Stone Jonathan, Johnstone Daniel M, Mitrofanis John, O'Rourke Michael
Bosch Institute, Sydney, Australia Discipline of Physiology, University of Sydney.
Bosch Institute, Sydney, Australia Discipline of Anatomy and Histology, University of Sydney.
J Alzheimers Dis. 2015;44(2):355-73. doi: 10.3233/JAD-141884.
This review traces evidence that age-related dementia (Alzheimer's disease) results from the destructive impact of the pulse on cerebral vasculature. Evidence is reviewed that the neuropathology of the dementia is caused by the breakdown of small cerebral vessels (silent microbleeds), that the microbleeds result from pulse-induced damage to the cerebral vessels, and that pulse becomes increasingly destructive with age, because of the age-related stiffening of the aorta and great arteries, which causes an increase in the intensity of the pressure pulse. Implications for therapy are discussed, and evidence is reviewed that pulse-induced destruction of the brain, and of another highly vascular organ, the kidney, are becoming the default forms of death, the way we die if we survive the infections, cardiovascular disease, and malignancies, which still, for a decreasing minority, inflict the tragedy of early death.
本综述追溯了与年龄相关的痴呆症（阿尔茨海默病）源于脉搏对脑血管系统的破坏性影响的证据。回顾的证据表明，痴呆症的神经病理学是由大脑小血管破裂（隐匿性微出血）所致，微出血是由脉搏对脑血管的损伤引起的，并且由于主动脉和大动脉随年龄增长而硬化，导致压力脉冲强度增加，脉搏随着年龄增长的破坏性越来越大。文中讨论了对治疗的启示，并回顾了证据表明，脉搏引起的脑部以及另一个血管丰富的器官——肾脏的破坏，正成为默认的死亡形式，即如果我们在感染、心血管疾病和恶性肿瘤中幸存下来，我们就会以这种方式死亡，而对于越来越少的一部分人来说，这些疾病仍然会造成过早死亡的悲剧。
