生物谷報(bào)道：美國(guó)研究人員進(jìn)行的一項(xiàng)長(zhǎng)期跟蹤調(diào)查發(fā)現(xiàn),，血液有炎癥跡象的人,，晚年罹患阿爾茨海默氏癥（早老性癡呆癥）的危險(xiǎn)性將大大增加。
這一研究成果將刊登在新一期美國(guó)《神經(jīng)病學(xué)》雜志上,。研究人員共選取了６９１名平均年齡為７９歲的健康人,，通過(guò)血液檢測(cè)確定其血液是否有炎癥跡象。隨后,，研究人員對(duì)他們進(jìn)行了歷時(shí)７年的跟蹤觀察,。這期間，共有４４人患上阿爾茨海默氏癥,。
研究人員說(shuō),，他們檢測(cè)了被調(diào)查者血液中的細(xì)胞因子水平，細(xì)胞因子是一類(lèi)可誘發(fā)炎癥的小分子多肽,。結(jié)果發(fā)現(xiàn),，血液中細(xì)胞因子水平最高的一組比最低一組患阿爾茨海默氏癥的危險(xiǎn)要高兩倍多。在被調(diào)查者中,，２８％的女性和３０％的男性屬于細(xì)胞因子水平最高的一組,，這些人中罹患阿爾茨海默氏癥的人占發(fā)病總?cè)藬?shù)的４２％。
參與研究的哈佛醫(yī)學(xué)院扎爾蒂·坦說(shuō),，上述研究進(jìn)一步證明,，炎癥在阿爾茨海默氏癥的發(fā)病過(guò)程中扮演了某種角色，那些可導(dǎo)致炎癥的細(xì)胞因子的生成很可能就是阿爾茨海默氏癥患病風(fēng)險(xiǎn)的一個(gè)生物標(biāo)記,。
原始出處:
NEUROLOGY 2007;68:1902-1908
Inflammatory markers and the risk of Alzheimer disease
The Framingham Study
Z. S. Tan, MD, MPH, A. S. Beiser, PhD, R. S. Vasan, MD, R. Roubenoff, MD, MHS, C. A. Dinarello, MD, T. B. Harris, MD, MS, E. J. Benjamin, MD, ScM, R. Au, PhD, D. P. Kiel, MD, MPH, P. A. Wolf, MD and S. Seshadri, MD
From the Department of Medicine, Institute for Aging Research, Hebrew Senior Life, Beth Israel Deaconess Medical Center and Harvard Medical School (Z.S.T., D.P.K.), Department of Neurology (S.S., P.A.W., R.A.) and Department of Medicine (R.S.V., E.J.B.), Boston University School of Medicine, Department of Epidemiology and Biostatistics, Boston University School of Public Health (A.B.); Tufts University School of Medicine (R.R.), Boston, MA; National Institute of Aging (T.B.H.), Bethesda, MD; and the University of Colorado Health Sciences Center (C.A.D.), Denver, CO.
Address correspondence and reprint requests to Dr. Zaldy S. Tan, Hebrew Senior Life Department of Medicine, 1200 Centre Street, Boston, MA 02131 [email protected]
Objective: To examine whether serum cytokines and spontaneous production of peripheral blood mononuclear cell (PBMC) cytokines are associated with the risk of incident Alzheimer disease (AD).
Methods: We followed 691 cognitively intact community-dwelling participants (mean age 79 years, 62% women) and related PBMC cytokine production (tertiles of spontaneous production of interleukin 1 [IL-1], IL-1 receptor antagonist, and tumor necrosis factor [TNF-]) and serum C-reactive protein and interleukin 6 (IL-6) to the risk of incident AD.
Results: Adjusting for clinical covariates, individuals in the top two tertiles (T2 and T3) of PBMC production of IL-1 or the top tertile (T3) of PBMC production of TNF- were at increased risk of developing AD (multivariable-adjusted hazard ratio [HR] for IL-1 T2 = 2.84, 95% CI 1.09 to 7.43; p = 0.03 and T3 = 2.61, 95% CI 0.96 to 7.07; p = 0.06; for TNF-, adjusted HR for T2 = 1.30, 95% CI 0.53 to 3.17; p = 0.57 and T3 = 2.59, 95% CI 1.09 to 6.12; p = 0.031]) compared with those in the lowest tertile (T1).
Interpretation: Higher spontaneous production of interleukin 1 or tumor necrosis factor by peripheral blood mononuclear cells may be a marker of future risk of Alzheimer disease (AD) in older individuals. These data strengthen the evidence for a pathophysiologic role of inflammation in the development of clinical AD.
