Hypertension-induced cognitive impairment: from pathophysiology to public health.

Hypertension-induced cognitive impairment: from pathophysiology to public health.
复制标题

DOI:
10.1038/s41581-021-00430-6
复制
发表时间:
2021-10
期刊:
Nature reviews. Nephrology
影响因子:
--
通讯作者:
Csiszar A
Csiszar A
中科院分区:
其他
文献类型:
--
作者:
Ungvari Z;Toth P;Tarantini S;Prodan CI;Sorond F;Merkely B;Csiszar A

文献摘要

参考文献

被引文献

相似文献

高血压影响三分之二的年龄>60岁的人,并显着增加血管性认知障碍和阿尔茨海默病的风险。高血压损害脑微循环的结构和功能完整性,促进微血管稀疏、微血管内皮功能障碍和神经血管解偶联,从而损害脑血液供应。此外,高血压破坏血脑屏障,促进神经炎症和淀粉样病变的恶化。衰老的特征是多方面的稳态功能障碍和受损的细胞应激恢复能力,这加剧了高血压的有害微血管效应。高血压诱发的脑小血管病的神经放射学标志物包括白色高信号、腔隙性梗死和微出血,所有这些都与认知能力下降有关。使用降低血压的药物和生活方式干预,结合促进微血管健康的治疗,有可能预防或延迟高血压患者血管性认知障碍和阿尔茨海默病的发病机制。高血压和衰老对大脑微循环有有害影响,可导致认知功能障碍。本文综述了脑血管对高血压的适应不良和微血管对老年高血压引起的认知障碍的作用,以及高血压在阿尔茨海默病发病机制中的作用。高血压与衰老有关,并显著增加血管性认知障碍和阿尔茨海默病的风险。在老年人中,高血压导致脑循环适应不良,导致脑血流失调、微血管稀疏、血脑屏障破坏、氧化应激和神经血管耦合受损。高血压引起脑微血管的病理改变,损害微血管结构、网络结构和功能,并促成脑微出血、腔隙性梗死和白色损伤的发生;这些因素与认知能力下降有关。高血压可能加剧阿尔茨海默病进展的潜在机制包括氧化性微血管损伤增加、脑炎症和血脑屏障破坏,以及淀粉样蛋白β的胶质淋巴(也称为神经胶质-淋巴)清除受损。使用降低血压的药物和/或生活方式干预措施与促进微血管健康的治疗相结合,可能会预防或延迟高血压患者的认知能力下降。
Hypertension affects two-thirds of people aged >60 years and significantly increases the risk of both vascular cognitive impairment and Alzheimer’s disease. Hypertension compromises the structural and functional integrity of the cerebral microcirculation, promoting microvascular rarefaction, cerebromicrovascular endothelial dysfunction and neurovascular uncoupling, which impair cerebral blood supply. In addition, hypertension disrupts the blood–brain barrier, promoting neuroinflammation and exacerbation of amyloid pathologies. Ageing is characterized by multifaceted homeostatic dysfunction and impaired cellular stress resilience, which exacerbate the deleterious cerebromicrovascular effects of hypertension. Neuroradiological markers of hypertension-induced cerebral small vessel disease include white matter hyperintensities, lacunar infarcts and microhaemorrhages, all of which are associated with cognitive decline. Use of pharmaceutical and lifestyle interventions that reduce blood pressure, in combination with treatments that promote microvascular health, have the potential to prevent or delay the pathogenesis of vascular cognitive impairment and Alzheimer’s disease in patients with hypertension. Hypertension and ageing have deleterious effects on the cerebral microcirculation that can lead to cognitive dysfunction. This Review discusses cerebrovascular maladaptation to hypertension and microvascular contributions to hypertension-induced cognitive impairment in ageing, as well as the role of hypertension in the pathogenesis of Alzheimer’s disease. Hypertension is associated with ageing and significantly increases the risk of vascular cognitive impairment and Alzheimer’s disease. In older individuals, hypertension leads to maladaptation of the cerebral circulation, resulting in dysregulation of cerebral blood flow, microvascular rarefaction, blood–brain barrier disruption, oxidative stress and impaired neurovascular coupling. Hypertension causes pathological alterations in cerebral microvessels that damage microvascular structure, network architecture and function, and contribute to the genesis of cerebral microhaemorrhages, lacunar infarcts and white matter injury; these factors are associated with cognitive decline. Potential mechanisms by which hypertension could exacerbate the progression of Alzheimer’s disease include increased oxidative microvascular damage, brain inflammation and blood–brain barrier disruption, as well as impaired glymphatic (also known as glial-lymphatic) clearance of amyloid-β. Use of pharmaceutical and/or lifestyle interventions that reduce blood pressure in combination with treatments that promote microvascular health could potentially prevent or delay cognitive decline in patients with hypertension.
DOI: 10.1097/wnr.0000000000000464
发表时间: 2015-12-02
期刊: NEUROREPORT
影响因子: 1.7
作者:
Fan, Yuhua;Yang, Xian;Sun, Jian
通讯作者: Sun, Jian
DOI: 10.1161/hypertensionaha.112.195511
发表时间: 2012-07
期刊: Hypertension (Dallas, Tex. : 1979)
影响因子: --
作者:
Carnevale D;Mascio G;D'Andrea I;Fardella V;Bell RD;Branchi I;Pallante F;Zlokovic B;Yan SS;Lembo G
通讯作者: Lembo G
DOI: 10.1038/ncomms2230
发表时间: 2012
影响因子: 16.6
作者:
通讯作者: --
DOI: 10.1152/ajpheart.00307.2014
发表时间: 2014-08-01
影响因子: 4.8
作者:
Csiszar, Anna;Gautam, Tripti;Ungvari, Zoltan
通讯作者: Ungvari, Zoltan
DOI: 10.1016/j.neurobiolaging.2010.08.013
发表时间: 2012-01-01
影响因子: 4.2
作者:
Carnevale, Daniela;Mascio, Giada;Minghetti, Luisa
通讯作者: Minghetti, Luisa