Mild Cognitive Impairment

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轻度认知障碍研究进展

轻度认知障碍（mild cognitive impairment,MCI）是介于正常衰老与痴呆之间的认知功能缺损状态,以获得性认知功能障碍,但不伴有显著的日常生活能力下降为特征。MCI患者每年约有10％～15％转化为阿尔茨海默病（Alzheimer’s disease,AD）,是AD的高危人群,如果在MCI阶段能给予治疗干预,有可能降低AD发病率。     

Role of hippocampal CA1 atrophy in memory encoding deficits in amnestic Mild Cognitive Impairment

Identifying the specific substrates of memory deficits in early Alzheimer's disease would help to develop clinically-relevant therapies. The present study assesses the relationships between encoding versus retrieval deficits in patients with amnestic Mild Cognitive Impairment (aMCI) and atrophy specifically within the hippocampus and throughout the white matter. Twenty-two aMCI patients underwent T1-weighted MRI scans and neuropsychological testing. Grey matter and white matter segments obtained from the MRI images were each entered in correlation analyses, assessed only in the hippocampus for grey matter segments, with encoding and retrieval memory performances. For the grey matter segments, the resulting spmT correlation maps were then superimposed onto a 3D surface view of the hippocampus to identify the relative involvement of the different subfields, a method already used and validated elsewhere. Memory encoding deficits specifically correlated with CA1 subfield atrophy, while no relationship was found with white matter atrophy. In contrast, retrieval deficits were weakly related to hippocampal atrophy and did not involve a particular subfield, while they strongly correlated with loss of white matter, specifically in medial parietal and frontal areas. In aMCI patients, encoding impairment appears specifically related to atrophy of the CA1 hippocampal subfield, consistent with the predominance of encoding deficits and CA1 atrophy in aMCI. In contrast, episodic retrieval deficits seem to be underlain by more distributed tissue losses, consistent with a disruption of a hippocampo-parieto-frontal network.     

Mild Cognitive Impairment and Mild Dementia: A Clinical Perspective

Mild cognitive impairment and mild dementia are common problems in the elderly. Primary care physicians are the first point of contact for most patients with these disorders and should be familiar with their diagnosis, prognosis, and management. Both mild cognitive impairment and mild dementia are characterized by objective evidence of cognitive impairment. The main distinctions between mild cognitive impairment and mild dementia are that in the latter, more than one cognitive domain is invariably involved and substantial interference with daily life is evident. The diagnosis of mild cognitive impairment and mild dementia is based mainly on the history and cognitive examination. The prognosis for mild cognitive impairment and mild dementia is an important motivation for diagnosis because in both, there is a heightened risk for further cognitive decline. The etiology of mild cognitive impairment and mild dementia can often be established through the clinical examination, although imaging and other laboratory tests may also contribute. Although Alzheimer disease is the most common cause of both, cerebrovascular disease and Lewy body disease make important contributions. Pharmacological treatments are of modest value in mild dementia due to Alzheimer disease, and there are no approved pharmacological treatments for mild cognitive impairment of any etiology. Nonetheless, new-onset cognitive impairment is a worrisome symptom to patients and families that demands answers and advice. If a patient is having difficulties managing medications, finances, or transportation independently, diagnosis and intervention are necessary to ensure the health and safety of the patient.     

Deep Fusion of Brain Structure-Function in Mild Cognitive Impairment

Multimodal fusion of different types of neural image data provides an irreplaceable opportunity to take advantages of complementary cross-modal information that may only partially be contained in single modality. To jointly analyze multimodal data, deep neural networks can be especially useful because many studies have suggested that deep learning strategy is very efficient to reveal complex and non-linear relations buried in the data. However, most deep models, e.g., convolutional neural network and its numerous extensions, can only operate on regular Euclidean data like voxels in 3D MRI. The interrelated and hidden structures that beyond the grid neighbors, such as brain connectivity, may be overlooked. Moreover, how to effectively incorporate neuroscience knowledge into multimodal data fusion with a single deep framework is understudied. In this work, we developed a graph-based deep neural network to simultaneously model brain structure and function in Mild Cognitive Impairment (MCI): the topology of the graph is initialized using structural network (from diffusion MRI) and iteratively updated by incorporating functional information (from functional MRI) to maximize the capability of differentiating MCI patients from elderly normal controls. This resulted in a new connectome by exploring “deep relations” between brain structure and function in MCI patients and we named it as Deep Brain Connectome. Though deep brain connectome is learned individually, it shows consistent patterns of alteration comparing to structural network at group level. With deep brain connectome, our developed deep model can achieve 92.7% classification accuracy on ADNI dataset.     

Evidence-based Evaluation of Cholinesterase Inhibitors for Mild Cognitive Impairment

The purpose of this article is to critically appraise the evidence concerning the use of cholinesterase inhibitors compared to no treatment to prevent the progression from mild cognitive impairment (MCI) to Alzheimer disease. The objective was addressed through the development of a structured, critically appraised topic (CAT). This evidence-based methodology incorporated a clinical scenario, background information, structured question, literature search strategy, results, critical appraisal, commentary, and clinical bottom line.     

轻度认知功能障碍患者的神经心理学特点初步探讨

目的 通过比较遗忘型轻度认知障碍(amnestic mild cognitive impairment,aMCI)和血管性认知障碍非痴呆型(vascular cognitive impairment-no dementia,VCFND)患者及正常老年人群在简易智能精神状态检查量表(mini mental state e...     

脑卒中轻度认知功能障碍的神经心理及神经影像学特点

【目的】探讨脑卒中轻度认知功能障碍（MCI）的神经心理及神经影像学特点。[方法]328例脑卒中患者,符合2005年中国防治认知功能障碍专家提出的标准者193例,从中筛检出31例脑卒中后合并MCl的患者;采用蒙特利尔认知量表对其评估。根据头颅CT或MRI确定病灶部位,并结合临床资料,分析脑卒中MCI的神经心理特点及影像学改变。【结果】193例脑卒中患者,MCI为31例,发生率16．06％。MCI患者临床表现为计算力下降,注意力受损,并以延迟记忆障碍和空间执行能力损害尤为明显,MCI与脑卒中的部位有关系。【结论】脑卒中患者MCI存在较高的发病率,且与病灶部位有一定的关系,脑叶卒中病灶更易引起MCI。     

轻度认知障碍患者的社区职业治疗

目的探讨社区职业治疗对轻度认知损害(MCI)患者的治疗作用。方法对南昌市某社区418例60岁以上老人进行认知筛查,有34例诊断为MCI。将这34例患者按随机数字表法分为2组,治疗组和对照组,每组17例。治疗组在治疗师指导下进行社区职业治疗;对照组则不做任何干预。治疗组每次治疗时间30~40 min,每周进行2次,连续进行6个月。治疗前后分别用简易智能状态检查量表(MMSE)、蒙特利尔认知评估量表(MOCA)和日常生活活动能力量表(ADL)进行认知功能检查和状态评定,评价干预治疗效果。结果 6个月后,治疗组治疗前后MMSE评分差异无统计学意义(P>0.05),但显著高于对照组治疗后(P<0.05),治疗组治疗后MOCA,ADL评分显著优于治疗组治疗前及对照组治疗后(P<0.05或P<0.01);对照组MMSE,MOCA评分显著低于治疗前,而ADL评分高于治疗前(均P<0.01)。结论轻度认知损害患者的认知水平可能随时间的推移而呈下降趋势,社区职业治疗可以延缓老年轻度认知损害的进程。     

脑白质疏松对轻度认知功能损害患者预后的影响

目的:探讨脑白质疏松(LA)对轻度认知功能损害(MCI)患者进展为痴呆的影响。方法:采用国际通用标准从门诊和住院患者中筛选MCI患者。通过MRI和CT扫描,确定这些患者是否存在LA。对MCI患者进行随访,用Kaplan-Meier生存分析法评定LA对MCI进展为痴呆的影响。结果:经临床和神经心理学评估,共有74例MCI患者入组。其中33例(44.6%)经影像学诊断为伴有LA,41例(55.4%)不伴LA。经6～24(13.2±6.8)个月随访,伴LA的患者有15例(45.5%)进展为痴呆,不伴LA的患者有9例(22.0%)进展为痴呆。随访期内伴有LA的MCI患者进展为痴呆的比例显著高于不伴LA的患者(P<0.05)。结论:伴有LA的MCI患者更容易进展为痴呆。这类MCI患者必须及早进行干预,去除可控危险因素,预防痴呆发生。     

老年人生活方式与轻度认知功能障碍相关性研究①

目的分析生活方式相关因素和老年轻度认知功能障碍的关系.方法以在宁波市社区流行病学调查中筛查出的120例患者作为实验组,对照组按照性别、年龄(±2岁)、文化程度作为配对条件,1∶2配比在病患同社区选择健康老年人入组,共入组240例,完成基线调查.结果单因素分析显示,实验组每天抽烟20支以上、每周至少1次家庭活动、退休后继续工作、旅游、积极参与社会活动、规律体育锻炼、休闲活动、棋牌、阅读、使用电脑、饮茶、食用咸菜及腌制品、认知功能训练、食用不饱和脂肪酸油类、食用鱼类及海产品、每天食用蔬菜均和老年痴呆相关(P<0.05).多因素分析证实:积极参与社会活动(OR=0.562,95%CI:0.359~0.723)、棋牌(OR=0.603,95%CI:0.323~0.884)、旅游(OR=0.683,95%CI:0.467~0.912)、退休后继续工作(OR=0.531,95%CI:0..326~0.724)、阅读(>30 min/d)(OR=0.272,95%CI:0.174~0.428)、使用电脑(>30 min/d)(OR=0.536,95%CI:0.427~0.869)、规律体育锻炼(OR=0.437,95%CI:0.316~0.732)、与朋友保持联系(OR=0.583,95%CI:0.385~0.765)、子女看望(OR=0.464,95%CI:0.316~0.745)、食用多不饱和脂肪酸(OR=0.524,95%CI:0.368~0.787)、经常食用鱼及海产品(OR=0.224,95%CI:0.171~0.383)、每天食用蔬菜水果(OR=0.485,95%CI:0.316~0.665)为轻度认知功能障碍的保护因素.结论实行积极、休闲生活方式,规律的体育锻炼,健康合理饮食,避免危险因素,可有效降低轻度认知功能障碍的发病风险.     

影像学技术在轻度认知障碍中的应用

轻度认知障碍是正常老化过程与老年性痴呆之间的一种过渡阶段,它向阿尔茨海默病转化的风险很高.神经影像学在轻度认知障碍的临床评价、早期诊断、预测向阿尔茨海默病转化的风险及检测治疗效果中起着重要的作用.     

虚拟现实技术在轻度认知障碍患者认知康复训练中的应用

目的：探讨虚拟现实认知康复训练对改善轻度认知障碍（MCI）患者认知功能、日常生活能力和睡眠质 量的效果。方法：60例MCI患者随机分为常规组和虚拟组,每组30例。常规组行常规认知训练,虚拟组行虚 拟现实认知康复训练,疗程均为6周。在训练前及训练6周后采用蒙特利尔认知评估量表（MCOA）、简易智 能精神状态量表（MMSE）、日常生活能力量表（ADL）、匹斯堡睡眠质量指数量表（PSQI）和半结构式访谈来 评价2种认知康复训练的临床疗效。结果：康复后,2组的MoCA、MMSE和ADL评分均高于同组康复前,且 虚拟组高于常规组（P＜0.05）;2组的PSQI评分与同组康复前差异无统计学意义（P＞0.05）,且2组间差异无 统计学意义（P＞0.05）。访谈结果显示,虚拟组患者均认为虚拟现实技术能提高其认知功能,并愿意继续虚 拟现实技术下的认知康复训练;常规组部分患者表示训练后认知功能没有明显变化。结论：虚拟现实认知康 复训练改善MCI患者的认知系统功能的疗效优于传统康复方法。     

社区老年人认知障碍与生活方式的相关性研究

目的：探讨社区老年人生活方式与认知障碍的相关性,为预防和控制认知障碍向痴呆的进展提供依据。方法采用一般资料问卷、中文版简易智力状态量表、日常生活自理能力量表和居民膳食营养与健康问卷对随机抽取的西安市815名社区老年人进行轻度认知障碍筛查。采用多元线性逐步回归分析轻度认知障碍的危险因素。结果西安市社区老年人轻度认知障碍的患病率为18.5%。多因素分析发现：无兴趣爱好、无宗教信仰是轻度认知障碍发生的独立危险因素;良好饮食习惯、体育锻炼是防止轻度认知障碍发生的保护因素（P<0.05）。结论日常生活饮食、宗教信仰、兴趣爱好、体育锻炼是影响认知障碍的主要因素,针对导致认知障碍的危险因素早期采取预防干预措施,以防止认知障碍向痴呆演变。     

团体认知干预对社区MCI老人认知功能的影响

目的：探讨团体认知干预对社区轻度认知功能障碍（MCI）老人认知功能的影响。方法：将80例MCI老人随机分为干预组和对照组,干预组进行团体认知干预,每天60min,持续6个月,对照组不作任何干预。用蒙特利尔认知评估量表（MoCA）、简易精神状态量表（MMSE）、日常生活活动能力量表（ADL）评价干预效果。结果：干预后,干预组MoCA、MMSE评分高于干预前及对照组,ADL评分低于干预前及对照组（P〈0.05）;干预后,干预组MoCA量表分项目中记忆力、注意力、视空间执行能力方面的分值高于对照组（P〈0.05）。结论：团体认知干预可以改善社区MCI老人的认知功能状况。     

Rosiglitazone and Cognitive Stability in Older Individuals With Type 2 Diabetes and Mild Cognitive Impairment

OBJECTIVE

Studies have suggested that insulin resistance plays a role in cognitive impairment in individuals with type 2 diabetes. We aimed to determine whether an improvement in insulin resistance could explain cognitive performance variations over 36 weeks in older individuals with mild cognitive impairment (MCI) and type 2 diabetes.

RESEARCH DESIGN AND METHODS

A total of 97 older individuals (mean ± SD age 76 ± 6 years) who had recently (<2 months) started an antidiabetes treatment of metformin (500 mg twice a day) (n = 30) or metformin (500 mg/day)+rosiglitazone (4 mg/day) (n = 32) or diet (n = 35) volunteered. The neuropsychological test battery consisted of the Mini-Mental State Examination (MMSE), Rey Verbal Auditory Learning Test (RAVLT) total recall, and Trail Making Tests (TMT-A and TMT-B) performed at baseline and every 12 weeks for 36 weeks along with clinical testing.

RESULTS

At baseline, no significant differences were found between groups in clinical or neuropsychological parameters. Mean ± SD values in the entire population were as follows: A1C 7.5 ± 0.5%, fasting plasma glucose (FPG) 8.6 ± 1.3 mmol/l, fasting plasma insulin (FPI) 148 ± 74 pmol/l, MMSE 24.9 ± 2.4, TMT-A 61.6 ± 42.0, TMT-B 162.8 ± 78.7, the difference between TMT-B and TMT-A [DIFFBA] 101.2 ± 58.1, and RAVLT 24.3 ± 2.1. At follow-up, ANOVA models tested changes in metabolic control parameters (FPI, FPG, and A1C). Such parameters improved in the metformin and metformin/rosiglitazone groups (P_trend < 0.05 in both groups). ANCOVA repeated models showed that results for the metformin/rosiglitazone group remained stable for all neuropsychological tests, and results for the diet group remained stable for the MMSE and TMT-A and declined for the TMT-B (P_trend = 0.024), executive efficiency (DIFFBA) (P_trend = 0.026), and RAVLT memory test (P_trend = 0.011). Results for the metformin group remained stable for the MMSE and TMTs but declined for the RAVLT (P_trend = 0.011). With use of linear mixed-effects models, the interaction term, FPI × time, correlated with cognitive stability on the RAVLT in the metformin/rosiglitazone group (β = −1.899; P = 0.009).

CONCLUSIONS

Rosiglitazone may protect against cognitive decline in older individuals with type 2 diabetes and MCI.Older individuals with type 2 diabetes have a significantly higher risk of cognitive decline, especially mild cognitive impairment (MCI) and dementia (1–3). The mechanisms explaining the association between type 2 diabetes and cognitive decline are still under investigation. It has been shown that individuals with type 2 diabetes who do not maintain optimal glycemic control (i.e., occurrences of hyperglycemic fluctuations) are more likely to start manifesting deficits in memory and mental processing speed functions (4). Interestingly, a decline in hyperglycemic levels has been associated with an improvement in cognitive function in older individuals with type 2 diabetes (4). Plasma glucose fluctuations are also considered to be responsible for a rise in reactive oxygen species (5), and a pro-oxidative effect of postprandial hyperglycemia may actively contribute to inappropriate regulation of vascular tone, leading to cognitive deficits (6). Alterations in the insulin signaling pathway have also been suggested as possible contributors to cognitive dysfunction, especially memory (7). Insulin receptors are selectively found in the hippocampus, and insulin modulates levels of important neurotransmitters involved in activating cognitive functions (7–9). Insulin resistance has been shown to be an independent determinant of lower cognitive performance in older individuals (10). Furthermore, impaired insulin response during midlife is associated with an increase risk of Alzheimer disease up to 35 years later (11). These findings strongly suggest that abnormal insulin action has deleterious effects on cognition.A decline in insulin resistance may be beneficial to cognition in older individuals with normal glucose tolerance (NGT) and MCI or Alzheimer disease (12). In particular, short-term treatment with rosiglitazone was associated with an improvement in delayed memory and selective attention tests in older individuals with NGT and MCI or early Alzheimer disease (12). However, whether a rosiglitazone-mediated decline in insulin resistance could be advantageous for cognitive function in older individuals with both type 2 diabetes and MCI is unknown. Considering that such individuals have an extremely high risk of cognitive decline, an improvement in insulin resistance may have a protective impact. To test this hypothesis, we performed neuropsychological tests at timely intervals in a group of older individuals with type 2 diabetes in poor metabolic control and MCI who had recently started an add-on antidiabetes agent, either metformin or rosiglitazone, to metformin monotherapy that was inadequate for control. We also included individuals who had recently begun a personalized diet program and had not previously used oral antidiabetes agents.     

一种新型认知训练方法对轻度认知障碍患者 各认知域功能的影响

目的:探讨一种新型认知训练方法对轻度认知障碍患者各认知域功能改善的情况。方法:收集简易智能精神状态检查量表(MMSE)>24分,蒙特利尔认知评估量表(MoCA)≤25分,临床痴呆量表为0.5分的MCI患者102例,随机分为训练组和对照组各51例,2组均给予健康宣教并进行痴呆危险因素的控制,训练组还通过一种新型认知训练方法进行系统性训练3月。在基线期(训练前)、访视期1(训练3月后)、访视期2(训练6月后),用MoCA和MoCA认知域指数得分(CDIS)进行评价。结果:训练组不同时间点的MoCA、MoCA MIS、MoCA EIS、MoCA VIS、MoCA LIS和MoCA AIS等量表评分差异均有统计学意义(P<0.05);对照组患者不同时间点的MoCA量表评分差异有统计学意义(P<0.05);训练组的MoCA、MoCA VIS、MoCA LIS和MoCA AIS等量表评分在访视期1和基线期相比差异均有统计学意义(P<0.05);训练组的MoCA、MoCA EIS、MoCA VIS、MoCA LIS和MoCA AIS等量表评分在访视期2与基线期相比差异均有统计...     

认知功能状况自评量表在社区轻度认知障碍患者中应用的信效度研究

目的 修订健康状况认知评价量表,并检验修订所得的认知功能状况自评量表在社区轻度认知障碍患者中应用的信效度.方法 本研究对美国学者Kessler编制的健康状况认知评价量表内容进行修订,形成认知功能状况自评量表,请6名相关领域专家进行调适和内容效度评价后形成终稿.于北京2家社区卫生服务中心筛查出188例轻度认知障碍患者,请其完成目标量表、老年抑郁量表的填写,其中25例患者在初次调查后的2～6周完成目标量表的重测.结果 认知功能状况自评量表的专家内容效度指数>0.833,量表水平内容效度指数/全体一致为0.870,量表水平内容效度指数/平均为0.982;对量表初级评价部分进行信效度检验,条目-总分相关系数均大于0.351(P<0.001);探索性因子分析该量表可提取4个因子,累计方差贡献率为56.375％;量表中威胁(r=0.375)、伤害/失去(r=0.454)2个维度的总分与老年抑郁量表总分呈正相关;Cronbachα系数为0.513～0.868;该量表总的重测信度为0.847,各维度为0.440～0.652.结论 认知功能状况自评量表在社区轻度认知障碍患者中应用的信效度可接受,可用于了解社区轻度认知障碍患者对认知功能改变影响和意义的主观评价.     

轻度认知损伤患者海马杏仁核体积的MRI测量及临床随访研究

目的 探讨轻度认知损伤（MCI）患者海马,杏仁核萎缩在Alzheimer病（AD）发病中的作用,方法 MCI组11例,AD组15例,正常老年人14例,GE 1．5T MR机,3D－FSPGR序列采样,冠状位,层厚1．3mm,层数60,计算机三维重建并进行杏仁核海马体积测量,经标准化校正后进行比较,随访MCI患者进展为AD的情况,结果 AD组海马杏仁核体积萎缩25％（P＜0．05）,MCI组萎缩5－13％（P＞0．05）,27．3％的MCI患者经1年随访进展为AD。结论 伴海马 杏仁核萎缩的MCI患者更易于进展为AD。     

脑白质疏松轻度认知功能障碍静息态默认网络研究

目的通过静息态功能磁共振成像(rs-fMRI)技术对脑白质疏松(LA)轻度认知障碍(MCI)患者脑默认网络进行分析。方法LA 患者31 例,临床痴呆评分(CDR) 0.5;年龄、性别和受教育程度匹配的正常对照组27 人,CDR 为0。对入组人群进行rs-fMRI 数据采集。使用SPM5 软件进行分析处理,使用fMRI 工具盒对预处理后的数据进行独立成分分析(ICA),组间差异进行双样本t 检验。结果静息状态下,对照组默认网络包括扣带回后部/楔前叶,双侧额叶内侧,双侧颞中回,双侧顶下回、角回,双侧海马。MCI组默认网络激活区域同对照组一致;同对照组相比,MCI患者扣带回前部/左侧额叶内侧、右侧海马旁回/钩回、右侧颞下回、左侧额叶深部白质/尾状核头部激活减低,左侧尾状核/扣带回前部、左侧额叶、左侧颞上回/顶下回的激活升高。结论LA患者静息状态默认网络活动异常,可能与认知障碍的发生有关。