Department of Internal Medicine and Therapeutics, Geriatric Section, University of Pavia, ASP, IDR S. Margherita, via Emilia 12, Pavia, Italy.
Autoimmun Rev. 2011 Dec;11(2):149-53. doi: 10.1016/j.autrev.2011.09.005. Epub 2011 Oct 5.
Alzheimer's disease (AD) has been recognized as the most common cause of sporadic dementia. It represents both a medical and social problem, as it affects 10% of over-65 population. Even if the elderly are the most involved population, aging alone cannot be considered as the only cause of this disease. In this review we wanted to focus on the last hypotheses on the possible causes of this neuronal affection. We focused in particular on the role of inflammation and alteration of the inflammatory status that is typical of the elderly and may lead to chronic inflammation. The inflammation seems to be a cause of neuronal impairment and loss. Some studies have proposed a protective role of antiinflammatory drugs. Then we analyzed the role of genetic polymorphisms of some pro-inflammatory substances that seem to be linked to some cases of dementia. The complement system seems to have a role too, as some factors have been found in senile plaques, representing a possible involvement of classical complement pathway. One of the latest hypotheses is about the role of blood-brain barrier (BBB), as its loss of integrity may lead to a passage of proteins in cerebro spinal fluid (CSF), causing a compromised role of BBB in preserving the brain as an "immune sanctuary".
阿尔茨海默病（AD）已被认为是散发性痴呆的最常见原因。它既是一个医学问题，也是一个社会问题，因为它影响了 65 岁以上人口的 10%。即使老年人是受影响最严重的人群，但仅年龄增长不能被视为这种疾病的唯一原因。在本次综述中，我们想重点关注关于这种神经元疾病可能病因的最新假说。我们特别关注炎症和炎症状态改变的作用，这种炎症状态是老年人的典型特征，可能导致慢性炎症。炎症似乎是神经元损伤和丧失的原因。一些研究提出了抗炎药物的保护作用。然后，我们分析了一些促炎物质的遗传多态性的作用，这些物质似乎与某些痴呆病例有关。补体系统似乎也有作用，因为在老年斑中发现了一些因子，代表经典补体途径的可能参与。最新的假说之一是关于血脑屏障（BBB）的作用，因为其完整性的丧失可能导致蛋白质在脑脊液（CSF）中的通过，从而使 BBB 在保护大脑作为“免疫避难所”方面的作用受到损害。
