有统计显示，受教育程度与患阿尔茨海默氏症的风险成反比例关系，但原因为何却一直不清。日前，英国和芬兰科学家最新发表在《大脑》杂志上的论文称，这是因为知识丰富的人可更好地应对阿尔茨海默氏症带来的大脑组织的变化，相比之下，多受一年教育者，其患上该症的风险会降低11%。
阿尔茨海默氏症俗称为老年痴呆症。过去十年关于其的研究不断显示，一个人受教育的程度越高，患病的风险就越低，但对于教育是否就可以防止阿尔茨海默氏症，却难有定论。相关研究也表明，该病与脑组织变化间并不是一一对应的关系，同样是患有阿尔茨海默氏症，有的人可能会有很多大脑病理学的表现，而有的人则可能很少。
英国和芬兰两国的研究人员对参与欧洲流行病临床病理学研究EClipSE项目的872名老年人的大脑进行了分析研究，这些人中有56%的人在死前患有阿尔茨海默氏症。他们发现，虽然人受教育的层次不同，但其大脑病理学表征是相似的，而之所以受教育多的人患阿尔茨海默氏症的风险较小，是因为他们能在出现阿尔茨海默氏症症状之前，更好地应对其大脑出现的变化，以抵消该病的负面影响。
领导该项研究的英国剑桥大学教授卡罗布雷恩表示，一个人的受教育程度关乎其社会经济地位和生活方式，而一个社会的教育水平则与整个社会的健康和谐发展息息相关。该研究表明，对早期教育的投资，无论是对社会，还是对个人生活，都是值得的(刘海英)。
推荐原文出处：
Brain 2010 133(8):2210-2216; doi:10.1093/brain/awq185
Education, the brain and dementia: neuroprotection or compensation?
Carol Brayne1, Paul G. Ince2, Hannah A. D. Keage1, Ian G. McKeith3, Fiona E. Matthews4, Tuomo Polvikoski3 and Raimo Sulkava5
1 Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 0SR, UK 2 School of Medical and Biomedical Sciences, University of Sheffield, Sheffield S10 2RX, UK 3 Institute for Ageing and Health, University of Newcastle, Newcastle NE4 5PL, UK 4 Medical Research Council Biostatistics Unit, Institute of Public Health, Cambridge CB2 0SR, UK 5 School of Public Health and Clinical Nutrition, University of Kuopio, Kuopio 70210, Finland
The potential protective role of education for dementia is an area of major interest. Almost all older people have some pathology in their brain at death but have not necessarily died with dementia. We have explored these two observations in large population-based cohort studies (Epidemiological Clinicopathological Studies in Europe; EClipSE) in an investigation of the relationships of brain pathology at death, clinical dementia and time in education, testing the hypothesis that greater exposure to education reduces the risk of dementia. EClipSE has harmonized longitudinal clinical data and neuropathology from three longstanding population-based studies that included post-mortem brain donation. These three studies started between 1985 and 1991. Number of years of education during earlier life was recorded at baseline. Incident dementia was detected through follow-up interviews, complemented by retrospective informant interviews, death certificate data and linked health/social records (dependent on study) after death. Dementia-related neuropathologies were assessed in each study in a comparable manner based on the Consortium to Establish a Registry for Alzheimer's Disease protocol. Eight hundred and seventy-two brain donors were included, of whom 56% were demented at death. Longer years in education were associated with decreased dementia risk and greater brain weight but had no relationship to neurodegenerative or vascular pathologies. The associations between neuropathological variables and clinical dementia differed according to the ‘dose’ of education such that more education reduced dementia risk largely independently of severity of pathology. More education did not protect individuals from developing neurodegenerative and vascular neuropathology by the time they died but it did appear to mitigate the impact of pathology on the clinical expression of dementia before death. The findings suggest that an understanding of the mechanisms leading to functional protection in the presence of pathology may be of considerable value to society.
