趙江民,詹 青. 上海交通大學(xué)醫(yī)學(xué)院附屬第九人民醫(yī)院醫(yī)學(xué)影像科,上海 0900;. 上海中醫(yī)藥大學(xué)附屬第七人民醫(yī)院神經(jīng)內(nèi)科,上海 0037
?
綜述Review
MRI早期診斷阿爾茨海默病的研究進(jìn)展
趙江民1,詹 青2
1. 上海交通大學(xué)醫(yī)學(xué)院附屬第九人民醫(yī)院醫(yī)學(xué)影像科,上海 201900;
2. 上海中醫(yī)藥大學(xué)附屬第七人民醫(yī)院神經(jīng)內(nèi)科,上海 200137
摘要
關(guān)鍵詞:阿爾茨海默病;早期診斷;磁共振成像
趙江民,詹 青. MRl早期診斷阿爾茨海默病的研究進(jìn)展[J]. 神經(jīng)病學(xué)與神經(jīng)康復(fù)學(xué)雜志, 2016, 12(1):47–51.
FUNDlNG/SUPPORT: Key Project of Scientific & Technological lnnovation Action Program Supported by Science and Technology Commission of Shanghai Municipality (No. 10411953400); Research Project Supported by Baoshan District Association for Science & Technology, Shanghai (No. 14–E–4); Medical Guidance Project of Science and Technology Commission of Shanghai Municipality (No. 114119a5800)
CONFLlCT OF lNTEREST: The authors have indicated they have no conflicts of interest to disclose.
Received Feb. 1, 2016; accepted for publication Mar. 1, 2016
Copyright ? 2016 by Journal of Neurology and Neurorehabilitation
ZHAN Qing
E-MAIL ADDRESS
zhanqing@#edu.cn
ABSTRACT
With the aging of global population, the incidence of Alzheimer’s disease (AD) shows a significant upward trend. So far, there is still a lack of effective treatment for AD, and diagnosis,prevention and treatment in early stage of AD is the only effective way to delay the progression of AD. Currently, the diagnosis of AD still mainly relies on the exclusive method and clinical neuropsychological scales with poor repeatability and being absent of objective evidence,lacking sensitive and accurate methods for early diagnosis of AD. With the development of medical imaging technology, "medical imaging+" transdisciplinary research has become the new norm, the interdisciplinary neuroimaging techniques can clearly show the finer structures and lesions in the brain, which provides a basis for the early diagnosis of AD. Due to the loss ofneurons in brain tissues of patients with AD, cerebral atrophy is developed, so the AD can be observed by measuring the degree of cerebral atrophy. This paper summarizes the research progress in measurement of hippocampal volume, entorhinal cortex thickness and the change of amygdale through magnetic resonance imaging (MRI), the application of double inversion recovery (DIR) sequence in diagnosis of AD, and the role of diffusion tensor imaging (DTI) in the assessment of injury in white matter related to hippocampus.
To cite: ZHAO J M, ZHAN Q. Advances in MRl in diagnosis of early–stage Alzheimer’s disease. J Neurol and Neurorehabil, 2016, 12(1):47–51.
阿爾茨海默病(Alzheimer's disease,AD)的主要臨床表現(xiàn)包括認(rèn)知功能障礙、日常生活能力下降和精神行為障礙。AD發(fā)病初期主要表現(xiàn)為以近期遺忘及學(xué)習(xí)和記憶新知識能力減退為特點(diǎn)的近期記憶力下降;隨著病情的進(jìn)展,逐漸出現(xiàn)計(jì)算困難、遠(yuǎn)期記憶障礙、時(shí)間及空間定向障礙、語言障礙、思維能力下降、理解及判斷能力下降以及情感障礙等認(rèn)知和行為障礙[1]。AD的特征性病理表現(xiàn)包括老年斑(senile plaque,SP)、神經(jīng)原纖維纏結(jié)(neurofibrillary tangle,NFT)以及神經(jīng)元及神經(jīng)突觸的喪失;此外,還包括神經(jīng)元顆??张葑冃院脱鼙诘矸蹣拥鞍鬃冃裕?]。
目前尚不清楚AD的確切病因及發(fā)病機(jī)制,相關(guān)學(xué)說包括遺傳學(xué)說、異常蛋白沉積學(xué)說、微管相關(guān)蛋白tau異常學(xué)說、神經(jīng)遞質(zhì)變化學(xué)說以及微量元素變化學(xué)說等[3-4]。目前對于AD的診斷仍主要依據(jù)排除法和臨床神經(jīng)心理量表法,但其可重復(fù)性差,且缺乏客觀依據(jù)。
近年來的研究發(fā)現(xiàn),在AD的輕度認(rèn)知障礙(mild cognition impairment,MCI)階段及AD早期,患者的腦組織結(jié)構(gòu)即表現(xiàn)出廣泛且較為明顯的變化[5-6]。AD患者由于腦組織神經(jīng)元的喪失,可出現(xiàn)腦萎縮改變,因此可以通過測量腦萎縮程度來觀察AD。目前,磁共振成像(magnetic resonance imaging,MRI)主要通過T2加權(quán)或液體衰減反轉(zhuǎn)恢復(fù)(fluid attenuated inversion recovery,F(xiàn)LAIR)序列來測量海馬體積和內(nèi)嗅區(qū)皮質(zhì)厚度以觀察AD;但對于AD早期的腦組織結(jié)構(gòu)變化,尚缺乏敏感且準(zhǔn)確的影像學(xué)診斷標(biāo)準(zhǔn)。本文對MRI形態(tài)學(xué)測量在AD早期診斷中的應(yīng)用進(jìn)展進(jìn)行綜述。
DOLEK等[7]發(fā)現(xiàn),AD患者海馬的萎縮程度比血管性癡呆和MCI更為明顯。有研究發(fā)現(xiàn),利用MRI可在AD的臨床前階段就能觀察到海馬結(jié)構(gòu)的明顯萎縮[2]。AD患者的海馬以每年3%~7%的速率逐漸萎縮,而正常老年人海馬的最大萎縮速率僅為0.9%。因此,動態(tài)跟蹤測量海馬體積的變化是監(jiān)測AD病情進(jìn)展的重要指標(biāo)之一。要測量海馬體積就必須首先確定海馬的邊界。手工勾畫海馬邊界非常費(fèi)時(shí),且誤差較大。雖然許多研究機(jī)構(gòu)及學(xué)者均對海馬體積測量法進(jìn)行了深入探討,試圖借助半自動或全自動分析程序以改進(jìn)海馬體積分析法,縮短測量時(shí)間;但結(jié)果顯示,體積測量誤差依然很大,且可重復(fù)性差。究其原因,主要包括以下幾個方面:(1)由于海馬形態(tài)欠規(guī)則,因此確定邊界較為困難;(2)難以清晰地勾畫海馬頭與其前上方杏仁核之間的分界;(3)在MRI T2加權(quán)或FLAIR序列圖像上,大腦灰質(zhì)與白質(zhì)的分界略模糊,增加了勾畫難度;(4)常有小部分海馬尾未被納入體積測量范圍之內(nèi),導(dǎo)致海馬體積的測量范圍只占海馬全部體積的90%~95%,進(jìn)一步增加了測量誤差。也有學(xué)者認(rèn)為,通過測量海馬CA1區(qū)來發(fā)現(xiàn)癡呆前期的腦組織結(jié)構(gòu)變化較測量海馬體積更為敏感[8],但海馬CA1區(qū)的萎縮不是AD特有的病理生理學(xué)改變。
近年來的研究發(fā)現(xiàn),內(nèi)嗅區(qū)皮質(zhì)是AD最早發(fā)生神經(jīng)變性的部位。AD早期的記憶損害可與內(nèi)嗅區(qū)萎縮有關(guān)。VARON等[9]認(rèn)為,內(nèi)嗅區(qū)皮質(zhì)的輕度萎縮與海馬的輕度萎縮相比,前者可引起更為嚴(yán)重的損害。通過測量新皮質(zhì)相關(guān)區(qū)域及內(nèi)嗅區(qū)皮質(zhì)厚度來區(qū)分AD患者與正常對照者的準(zhǔn)確率>90%。內(nèi)嗅區(qū)皮質(zhì)的體積變化在AD的早期診斷及鑒別診斷中具有一定的價(jià)值[10]。測量皮質(zhì)厚度最常采用的檢測方法就是基于體素的容積分析法,這種方法是通過高分辨率影像掃描將大腦圖像轉(zhuǎn)換成一種標(biāo)準(zhǔn)模板的大腦,可以在頭部位置及大腦體積大小等方面抵消其總體差異,因而能消除個體之間大腦的解剖學(xué)差異,但是在灰質(zhì)分布方面仍然保留了局部差異,因此可依據(jù)此差異進(jìn)行分析。然而,這種檢測方法的精度不高,且在隨訪時(shí)也難以確保重復(fù)定位的準(zhǔn)確性。近期有研究發(fā)現(xiàn),海馬細(xì)微結(jié)構(gòu)的變化可能是神經(jīng)變性疾病的早期指標(biāo)之一[11]。因此,應(yīng)用MRI對海馬細(xì)微結(jié)構(gòu)的變化進(jìn)行觀察已成為AD早期診斷研究的熱點(diǎn)之一。
在AD早期階段,杏仁核發(fā)生的病理變化涉及抑郁的發(fā)病機(jī)制,可能是二十碳五烯酸與認(rèn)知功能降低及抑郁綜合征相互關(guān)聯(lián)的重要腦部結(jié)構(gòu)[12]。CAVEDO等[13]發(fā)現(xiàn)AD患者杏仁核的局部結(jié)構(gòu)與正常對照者有所不同,并認(rèn)為其連接了海馬(外側(cè)核和基底腹內(nèi)側(cè)核)、內(nèi)嗅區(qū)以及膽堿能神經(jīng)通路。在路易小體癡呆(dementia with Lewy bodies,DLB)患者中,杏仁核組織喪失引起的彌散增加可能與微空泡有關(guān)。彌散加權(quán)成像(diffusion-weighted imaging,DWI)是對MRI的補(bǔ)充。研究表明,彌散張量成像(diffusion tensor imaging,DTI)的彌散系數(shù)在鑒別AD 與DLB中具有重要價(jià)值[2]。BURTON等[15]認(rèn)為,是海馬和杏仁核而不是內(nèi)嗅區(qū)皮質(zhì)導(dǎo)致AD和DLB患者顳葉內(nèi)側(cè)結(jié)構(gòu)的萎縮。杏仁核萎縮在AD發(fā)病機(jī)制中的作用是當(dāng)前的研究熱點(diǎn)之一。
DIR序列可以清晰地顯示腦皮質(zhì)(呈現(xiàn)高信號)與腦白質(zhì)和腦脊液之間的分界[16],還可以清晰地顯示靠近皮層的多發(fā)性硬化病灶,較FLAIR序列具有更高的敏感度[17]。有研究將DIR序列應(yīng)用于癲癇腦皮質(zhì)異位和頸動脈斑塊的檢測,還有極少數(shù)研究將DIR序列應(yīng)用于癡呆的研究,并認(rèn)為DIR序列為癡呆腦內(nèi)微梗死灶的顯示提供了新方法[18]。
有研究發(fā)現(xiàn),AD的早期表現(xiàn)為雙側(cè)海馬、內(nèi)嗅區(qū)和右側(cè)杏仁核體積縮?。?9]。鑒于海馬體積測量難度高且誤差大,同時(shí)難以進(jìn)行準(zhǔn)確的重復(fù)性定位,因此尋找一種更加簡便、準(zhǔn)確且重復(fù)性較好的MRI檢查方法就成為當(dāng)前AD影像學(xué)研究的熱點(diǎn)之一。目前普遍認(rèn)為,顳葉萎縮和海馬萎縮均為AD早期診斷的指標(biāo)之一。盡管DIR序列可以清楚地區(qū)分灰白質(zhì),但應(yīng)用DIR序列進(jìn)行AD腦皮質(zhì)厚度檢測的研究還未見報(bào)道。
BOZZALI等[20]研究發(fā)現(xiàn),AD可選擇性地累及與皮層相聯(lián)系的相關(guān)腦白質(zhì)區(qū),如胼胝體、顳葉、額葉和頂葉,提示與皮層聯(lián)系的神經(jīng)元的喪失導(dǎo)致了腦白質(zhì)束的變性,但其余腦白質(zhì)區(qū)則不易受累。MCMILLAN等[21]認(rèn)為,通過MRI可以檢測AD患者灰質(zhì)和白質(zhì)的丟失情況,應(yīng)用DTI可以測量腦白質(zhì)體積。AD以扣帶回后部及楔前回腦灰質(zhì)的萎縮最為明顯,而額顳葉性癡呆則是以額顳葉皮質(zhì)萎縮最為明顯。采用DTI可以顯示腦白質(zhì)纖維束的走行,有助于觀察白質(zhì)纖維束的空間方向性及完整性。目前最常用的DTI量化指標(biāo)包括表觀彌散系數(shù)(apparentdiffusion coefficient,ADC)、平均彌散率(mean diffusivity,MD)和各向異性分?jǐn)?shù)(fractional anisotropy,F(xiàn)A)。MD是ADC的平均值,其消除了各向異性的影響,顯示了水分子的擴(kuò)散程度,但會受到細(xì)胞大小和細(xì)胞膜完整性的影響;FA則是擴(kuò)散張量的各向異性成分與整個擴(kuò)散張量的比值。TAKAHASHI等[22]應(yīng)用3.0T磁共振(magnetic resonance,MR)儀進(jìn)行DTI來研究AD患者,結(jié)果發(fā)現(xiàn)額葉皮層下白質(zhì)、胼胝體壓部及前后扣帶束的FA均較正常人顯著下降。
DTI可用于評估癡呆患者的白質(zhì)損傷。與AD患者相比,皮質(zhì)下缺血性血管性癡呆(subcortical ischemic vascular dementia,SIVD)患者的多發(fā)局灶性FA降低及ADC升高更加明顯,可以作為鑒別AD與SIVD患者的一種方法[23]。研究表明,病理變化的差異與不同的穹隆損傷機(jī)制相關(guān)。例如,特發(fā)性正常壓力性腦積水系通過機(jī)械的伸展,引起腦室擴(kuò)張及胼胝體變形;AD則是繼發(fā)于海馬萎縮的退行性病變[24]。AD患者海馬纖維結(jié)構(gòu)的變化較體積變化更為敏感。AD、特發(fā)性正常壓力性腦積水和正常人的FA呈遞增變化,而MD呈遞減變化,可能與AD的神經(jīng)元喪失有關(guān),而DTI有助于對此進(jìn)行鑒別[25]。與單純AD相比,AD并發(fā)腦血管病對MD的影響更大。腦白質(zhì)MD升高[26]及FA降低[27]可能與AD伴腦血管病有關(guān)。穹隆是海馬發(fā)出的纖維束的主要結(jié)構(gòu),其可能成為提示AD進(jìn)展的一項(xiàng)重要指標(biāo)。有學(xué)者認(rèn)為,通過DTI可以觀察海馬細(xì)微結(jié)構(gòu)的變化,是早期診斷AD的潛在指標(biāo)[28]。
總之,尋找一種敏感度及特異度較高且重復(fù)性較好的簡便易行的檢測方法,已成為AD研究的重點(diǎn)及熱點(diǎn)。要實(shí)現(xiàn)對腦皮質(zhì)進(jìn)行可重復(fù)的、準(zhǔn)確的MRI檢查,必須滿足如下條件:(1)擁有最大的空間分辨率,層厚盡可能薄,以減少容積效應(yīng)的影響;(2)擁有良好的軟組織分辨率,能夠很好地顯示腦皮質(zhì)邊界,使邊界劃分更加可靠;(3)應(yīng)采用恒定的定位解剖標(biāo)志,以確保MRI檢查的可重復(fù)性;(4)測量操作應(yīng)簡便可行,使人為誤差盡可能地降至最低;(5)圖像采集時(shí)間不宜過長,使大多數(shù)患者能夠配合完成檢查。因此,可重復(fù)性好、易于評價(jià)早期AD的客觀影像學(xué)指標(biāo)的研究,將成為神經(jīng)科學(xué)領(lǐng)域未來重點(diǎn)的探索方向。
此外,基于MRI的生物學(xué)指標(biāo)的定量分析可用于AD的早期檢測[29]。例如,有研究發(fā)現(xiàn)神經(jīng)毒性β-淀粉樣蛋白低聚物與AD相關(guān),靶向β-淀粉樣蛋白低聚物的納米材料(攜帶低聚物特異性抗體)在新藥療效評價(jià)及AD的早期診斷和治療中均具有潛在的應(yīng)用價(jià)值;通過MRI測量β-淀粉樣蛋白低聚物可以直接做出AD診斷,并可提供結(jié)構(gòu)性信息及分子靶向?qū)Ρ葎┑亩ㄎ恍畔ⅲ?0]。今后,有待對生物學(xué)指標(biāo)在AD診斷中的應(yīng)用開展更為深入的研究。
參考文獻(xiàn)
[1] ALMKVlST O, TALLBERG l M. Cognitive decline from estimated premorbid status predicts neurodegeneration in Alzheimer's disease[J]. Neuropsychology, 2009,23(1):117–124.
[2] OKONKWO O C, XU G, DOWLlNG N M, et al. Family history of Alzheimer disease predicts hippocampal atrophy in healthy middle–aged adults[J]. Neurology, 2012, 78(22):1769–1776.
[3] KOREN J 3RD, JlNWAL U K, LEE D C, et al. Chaperone signalling complexes in Alzheimer's disease[J]. J Cell Mol Med,2009, 13(4):619–630.
[4] ZHANG Y, LONDOS E, MlNTHON L, et al. Medial temporal lobe atrophy increases the specificity of cerebrospinal fluid biomarkers in Alzheimer disease with minor cerebrovascular changes[J]. Acta Radiol,2009, 50(6):674–681.
[5] BERTELSON J A, AJTAl B. Neuroimaging of dementia[J]. Neurol Clin, 2014, 32(1):59–93.
[6] ROPELE S, SCHMlDT R, ENZlNGER C, et al. Longitudinal magnetization transfer imaging in mild to severe Alzheimer disease[J]. AJNR Am J Neuroradiol, 2012, 33(3):570–575.
[7] DOLEK N, SAYLlSOY S, OZBABALlK D, et al. Comparison of hippocampal volume measured using magnetic resonance imaging in Alzheimer's disease, vascular dementia, mild cognitive impairment and pseudodementia[J]. J lnt Med Res, 2012,40(2):717–725.
[8] LA JOlE R, PERROTlN A, DE LA SAYETTE V,et al. Hippocampal subfield volumetry in mild cognitive impairment, Alzheimer's disease and semantic dementia[J]. Neuroimage Clin,2013(3):155–162.
[9] VARON D, LOEWENSTElN D A, POTTER E, et al. Minimal atrophy of the entorhinal cortex and hippocampus: progression of cognitive impairment[J]. Dement Geriatr Cogn Disord,2011, 31(4):276–283.
[10] TAPlOLA T, PENNANEN C, TAPlOLA M,et al. MRl of hippocampus and entorhinal cortex in mild cognitive impairment: a follow–up study[J]. Neurobiol Aging, 2008,29(1):31–38.
[11] VAN NORDEN A G, DE LAAT K F, FlCK l, et al. Diffusion tensor imaging of the hippocampus and verbal memory performance: the RUN DMC study[J]. Hum Brain Mapp, 2012,33(3):542–551.
[12] SAMlERl C, MAlLLARD P, CRlVELLO F, et al. Plasma long–chain omega–3 fatty acids and atrophy of the medial temporal lobe[J]. Neurology, 2012, 79(7):642–650.
[13] CAVEDO E, BOCCARDl M, GANZOLA R, et al. Local amygdala structural differences with 3T MRl in patients with Alzheimer disease[J]. Neurology, 2011, 76(8):727–733.
[14] KANTARCl K, AVULA R, SENJEM M L, et al. Dementia with Lewy bodies and Alzheimer disease: neurodegenerative patterns characterized by DTl[J]. Neurology, 2010,74(22):1814–1821.
[15] BURTON E J, MUKAETOVA–LADlNSKA E B, PERRY R H, et al. Quantitative neurodegenerative pathology does not explain the degree of hippocampal atrophy on MRl in degenerative dementia[J]. lnt J Geriatr Psychiatry, 2012, 27(12):1267–74.
[16] POUWELS P J, KUlJER J P, MUGLER J P 3RD, et al. Human gray matter: feasibility of single–slab 3D double inversion–recovery high–spatial–resolution MR imaging[J]. Radiology, 2006, 241(3):873–879.
[17] SlMON B, SCHMlDT S, LUKAS C, et al. lmproved in vivo detection of cortical lesions in multiple sclerosis using double inversion recovery MR imaging at 3 Tesla[J]. Eur Radiol, 2010, 20(7):1675–1683.
[18] ll Y, MAEDA M, KlDA H, et al. ln vivo detection of cortical microinfarcts on ultrahigh–field MRl[J]. J Neuroimaging, 2013,23(1):28–32.
[19] STRlEPENS N, SCHEEF L, WlND A, et al. Volume loss of the medial temporal lobe structures in subjective memory impairment[J]. Dement Geriatr Cogn Disord,2010, 29(1):75–81.
[20] BOZZALl M, FALlNl A, FRANCESCHl M, et al. White matter damage in Alzheimer’s disease assessed in vivo using diffusion tensor magnetic resonance imaging[J]. J NeurolNeurosurg Psychiatry, 2002,72(6):742–746.
[21] MCMlLLAN C T, BRUN C, SlDDlQUl S, et al. White matter imaging contributes to the multimodal diagnosis of frontotemporal lobar degeneration[J]. Neurology, 2012,78(22):1761–1768.
[22] TAKAHASHl S, YONEZAWA H, TAKAHASHl J, et al. Selective reduction of diffusion anisotropy in white matter of Alzheimer disease brains measured by 3.0 Tesla magnetic resonance imaging[J]. Neurosci Lett, 2002,332(1):45–48.
[23] FU J L, ZHANG T, CHANG C, et al. The value of diffusion tensor imaging in the differential diagnosis of subcortical ischemic vascular dementia and Alzheimer’s disease in patients with only mild white matter alterations on T2–weighted images[J]. Acta Radiol, 2012, 53(3):312–317.
[24] HATTORl T, SATO R, AOKl S, et al. Different patterns of fornix damage in idiopathic normal pressure hydrocephalus and Alzheimer disease[J]. AJNR Am J Neuroradiol, 2012, 33(2):274–279.
[25] HONG Y J, YOON B, SHlM Y S, et al. Differences in microstructural alterations of the hippocampus in Alzheimer disease and idiopathic normal pressure hydrocephalus: a diffusion tensor imaging study[J]. AJNR Am J Neuroradiol, 2010, 31(10):1867–1872.
[26] CHEN S Q, KANG Z, HU X Q, et al. Diffusion tensor imaging of the brain in patients with Alzheimer‘s disease and cerebrovascular lesions[J]. J Zhejiang Univ Sci B, 2007,8(4):242–247.
[27] MlELKE M M, KOZAUER N A, CHAN K C,et al. Regionally–specific diffusion tensor imaging in mild cognitive impairment and Alzheimer’s disease[J]. Neuroimage, 2009,46(1):47–55.
[28] ZHANG B, XU Y, ZHU B, et al. The role of diffusion tensor imaging in detecting microstructural changes in prodromal Alzheimer’s disease[J]. NS Neurosci Ther,2014, 20(1):3–9.
[29] ZHOU Y, YU F, DUONG T Q, et al. White matter lesion load is associated with resting state functional MRl activity and amyloid PET but not FDG in mild cognitive impairment and early Alzheimer's disease patients[J]. J Magn Reson lmaging, 2015, 41(1):102–109.
[30] VlOLA KL, SBARBORO J, SUREKA R, et al. Towards non–invasive diagnostic imaging of early–stage Alzheimer's disease[J]. Nat Nanotechnol, 2015, 10(1):91–98.
隨著全球人口老齡化,阿爾茨海默?。ˋlzheimer's disease,AD)發(fā)病率呈明顯上升趨勢。迄今為止,尚缺乏有效的AD治療方法,早期診斷及防治是延緩AD進(jìn)展的唯一有效方法。目前,AD的診斷仍主要依靠排除法和臨床神經(jīng)心理量表法,但其可重復(fù)性差且缺乏客觀依據(jù);因此,尚缺乏敏感且準(zhǔn)確的AD早期診斷方法。隨著影像學(xué)技術(shù)的發(fā)展,“醫(yī)學(xué)影像學(xué)+”的學(xué)科交叉已成為新常態(tài),由此產(chǎn)生的神經(jīng)影像學(xué)技術(shù)可以清晰地顯示腦內(nèi)更細(xì)小的結(jié)構(gòu)和病灶,這為AD的早期影像學(xué)診斷研究提供了基礎(chǔ)。本文對磁共振成像(magnetic resonance imaging,MRI)應(yīng)用于海馬體積、內(nèi)嗅區(qū)皮質(zhì)厚度及杏仁核變化的檢測以及雙反轉(zhuǎn)恢復(fù)(double inversion recovery,DIR)序列應(yīng)用于AD診斷及彌散張量成像(diffusion tensor imaging,DTI)應(yīng)用于海馬相關(guān)腦白質(zhì)損傷評估的最新研究進(jìn)展進(jìn)行綜述。
DOI:10.12022/jnnr.2016-0015
通信作者
詹 青
zhanqing@#edu.cn
基金項(xiàng)目:上海市科學(xué)技術(shù)委員會科技創(chuàng)新行動計(jì)劃重點(diǎn)項(xiàng)目(編號:10411953400);上海市寶山區(qū)科學(xué)技術(shù)委員會科研項(xiàng)目(編號:14–E–4);上海市科學(xué)技術(shù)委員會醫(yī)學(xué)引導(dǎo)類科技項(xiàng)目(編號:114119a5800)
CORRESPONDING AUTHOR
Advances in MRI in diagnosis of early-stage Alzheimer’s disease
ZHAO Jiangmin1, ZHAN Qing2
1. Department of Medical lmaging, Ninth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,Shanghai 201900, China;
2. Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China
KEy WORDS:Alzheimer disease; Early diagnosis; Magnetic resonance imaging