中国阿尔茨海默病临床前期主观认知下降的诊治策略

doi:DOI:10.12117/jccmi.2018.08.002

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摘要当前，中国已经成为世界上阿尔茨海默病（Alzheimer disease，AD）患者人数最多的国家。而AD的治疗尚未取得突破性进展。因此，AD对我国老年人群的健康和经济社会的可持续发展构成重大威胁。新形势下，应转变工作思路，扭转重治疗轻预防的误区。就目前情况而言，攻克AD的真正希望在于二级预防乃至一级预防。主观认知下降（Subjective cognitive decline，SCD）作为AD的高危人群，是AD防治的重要关口。为贯彻落实“健康中国2030”实施方案，实现重大慢性病早诊早治技术纳入诊疗常规，由国家老年疾病临床医学研究中心（宣武医院）——中国AD临床前期联盟牵头，会同有关专家组成工作组制定了我国AD临床前期SCD的诊疗策略。本策略涵盖了AD临床前期SCD的概念、流行病学、神经心理学检查、影像学检查及非药物干预等主要方面，以期提高我国医务人员对AD的认识，最终实现“The End of Alzheimer’s”的终极目标。

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	韩璎

关键词 ：阿尔兹海默病, 诊断, 治疗, 磁共振成像

Abstract：At present, China is the country with the largest number of people with Alzheimer disease(AD) over the world. This has posed a major burden to the health of the elderly people and the sustainable development of economy in China. There are yet no medication that can prevent the progression of AD. Given the current circumstances, the greatest possibility of combating AD should start even before the disease begins to manifest. Subjective cognitive decline(SCD), a high-risk group of AD, has been identified as the most important target persons for prevention. The National Clinical Research Center for Geriatric Disorders of Xuanwu Hospital convened a workgroup to develop recommendations for diagnosis and treatment of SCD as a part of the plan of “healthy China 2030”, a national health strategy proposed by the Chinese government in 2016, to advance early diagnosis and treatment technology for major chronic diseases as clinical practice. These recommendations include the concept of defining SCD, epidemiology, neuropsychological examinations, neuroimaging and non-pharmalogical interventions of SCD in oder to improve the understanding of AD among medical staff, and ultimately achieve the final goal of “The End of Alzheimer’s”.

Key words： Alzheimer disease Diagnosis Theraphy Magnetic resonance imaging

收稿日期: 2018-04-18

PACS:	Ｒ749.16
	Ｒ445.2

基金资助:《国家重点研发计划》“重大慢性非传染性疾病防控研究”专项阿尔茨海默病的早期诊断新技术研发（2016YFC1306300）；国家自然科学基金重点项目（61633018）；北京市卫计委老年重大疾病关键技术研究（PXM2018_026283_000002）；顺义区卫计委、德国科学基金会资助（German Research Council, DFG; JE 2707/7-1）

通讯作者: 韩璎，国家老年疾病临床医学研究中心首都医科大学宣武医院神经内科，100053。E-mail：hanying@xwh.ccmu.edu.cn

作者简介: 韩璎（1964-），女，山东人，主任医师。E-mail：hanying@xwh.ccmu.edu.cn

引用本文:

韩璎. 中国阿尔茨海默病临床前期主观认知下降的诊治策略[J]. 中国临床医学影像杂志, 2018, 29(8): 534-538.
HAN Ying. Recommendations for diagnosis and treatment of subjective cognitive decline due to preclinical Alzheimer disease in China. JOURNAL OF CHINA MEDICAL IMAGING, 2018, 29(8): 534-538.

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http://www.jccmi.com.cn/CN/DOI:10.12117/jccmi.2018.08.002 或 http://www.jccmi.com.cn/CN/Y2018/V29/I8/534

[1]Prince M, Wimo A, Guerchet M, et al. World Alzheimer Report 2015[R]. 2015 [2018-07-26]. https://www.researchgate.net/publication/309637438_World_Alzheimer_Report_2015.
[2]McDade E, Bateman RJ. Stop Alzheimer’s before it starts[J]. Nature, 2017, 547(7662): 153-155.
[3]Scheltens P, Blennow K, Breteler MM, et al. Alzheimer’s disease[J]. Lancet, 2016, 388(10043): 505-517.
[4]Karran E, De Strooper B. The amyloid cascade hypothesis: are we poised for success or failure?[J]. J Neurochem, 2016, 139(Suppl 2): 237-252.
[5]Ngandu T, Lehtisalo J, Solomon A, et al. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people(FINGER): a randomised controlled trial[J]. Lancet, 2015, 385(9984): 2255-2263.
[6]Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care[J]. Lancet, 2017, 390(10113): 2673-2734.
[7]Reisberg B, Ferris SH, de Leon MJ, et al. The Global Deterioration Scale for assessment of primary degenerative dementia[J]. Am J Psychiatry, 1982, 139(9): 1136-1139.
[8]Jessen F, Amariglio RE, van Boxtel M, et al. A conceptual framework for research on subjective cognitive decline in preclinical Alzheimer’s disease[J]. Alzheimers Dement, 2014, 10(6): 844-852.
[9]Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease[J]. Alzheimers Dement, 2011, 7(3): 280-292.
[10]Westoby CJ, Mallen CD, Thomas E. Cognitive complaints in a general population of older adults: prevalence, association with pain and the influence of concurrent affective disorders[J]. Eur J Pain, 2009, 13(9): 970-976.
[11]Buffart LM, de Bree R, Altena M, et al. Demographic, clinical, lifestyle-related, and social-cognitive correlates of physical activity in head and neck cancer survivors[J]. Support Care Cancer, 2018, 26(5): 1447-1456.
[12]Luck T, Luppa M, Matschinger H, et al. Incident subjective memory complaints and the risk of subsequent dementia[J]. Acta Psychiatr Scand, 2015, 131(4): 290-296.
[13]Luck T, Roehr S, Jessen F, et al. Mortality in Individuals with Subjective Cognitive Decline: Results of the Leipzig Longitudinal Study of the Aged(LEILA75+)[J]. J Alzheimers Dis, 2015, 48(Suppl 1): S33-42.
[14]Mitchell AJ, Beaumont H, Ferguson D, et al. Risk of dementia and mild cognitive impairment in older people with subjective memory complaints: meta-analysis[J]. Acta Psychiatr Scand, 2014, 130(6): 439-451.
[15]Wolfsgruber S, Kleineidam L, Wagner M, et al. Differential Risk of Incident Alzheimer’s Disease Dementia in Stable Versus Unstable Patterns of Subjective Cognitive Decline[J]. J Alzheimers Dis, 2016, 54(3): 1135-1146.
[16]Jessen F, Wolfsgruber S, Wiese B, et al. AD dementia risk in late MCI, in early MCI, and in subjective memory impairment[J]. Alzheimers Dement, 2014, 10(1): 76-83.
[17]Chen KL, Xu Y, Chu AQ, et al. Validation of the Chinese Version of Montreal Cognitive Assessment Basic for Screening Mild Cognitive Impairment[J]. J Am Geriatr Soc, 2016, 64(12): e285-e290.
[18]Bondi MW, Edmonds EC, Jak AJ, et al. Neuropsychological criteria for mild cognitive impairment improves diagnostic precision, biomarker associations, and progression rates[J]. J Alzheimers Dis, 2014, 42(1): 275-289.
[19]Edmonds EC, Delano-Wood L, Galasko DR, et al. Subtle Cognitive Decline and Biomarker Staging in Preclinical Alzheimer’s Disease[J]. J Alzheimers Dis, 2015, 47(1): 231-242.
[20]Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium[J]. JAMA, 1997, 278(16): 1349-1356.
[21]Olsson B, Lautner R, Andreasson U, et al. CSF and blood biomarkers for the diagnosis of Alzheimer’s disease: a systematic review and meta-analysis[J]. Lancet Neurol, 2016, 15(7): 673-684.
[22]Jessen F, Feyen L, Freymann K, et al. Volume reduction of the entorhinal cortex in subjective memory impairment[J]. Neurobiol Aging, 2006, 27(12): 1751-1756.
[23]Meiberth D, Scheef L, Wolfsgruber S, et al. Cortical thinning in individuals with subjective memory impairment[J]. J Alzheimers Dis, 2015, 45(1): 139-146.
[24]Peter J, Scheef L, Abdulkadir A, et al. Gray matter atrophy pattern in elderly with subjective memory impairment[J]. Alzheimers Dement, 2014, 10(1): 99-108.
[25]Perrotin A, de Flores R, Lamberton F, et al. Hippocampal Subfield Volumetry and 3D Surface Mapping in Subjective Cognitive Decline[J]. J Alzheimers Dis, 2015, 48(Suppl 1): S141-150.
[26]Wang PJ, Saykin AJ, Flashman LA, et al. Regionally specific atrophy of the corpus callosum in AD, MCI and cognitive complaints[J]. Neurobiol Aging, 2006, 27(11): 1613-1617.
[27]Verfaillie SC, Tijms B, Versteeg A, et al. Thinner temporal and parietal cortex is related to incident clinical progression to dementia in patients with subjective cognitive decline[J]. Alzheimers Dement(Amst), 2016, 5: 43-52.
[28]Engvig A, Fjell AM, Westlye LT, et al. Hippocampal subfield volumes correlate with memory training benefit in subjective memory impairment[J]. Neuroimage, 2012, 61(1): 188-194.
[29]Engvig A, Fjell AM, Westlye LT, et al. Effects of cognitive training on gray matter volumes in memory clinic patients with subjective memory impairment[J]. J Alzheimers Dis, 2014, 41(3): 779-791.
[30]Selnes P, Fjell AM, Gjerstad L, et al. White matter imaging changes in subjective and mild cognitive impairment[J]. Alzheimers Dement, 2012, 8(5 Suppl): S112-121.
[31]Selnes P, Aarsland D, Bjornerud A, et al. Diffusion tensor imaging surpasses cerebrospinal fluid as predictor of cognitive decline and medial temporal lobe atrophy in subjective cognitive impairment and mild cognitive impairment[J]. J Alzheimers Dis, 2013, 33(3): 723-736.
[32]Shu N, Wang X, Bi Q, et al. Disrupted Topologic Efficiency of White Matter Structural Connectome in Individuals with Subjective Cognitive Decline[J]. Radiology, 2018, 286(1): 229-238.
[33]Wang Y, Risacher SL, West JD, et al. Altered default mode network connectivity in older adults with cognitive complaints and amnestic mild cognitive impairment[J]. J Alzheimers Dis, 2013, 35(4): 751-760.
[34]Sun Y, Yang FC, Lin CP, et al. Biochemical and neuroimaging studies in subjective cognitive decline: progress and perspectives[J]. CNS Neurosci Ther, 2015, 21(10): 768-775.
[35]Rodda J, Dannhauser T, Cutinha DJ, et al. Subjective cognitive impairment: functional MRI during a divided attention task[J]. Eur Psychiatry, 2011, 26(7): 457-462.
[36]Erk S, Spottke A, Meisen A, et al. Evidence of neuronal compensation during episodic memory in subjective memory impairment[J]. Arch Gen Psychiatry, 2011, 68(8): 845-852.
[37]Hu X, Uhle F, Fliessbach K, et al. Reduced future-oriented decision making in individuals with subjective cognitive decline: A functional MRI study[J]. Alzheimers Dement (Amst), 2017, 6: 222-231.
[38]Scheef L, Spottke A, Daerr M, et al. Glucose metabolism, gray matter structure, and memory decline in subjective memory impairment[J]. Neurology, 2012, 79(13): 1332-1339.
[39]Snitz BE, Lopez OL, McDade E, et al. Amyloid-beta Imaging in Older Adults Presenting to a Memory Clinic with Subjective Cognitive Decline: A Pilot Study[J]. J Alzheimers Dis, 2015, 48(Suppl 1): S151-159.
[40]Perrotin A, La Joie R, de La Sayette V, et al. Subjective cognitive decline in cognitively normal elders from the community or from a memory clinic: Differential affective and imaging correlates[J]. Alzheimers Dement, 2017, 13(5): 550-560.
[41]Teipel SJ, Cavedo E, Weschke S, et al. Cortical amyloid accumulation is associated with alterations of structural integrity in older people with subjective memory complaints[J]. Neurobiol Aging, 2017, 57: 143-152.
[42]Scholl M, Wall A, Thordardottir S, et al. Low PiB PET retention in presence of pathologic CSF biomarkers in Arctic APP mutation carriers[J]. Neurology, 2012, 79(3): 229-236.
[43]Greenwood PM, Parasuraman R. Neuronal and cognitive plasticity: a neurocognitive framework for ameliorating cognitive aging[J]. Front Aging Neurosci, 2010, 2: 150.
[44]Jellinger KA, Attems J. Neuropathological approaches to cerebral aging and neuroplasticity[J]. Dialogues Clin Neurosci, 2013, 15(1): 29-43.
[45]Cespon J, Miniussi C, Pellicciari MC. Interventional programmes to improve cognition during healthy and pathological ageing: Cortical modulations and evidence for brain plasticity[J]. Ageing Res Rev, 2018, 43: 81-98.
[46]Smart CM, Karr JE, Areshenkoff CN, et al. Non-Pharmacologic Interventions for Older Adults with Subjective Cognitive Decline: Systematic Review, Meta-Analysis, and Preliminary Recommendations[J]. Neuropsychol Rev, 2017, 27(3): 245-257.
[47]Clare L, Woods RT. Cognitive training and cognitive rehabilitation for people with early-stage Alzheimer’s disease: A review[J]. Neuropsychol Rehabil, 2004, 14(4): 385-401.
[48]Stern Y. Cognitive reserve[J]. Neuropsychologia, 2009, 47(10): 2015-2028.
[49]Stern Y. Cognitive reserve in ageing and Alzheimer’s disease[J]. Lancet Neurol, 2012, 11(11): 1006-1012.