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当代阿耳茨海默病研究

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Research Article

Tau PET在视空间功能障碍患者中的分布模式

卷 16, 期 11, 2019

页: [1055 - 1062] 页: 8

弟呕挨: 10.2174/1567205016666191113152434

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摘要

背景:视空间功能障碍是许多非典型阿尔茨海默病(AD)患者的主要症状之一,但是直到现在,其神经相关性仍不清楚。由于胞内高磷酸化tau蛋白的积累是AD神经退行性变的主要致病因素,因此tau的分布方式可能会突出显示与特定认知缺陷相关的受影响的大脑区域。 目的:我们研究了视觉空间功能障碍患者特别受tau积累影响的大脑区域,以探讨其神经相关性。 方法:使用18F-AV-1451 tau正电子发射断层扫描(PET),对视觉空间功能障碍(VS-AD)明显的AD患者和认知正常的AD患者,体力不高的AD患者进行体素明智的两次抽样t检验。 -无视觉空间功能障碍(非VS-AD)和认知正常的受试者。 结果:结果显示VS-AD患者的tau积累增加主要位于枕顶叶皮质,扣带回后皮质,前突神经,颞下内侧和中间皮质,而tau积累的增加主要发生于非VS-AD患者的下颞内侧。 结论:这些发现表明,枕顶叶皮质,扣带回后皮质和前突神经尤其受VS-AD患者tau积累增加的影响,可能与AD的视觉空间功能障碍有关。

关键词: 阿尔茨海默氏病,视觉空间功能障碍,tau PET,高磷酸化tau,Aβ斑块,NFT。

[1]
Scheltens P, Blennow K, Breteler MMB, de Strooper B, Frisoni GB, Salloway S, et al. Alzheimer’s disease. Lancet 388(10043): 505-17.(2016);
[2]
Mattson MP. Pathways towards and away from Alzheimer’s disease. Nature 430(7000): 631-9.(2004);
[3]
Walsh DM, Selkoe DJ. Deciphering the molecular basis of memory failure in Alzheimer’s disease. Neuron 44(1): 181-93.(2004);
[4]
Buckner RL. Memory and executive function in aging and AD: Multiple factors that cause decline and reserve factors that compensate. Neuron 44(1): 195-208.(2004);
[5]
Geldmacher DS. Visuospatial dysfunction in the neurodegenerative diseases. Front Biosci 8: E428-36.(2003);
[6]
Mels JL, Noll ES, Hewitt BM, Dubovsky SL, Filley CM. Visuospatial dysfunction in Alzheimer’s disease. J Investig Med 47(2): 80A-A.(1999);
[7]
Cogan DG. VISUOSPATIAL DYSGNOSIA. Am J Ophthalmol 88(3): 361-8.(1979);
[8]
Mandal PK, Joshi J, Saharan S. Visuospatial Perception: An Emerging Biomarker for Alzheimer’s Disease. J Alzheimers Dis 31: S117-35.(2012);
[9]
Lee DY, Seo EH, Choo IH, Kim SG, Lee JS, Lee DS, et al. Neural Correlates of the Clock Drawing Test Performance in Alzheimer’s Disease: A FDG-PET Study. Dement Geriatr Cogn Disord 26(4): 306-13.(2008);
[10]
Jacobs HIL, Gronenschild E, Evers EAT, Ramakers I, Hofman PAM, Backes WH, et al. Visuospatial processing in early Alzheimer’s disease: A multimodal neuroimaging study. Cortex 64: 394-406.(2015);
[11]
Gron G, Wunderlich AP, Spitzer M, Tomczak R, Riepe MW. Brain activation during human navigation: gender-different neural networks as substrate of performance. Nat Neurosci 3(4): 404-8.(2000);
[12]
Hall B, Mak E, Cervenka S, Aigbirhio FI, Rowe JB, O’Brien JT. In vivo tau PET imaging in dementia: Pathophysiology, radiotracer quantification, and a systematic review of clinical findings. Ageing Res Rev 36: 50-63.(2017);
[13]
Kidemet-Piskac S, Leko MB, Blazekovic A, Horvat LL, Klepac N, Sonicki Z, et al. Evaluation of cerebrospinal fluid phosphorylated tau(231) as a biomarker in the differential diagnosis of Alzheimer’s disease and vascular dementia. CNS Neurosci Ther 24(8): 734-40.(2018);
[14]
Santangelo R, Dell’Edera A, Sala A, Cecchetti G, Masserini F, Caso F, et al. The CSF p-tau181/A beta 42 Ratio Offers a Good Accuracy “In Vivo” in the Differential Diagnosis of Alzheimer’s Dementia. Curr Alzheimer Res 16(7): 587-95.(2019);
[15]
Schwarz AJ, Yu P, Miller BB, Shcherbinin S, Dickson J, Navitsky M, et al. Regional profiles of the candidate tau PET ligand F-18-AV-1451 recapitulate key features of Braak histopathological stages. Brain 139: 1539-50.(2016);
[16]
Braak H, Alafuzoff I, Arzberger T, Kretzschmar H, Del Tredici K. Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 112(4): 389-404.(2006);
[17]
Okamura N, Yanai K. Applications of tau PET imaging. Nat Rev Neurol 13(4): 2.(2017);
[18]
Robertson JS, Rowe CC, Vilemagne VL. Tau imaging with PET: an overview of challenges, current progress, and future applications. Q J Nucl Med Mol Imaging 61(4): 405-13.(2017);
[19]
Galasko D, Klauber MR, Hofstetter CR, Salmon DP, Lasker B, Thal LJ. The mini-mental state examination in the early diagnosis of Alzheimers-disease. Arch Neurol 47(1): 49-52.(1990);
[20]
Smith T, Gildeh N, Holmes C. The Montreal Cognitive Assessment: Validity and utility in a memory clinic setting. Can J Psychiat-Rev Can Psychiat 52(5): 329-32.(2007);
[21]
Gauthier S, Wirth Y, Mobius HJ. Effects of memantine on behavioural symptoms in Alzheimer’s disease patients: an analysis of the Neuropsychiatric Inventory (NPI) data of two randomised, controlled studies. Int J Geriatr Psychiatry 20(5): 459-64.(2005);
[22]
Galasko D, Bennett D, Sano M, Ernesto C, Thomas R, Grundman M, et al. An inventory to assess activities of daily living for clinical trials in Alzheimer’s disease. Alzheimer Dis Assoc Disord 11: S33-9.(1997);
[23]
Marshall GA, Rentz DM, Frey MT, Locascio JJ, Johnson KA, Sperling RA, et al. Executive function and instrumental activities of daily living in mild cognitive impairment and Alzheimer’s disease. Alzheimers Dement 7(3): 300-8.(2011);
[24]
Vida S, Des Rosiers P, Carrier L, Gauthier S. Depression in Alzheimer’s disease: receiver operating characteristic analysis of the Cornell Scale for Depression in Dementia and the Hamilton Depression Scale. Journal of geriatric psychiatry and neurology 7(3): 159-62.(1994);
[25]
Williams BW, Mack W, Henderson VW. Boston naming test in Alzheimers-disease. Neuropsychologia 27(8): 1073-9.(1989);
[26]
Agrell B, Dehlin O. The clock-drawing test. Age Ageing 27(3): 399-403.(1998);
[27]
McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR, Kawas CH, et al. The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement 7(3): 263-9.(2011);
[28]
Serrano-Pozo A, Qian J, Monsell SE, Blacker D, Gomez-Isla T, Betensky RA, et al. Mild to Moderate Alzheimer Dementia with Insufficient Neuropathological Changes. Ann Neurol 75(4): 597-601.(2014);
[29]
Herholz K, Salmon E, Perani D, Baron JC, Holthoff V, Frolich L, et al. Discrimination between Alzheimer dementia and controls by automated analysis of multicenter FDG PET. Neuroimage 17(1): 302-16.(2002);
[30]
Takenoshita N, Fukasawa R, Ogawa Y, Shimizu S, Umahara T, Ishii K, et al. Amyloid and tau positron emission tomography in suggested diabetes-related dementia. Curr Alzheimer Res 15(11): 1062-9.(2018);
[31]
Mainta IC, Perani D, Delattre BMA, Assal F, Haller S, Vargas MI, et al. FDG PET/MR imaging in major neurocognitive disorders. Curr Alzheimer Res 14(2): 186-97.(2017);
[32]
Nakashima H, Umegaki H, Makino T, Kato K, Abe S, Suzuki Y, et al. Neuroanatomical correlates of error types on the Clock Drawing Test in Alzheimer’s disease patients. Geriatr Gerontol Int 16(7): 777-84.(2016);
[33]
Pinto E, Peters R. Literature Review of the Clock Drawing Test as a Tool for Cognitive Screening. Dement Geriatr Cogn Disord 27(3): 201-13.(2009);
[34]
Samton JB, Ferrando SJ, Sanelli P, Karimi S, Raiteri V, Barnhill JW. The clock drawing test: Diagnostic, functional, and neuroimaging correlates in older medically ill adults. J Neuropsychiatry Clin Neurosci 17(4): 533-40.(2005);
[35]
Terwindt PW, Hubers AAM, Giltay EJ, van der Mast RC, van Duijn E. Screening for cognitive dysfunction in Huntington’s disease with the clock drawing test. Int J Geriatr Psychiatry 31(9): 1013-20.(2016);
[36]
Park J, Jeong E, Seomun G. The clock drawing test: A systematic review and meta-analysis of diagnostic accuracy. J Adv Nurs 74(12): 2742-54.(2018);
[37]
Chau W, McIntosh AR. The Talairach coordinate of a point in the MNI space: how to interpret it. Neuroimage 25(2): 408-16.(2005);
[38]
Ossenkoppele R, Schonhaut DR, Scholl M, Lockhart SN, Ayakta N, Baker SL, et al. Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer’s disease. Brain 139: 1551-67.(2016);
[39]
Pontecorvo MJ, Devous MD, Navitsky M, Lu M, Salloway S, Schaerf FW, et al. Relationships between flortaucipir PET tau binding and amyloid burden, clinical diagnosis, age and cognition. Brain 140: 748-63.(2017);
[40]
Lewis J, Dickson DW. Propagation of tau pathology: hypotheses, discoveries, and yet unresolved questions from experimental and human brain studies. Acta Neuropathol 131(1): 27-48.(2016);
[41]
Guan ZZ, Zhang X, Ravid R, Nordberg A. Decreased protein levels of nicotinic receptor subunits in the hippocampus and temporal cortex of patients with Alzheimer’s disease. J Neurochem 74(1): 237-43.(2000);
[42]
Grundman M. CoreyBloom J, Jernigan T, Archibald S, Thal LJ. Low body weight in Alzheimer’s disease is associated with mesial temporal cortex atrophy. Neurology 46(6): 1585-91.(1996);
[43]
Del Sole A, Clerici F, Chiti A, Lecchi M, Mariani C, Maggiore L, et al. Individual cerebral metabolic deficits in Alzheimer’s disease and amnestic mild cognitive impairment: an FDG PET study. Eur J Nucl Med Mol Imaging 35(7): 1357-66.(2008);
[44]
Pei JJ, Gong CX, Iqbal K, Grundke-Iqbal I, Wu QL, Winblad B, et al. Subcellular distribution of protein phosphatases and abnormally phosphorylated tau in the temporal cortex from Alzheimer’s disease and control brains. J Neural Transm 105(1): 69-83.(1998);
[45]
Thiyagesh SN, Farrow TFD, Parks RW, Accosta-Mesa H, Young C, Wilkinson ID, et al. The neural basis of visuospatial perception in Alzheimer’s disease and healthy elderly comparison subjects: An fMRI study. Psychiatry Res Neuroimaging 172(2): 109-16.(2009);
[46]
Kravitz DJ, Saleem KS, Baker CI, Mishkin M. A new neural framework for visuospatial processing. Nat Rev Neurosci 12(4): 217-30.(2011);
[47]
Grieves RM, Jeffery KJ. The representation of space in the brain. Behav Processes 135: 113-31.(2017);
[48]
Whittingstall K, Bernier M, Houde JC, Fortin D, Descoteaux M. Structural network underlying visuospatial imagery in humans. Cortex 56: 85-98.(2014);
[49]
Chien HY, Gau SSF, Tseng WYI. Deficient visuospatial working memory functions and neural correlates of the default-mode network in adolescents with autism spectrum disorder. Autism Res 9(10): 1058-72.(2016);

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