麻省總醫(yī)院的Bradford Dickerson博士等人近日在《神經(jīng)學》（Neurology）雜志上報道稱,，大腦皮質(zhì)變薄與認知能力下降有關(guān),。該報道中研究人員觀察了大腦的9個區(qū)域，發(fā)現(xiàn)這些區(qū)域大腦皮質(zhì)厚度較低而認知能力正常的患者,，其認知能力在3年后有所下降,。
此前研究人員發(fā)現(xiàn)了一種名為ADsig的生物標記，可用來標記大腦皮質(zhì)的厚度,，并證實大腦皮質(zhì)變薄是輕度阿爾茨海默病性癡呆的可靠標記,，并能預(yù)測阿爾茨海默病患者的認知障礙。
該研究中,，通過MRI檢查受試者的腦皮質(zhì)厚度,，并將159名認知能力正常者依照ADsig分為3組。19名腦皮質(zhì)厚度至少比平均水平低一個標準差者被認為是發(fā)生認知障礙的高風險者,，稱為低ADsig組,；另外116名受試者為平均ADsig組，其腦皮質(zhì)厚度在平均水平上下一個標準差范圍內(nèi),；最后24名為高ADsig組,，其腦皮質(zhì)厚度比平均水平至少高一個標準差。
3年后,，125名受試者的測試數(shù)據(jù)被認為有認知能力改變,，其中包括：9名受試者的綜合測試結(jié)果顯示有認知能力下降；高危險組的14名受試者中有3名發(fā)生了認知能力下降,，占21.4%,；平均ADsig組的90名受試者中有6名發(fā)生了認知能力下降，占6.6%,；高ADsig組的21名受試者其認知能力均沒有下降,。Logistic回歸分析發(fā)現(xiàn)，基線ADsig水平與認知能力下降的相關(guān)性較強,，其腦皮質(zhì)厚度每下降一個標準差,，認知能力的下降程度約為3倍。
作者稱,，該研究為檢測發(fā)生阿爾茨海默病的風險提供了新的方法,，在老年癡呆疾病的檢測及預(yù)后判斷中具有重要意義。（生物谷bioon.com）
doi:10.1212/WNL.0b013e31823e
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PMID:
MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults
Bradford C. Dickerson, MD and David A. Wolk, MD On behalf of the Alzheimer's Disease Neuroimaging Initiative.
Objective: New preclinical Alzheimer disease (AD) diagnostic criteria have been developed using biomarkers in cognitively normal (CN) adults. We implemented these criteria using an MRI biomarker previously associated with AD dementia, testing the hypothesis that individuals at high risk for preclinical AD would be at elevated risk for cognitive decline.
Methods: The Alzheimer's Disease Neuroimaging Initiative database was interrogated for CN individuals. MRI data were processed using a published set of a priori regions of interest to derive a single measure known as the AD signature (ADsig). Each individual was classified as ADsig-low (≥1 SD below the mean: high risk for preclinical AD), ADsig-average (within 1 SD of mean), or ADsig-high (≥1 SD above mean). A 3-year cognitive decline outcome was defined a priori using change in Clinical Dementia Rating sum of boxes and selected neuropsychological measures.
Results: Individuals at high risk for preclinical AD were more likely to experience cognitive decline, which developed in 21% compared with 7% of ADsig-average and 0% of ADsig-high groups (p = 0.03). Logistic regression demonstrated that every 1 SD of cortical thinning was associated with a nearly tripled risk of cognitive decline (p= 0.02). Of those for whom baseline CSF data were available, 60% of the high risk for preclinical AD group had CSF characteristics consistent with AD while 36% of the ADsig-average and 19% of the ADsig-high groups had such CSF characteristics (p = 0.1).
Conclusions: This approach to the detection of individuals at high risk for preclinical AD-identified in single CN individuals using this quantitative ADsig MRI biomarker-may provide investigators with a population enriched for AD pathobiology and with a relatively high likelihood of imminent cognitive decline consistent with prodromal AD.
