)导致与 AD 观察到的相似的随年龄增长的实质 Aβ积累。这些数据证实了 CSVD 和 AD 之间的神经病理学联系,证实了实质 Aβ沉积是 AD 的特异性标志物这一挑战,并揭示了 SHRSP 作为研究高血压、CSVD 和 Aβ斑块之间关联的有效实验模型的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c0f/4212487/c2d7fc4ffeee/acn30001-0124-f1.jpg

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