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Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease

机译：脑淀粉样血管病在阿尔茨海默病的病因和免疫治疗中的作用

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Amyloid is deposited in the walls of arteries and capillaries as cerebral amyloid angiopathy (CAA) in the brains of older individuals and of those with Alzheimer disease (AD). CAA in AD reflects an age-related failure of elimination of amyloid-beta (Aβ) from the brain along perivascular lymphatic drainage pathways. In the absence of conventional lymphatic vessel in the brain, interstitial fluid and solutes drain from the brain to cervical lymph nodes along narrow basement membranes in the walls of capillaries and arteries, a pathway that is largely separate from the cerebrospinal fluid. In this review we focus on the pathology and pathogenesis of CAA, its role in the aetiology of AD and its impact on immunotherapy for AD. The motive force for lymphatic drainage of the brain appears to be generated by arterial pulsations. Failure of elimination of Aβ along perivascular pathways coincides with a reduction in enzymic degradation of Aβ, reduced absorption of Aβ into the blood and age-related stiffening of artery walls that appears to reduce the motive force for lymphatic drainage. Reduced clearances of Aβ and CAA are associated with the accumulation of insoluble and soluble Aβs in the brain in AD and the probable loss of homeostasis of the neuronal environment due to retention of soluble metabolites within the brain. Tau metabolism may also be affected. Immunotherapy has been successful in removing insoluble plaques of Aβ from the brain in AD but with little effect on cognitive decline. One major problem is the increase in CAA in immunised patients that probably prevents the complete removal of Aβ from the brain. Increased knowledge of the physiology and structural and genetic aspects of the lymphatic drainage of Aβ from the brain will stimulate the development of therapeutic strategies for the prevention and treatment of AD.
机译：淀粉样蛋白在老年人和患有阿尔茨海默氏病（AD）的人的大脑中作为脑淀粉样蛋白血管病（CAA）沉积在动脉和毛细血管壁中。 AD中的CAA反映了与年龄相关的沿血管周围淋巴引流途径从大脑消除淀粉样蛋白（Aβ）的失败。在大脑中不存在常规淋巴管的情况下，间质液和溶质沿着毛细血管和动脉壁的狭窄基底膜从大脑流到颈淋巴结，这是一条与脑脊髓液基本分开的途径。在这篇综述中，我们关注CAA的病理学和发病机理，其在AD病因中的作用及其对AD免疫疗法的影响。脑部淋巴引流的动力似乎是由动脉搏动产生的。沿血管周围途径消除Aβ的失败与Aβ的酶促降解减少，Aβ吸收到血液中的减少以及年龄相关的动脉壁僵硬相吻合，这似乎减少了淋巴引流的动力。 Aβ和CAA清除率的降低与AD中大脑中不溶性和可溶性Aβ的积累以及由于大脑中可溶性代谢物的保留而可能导致神经元环境的稳态丧失有关。牛磺酸的代谢也可能受到影响。免疫疗法已成功地从AD的大脑中清除了Aβ的不溶性斑块，但对认知功能下降的影响很小。一个主要问题是免疫患者中CAA的增加，这可能会阻止Aβ从大脑中完全清除。对大脑Aβ淋巴引流的生理学，结构和遗传学方面的了解不断增加，将刺激预防和治疗AD的治疗策略的发展。

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