生物谷報道：荷蘭科學(xué)家最近發(fā)表研究論文說,，與已經(jīng)成功戒煙和從不吸煙的人比起來,，吸煙者日后罹患早老性癡呆癥及其他種類癡呆癥的風(fēng)險要高出不少,。
據(jù)路透社9月3日報道,，荷蘭鹿特丹伊拉斯默斯醫(yī)學(xué)中心的莫尼克·布萊特勒博士及其同事通過研究發(fā)現(xiàn),，年齡超過55歲的吸煙者出現(xiàn)癡呆癥狀的可能性,，較之年齡相仿的不吸煙者高出50％,。
布萊特勒和同事在其發(fā)表于Neurology雜志上的論文中表示，他們曾經(jīng)對將近7000名年齡不小于55歲的人進(jìn)行了平均為期7年的追蹤研究,。在此期間,，總共有706名被研究者患上了各種不同類型的癡呆癥。
目前人們已經(jīng)確知有一種名叫APOE4（也叫做阿樸脂蛋白E4）的基因能夠增加一個人罹患癡呆的風(fēng)險,。研究發(fā)現(xiàn),，對于那些體內(nèi)已經(jīng)存在著此種基因的人來說，吸煙并不會對他們今后是否患上早老性癡呆癥產(chǎn)生任何影響,。但如果那些體內(nèi)沒有該基因的人持續(xù)吸煙的話,，他們未來患上早老性癡呆癥的危險會提高70％。
吸煙可能會導(dǎo)致人體出現(xiàn)中風(fēng)癥狀,，而此種情況反過來也會對大腦造成損傷并最終發(fā)展到癡呆這一步,，布萊特勒說。布萊特勒說,，“吸煙會增加患腦血管疾?。ㄖ酗L(fēng)）的風(fēng)險，而這與癡呆同樣有著密不可分的聯(lián)系,。”
他還說：“所謂氧化應(yīng)激(Oxidative Stress)是導(dǎo)致癡呆癥狀出現(xiàn)的另外一項作用機制,，它會對人體血管內(nèi)的細(xì)胞造成傷害,，并導(dǎo)致動脈硬化。與不吸煙者相比,，吸煙者體內(nèi)的氧化應(yīng)激現(xiàn)象往往會表現(xiàn)得更為激烈,，而在早老性癡呆癥患者身上，人們同樣發(fā)現(xiàn)了這種氧化應(yīng)激水平有所升高,。”
所謂氧化應(yīng)激的過程其實與生銹十分類似,，就是通過化學(xué)反應(yīng)對人體DNA造成損傷。
英文原文：http://www.consumeraffairs.com/news04/2007/09/dementia_smoking.html
原始出處:
NEUROLOGY 2007;69:998-1005
Relation between smoking and risk of dementia and Alzheimer disease
The Rotterdam Study
C. Reitz, MD, PhD, T. den Heijer, MD, PhD, C. van Duijn, PhD, A. Hofman, MD, PhD and M.M.B. Breteler, MD, PhD
From the Departments of Epidemiology & Biostatistics (C.R., T.d.H., C.v.D., A.H., M.M.B.B.) and Neurology (T.d.H.), Erasmus Medical Center, Rotterdam, The Netherlands.
Address correspondence and reprint requests to DrB. Breteler, Department of Epidemiology & Biostatistics, Erasmus Medical Center, PO Box 1738, 3000DR Rotterdam, The Netherlands m.breteler@erasmusmc.nl
Background and Objective: Previous studies relating smoking with the risk of dementia have been inconsistent and limited in their validity by short follow-up times, large intervals between baseline and follow-up assessments, and unspecific determination of dementia diagnosis. We re-assessed after longer follow-up time in the large population-based cohort of the Rotterdam Study whether smoking habits and pack-years of smoking are associated with the risk of dementia, Alzheimer disease (AD), and vascular dementia (VaD).
Methods: Prospective population-based cohort study in 6,868 participants, 55 years or older and free of dementia at baseline. First, Cox proportional hazard models were used to relate smoking status at baseline with the risks of incident dementia, VaD, and AD, using never smokers as the reference category in all analyses. Then Cox proportional hazard models were used to relate pack-years of smoking with the risks of incident dementia, VaD, and AD. To explore the impact of the APOE4 allele, sex, and age on the association between smoking status and dementia, we repeated all analyses stratifying, in separate models, by APOE4 genotype, sex, and median of age.
Results: After a mean follow-up time of 7.1 years, current smoking at baseline was associated with an increased risk of dementia (HR 1.47, 95% CI 1.18 to 1.86) and AD (HR 1.56, 95% CI 1.21 to 2.02). This increase in disease risk was restricted to persons without the APOE4 allele. There was no association between current smoking and risk of VaD, and there was no association between past smoking and risk of dementia, AD, or VaD.
Conclusion: Current smoking increases the risk of dementia. This effect is more pronounced in persons without the APOE4 allele than APOE4 carriers.
