麻省總醫(yī)院的Bradford Dickerson博士等人近日在《神經(jīng)學(xué)》（Neurology）雜志上報(bào)道稱,，大腦皮質(zhì)變薄與認(rèn)知能力下降有關(guān),。該報(bào)道中研究人員觀察了大腦的9個(gè)區(qū)域,，發(fā)現(xiàn)這些區(qū)域大腦皮質(zhì)厚度較低而認(rèn)知能力正常的患者，其認(rèn)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(biāo)記,，可用來標(biāo)記大腦皮質(zhì)的厚度，并證實(shí)大腦皮質(zhì)變薄是輕度阿爾茨海默病性癡呆的可靠標(biāo)記,，并能預(yù)測阿爾茨海默病患者的認(rèn)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(rèn)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(gè)標(biāo)準(zhǔn)差者被認(rèn)為是發(fā)生認(rèn)知障礙的高風(fēng)險(xiǎn)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(gè)標(biāo)準(zhǔn)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(gè)標(biāo)準(zhǔn)差,。
3年后，125名受試者的測試數(shù)據(jù)被認(rèn)為有認(rèn)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(rèn)知能力下降,；高危險(xiǎn)組的14名受試者中有3名發(fā)生了認(rèn)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(rèn)知能力下降,，占6.6%；高ADsig組的21名受試者其認(rèn)知能力均沒有下降,。Logistic回歸分析發(fā)現(xiàn),，基線ADsig水平與認(rèn)知能力下降的相關(guān)性較強(qiáng),，其腦皮質(zhì)厚度每下降一個(gè)標(biāo)準(zhǔn)差，認(rèn)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(fēng)險(xiǎn)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.
