美國研究人員日前找到查出早期老年癡呆癥(Alzheimer's)的方法,，檢驗(yàn)的準(zhǔn)確率達(dá)87%,。
據(jù)新加坡《聯(lián)合早報》報道,，另一組研究人員發(fā)現(xiàn),，糖尿病人患上老年癡呆癥的幾率較高,，而且癡呆癥狀惡化較快,。
據(jù)報道,，新方法是通過測量脊髓液中的蛋白質(zhì)含量,，在人體出現(xiàn)癡呆癥狀和其他認(rèn)知損害發(fā)生之前,，就能驗(yàn)出疾病,。賓夕法尼亞大學(xué)醫(yī)學(xué)院的萊斯利·肖說：“我們可以通過新方法檢查和追蹤老年癡呆癥的發(fā)展。”
在試驗(yàn)中,，研究人員對410名參加大規(guī)模老年癡呆調(diào)查的病人進(jìn)行了脊髓液分析,。結(jié)果發(fā)現(xiàn),，一種名為β-淀粉樣蛋白42(amyloid beta 42)的蛋白質(zhì)濃度低的人,，容易發(fā)展為老年癡呆癥,，可能是因?yàn)檫@種蛋白質(zhì)堆積在大腦血斑中的緣故。
他們還發(fā)現(xiàn),，脊椎液中tau蛋白含量低的人也容易變成老年癡呆,。萊斯利·肖說：“tau蛋白進(jìn)入脊髓液，可能是神經(jīng)細(xì)胞將要死亡時,，細(xì)胞內(nèi)物質(zhì)釋放出來造成的,。”
他們的研究成果發(fā)表在《神經(jīng)學(xué)年鑒》(Annals of Neurology)上,。（生物谷Bioon.com）
生物谷推薦原始出處：
Annals of Neurology Volume 65 Issue 2, Pages 176 - 183
Decreased cerebrospinal fluid Aβ42 correlates with brain atrophy in cognitively normal elderly
Anne M. Fagan, PhD 1 2 3 *, Denise Head, PhD 3 4 5, Aarti R. Shah, MS 1, Daniel Marcus, PhD 4, Mark Mintun, MD 3 4, John C. Morris, MD 1 3 6, David M. Holtzman, MD 1 2 3 7
1Department of Neurology, Washington University School of Medicine, St. Louis, MO
2Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO
3Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO
4Department of Radiology, Washington University School of Medicine, St. Louis, MO
5Department of Psychology, Washington University School of Medicine, St. Louis, MO
6Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO
7Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO
Objective
For therapies for Alzheimer's disease (AD) to have the greatest impact, it will likely be necessary to treat individuals in the preclinical (presymptomatic) stage. Fluid and neuroimaging measures are being explored as possible biomarkers of AD pathology that could aid in identifying individuals in this stage to target them for clinical trials and to direct and monitor therapy. The objective of this study was to determine whether cerebrospinal fluid (CSF) biomarkers for AD suggest the presence of brain damage in the preclinical stage of AD.
Methods
We investigated the relation between structural neuroimaging measures (whole-brain volume) and levels of CSF amyloid- (A)β40, Aβ42, tau, and phosphorylated tau181 (ptau181), and plasma A40 and Aβ42 in well-characterized research subjects with very mild and mild dementia of the Alzheimer type (n = 29) and age-matched, cognitively normal control subjects (n = 69).
Results
Levels of CSF tau and ptau181, but not Aβ42, correlated inversely with whole-brain volume in very mild and mild dementia of the Alzheimer type, whereas levels of CSF Aβ42, but not tau or ptau181, were positively correlated with whole-brain volume in nondemented control subjects.
Interpretation
Reduction in CSF Aβ42, likely reflecting A aggregation in the brain, is associated with brain atrophy in the preclinical phase of AD. This suggests that there is toxicity associated with A aggregation before the onset of clinically detectable disease. Increases in CSF tau (and ptau181) are later events that correlate with further structural damage and occur with clinical onset and progression. Ann Neurol 2009;65:176-183
