背景 老龄化社会背景下，老年痴呆患病数量逐年增加，且共病状态越发常见，但目前湖南省关于老年痴呆的广泛调查不足，疾病之间的共病关系尚不明确。 目的 全面了解湖南省≥65岁居民老年痴呆患病情况并分析其与常见11种慢性病的共病关系。 方法 于2021年4—5月，采用分层多阶段抽样方法，在湖南省30个区（县）、60个街道（乡镇）、180个居（村）委会随机调查≥65岁居民。以痴呆社区筛查量表（CSI-D）或8条目痴呆筛查问卷（AD8）为筛查工具，神经内科或精神科医生结合简易精神状态检查量表（MMSE）和蒙特利尔认知评估量表（MoCA）诊断痴呆。同时调查居民高血压、脑血管病、缺血性心脏病、类风湿关节炎、椎间盘疾病、糖尿病、胃肠炎、慢性阻塞性肺疾病、胆结石胆囊炎、消化性溃疡、癌症的患病情况。 结果 本次共抽样5 979人，共5 616人完成调查，785例（13.98%）检出痴呆。不同地区、性别、年龄、吸烟史及有无慢性病者老年痴呆患病率比较，差异均有统计学意义（P<0.05）。共收集到5 606份慢性病患病情况数据，排名前五位的疾病分别是高血压〔2 205（39.33%）〕、椎间盘疾病〔553（9.86%）〕、糖尿病〔526（9.38%）〕、脑血管病〔492（8.78%）〕、缺血性心脏病〔467（8.33%）〕。老年痴呆群体中排名前五位的疾病分别是高血压〔325（41.40%）〕、脑血管病〔111（14.14%）〕、缺血性心脏病〔91（11.59%）〕、类风湿关节炎〔89（11.33%）〕、椎间盘疾病〔81（10.31%）〕。0、1、2、≥3种不同慢性病患病数量群体的老年痴呆患病率依次为11.46%（214/1 867）、13.66%（309/2 262）、17.50%（176/1 006）、18.26%（86/471）。有无胃肠炎、类风湿关节炎、脑血管病、慢性阻塞性肺疾病、缺血性心脏病者老年痴呆患病率比较，差异均有统计学意义（P<0.05）。二元Logistic回归分析结果显示，居住在农村〔OR=2.048，95%CI（1.655，2.536）〕、女性〔OR=1.388，95%CI（1.163，1.655）〕、年龄增大〔OR=1.348，95%CI（1.270，1.431）〕、患有慢性病〔OR=1.195，95%CI（1.101，1.297）〕是≥65岁居民发生老年痴呆的危险因素（P<0.05）。老年痴呆患者按时服药情况：12.79%（99/774）表示有困难、6.59%（51/774）需要帮助、2.97%（23/774）根本无法独立完成。 结论 湖南省≥65岁居民老年痴呆患病率随慢性病患病数量增加而增加，且与多种疾病相关。共病背景下老年痴呆患者的自理能力及家庭照护负担应引起全社会的重视。此次大调查基本掌握了湖南省老年痴呆的患病情况及与慢性病共病情况，旨在为制订疾病防治相关政策提供客观依据。

目的：分析广州市痴呆共病患者直接经济负担及其影响因素，为痴呆共病患者的经济成本测算与家庭照护负担评估提供参考依据。方法：采用自编问卷，收集广州市痴呆共病患者社会人口学特征、治疗情况、疾病直接经济负担等情况；使用Charlson 查尔森合并症指数（charlson comorbidity index, CCI）评估共病负担；使用直接法估算直接经济负担费用，经正态性检验服从偏态分布，对数转换使其呈近似正态化后应用于多元线性回归模型。结果：广州市痴呆共病患者过去1年产生的人均直接经济负担费用为7180.00（3600.00，15 568.67）元，其中人均直接医疗费用为6150.00（3185.00，12 590.00）元，人均直接非医疗费用为0.00（0.00，2082.50）；CCI共病负担指数为5.00（5.00，6.00），共病负担与直接经济负担均较重。多元线性回归结果显示疾病直接经济负担的主要影响因素为患者所在区域、就诊地点、合并慢性阻塞性肺疾病（chronic obstructive pulmonary disease, COPD）或老年慢性支气管炎、合并心脏病及服用痴呆药物种类。结论：广州市痴呆共病患者直接经济负担较重，影响因素具有多维度与复杂性的特征，需要政府、社会和医疗机构等多方面共同努力与探索。

老年人痴呆或认知障碍多由一种以上年龄相关的常见脑部疾病所致。阿尔茨海默病（Alzheimer's disease, AD）是其中最常见的神经变性疾病，且是全球前10位死因中唯一无法治愈或缺乏长期对症疗效的疾病，给个人、家庭和全球经济都带来了巨大的负担。早期及时发现和干预是对抗AD的最佳策略。在过去的 30 年中，许多研究都提出了降低痴呆风险的方法，2020年《柳叶刀》杂志的痴呆预防报告已阐明通过应对风险因素可以预防或延缓超过40%的痴呆。然而，目前全球医疗体系尚未具备早期或及时发现AD的足够能力。最近的一项研究发现，只有不到 10%的轻度认知障碍（mild cognitive impairment, MCI）是在初级医疗机构中诊断出来的。近来，抗淀粉样蛋白β（Amyloid beta，Aβ）抗体药物lecanemab和donanemab被批准上市用于早期AD治疗，以及30年的随访研究证明改善风险因素显著减少AD痴呆的发病率并延长了寿命，使得人们对AD早期识别的关注迅速增加。阿尔茨海默病防治协会（China Association for Alzheimer's Disease，CAAD）认识到居家早期和及时发现 AD 的重要性，并成立了一个由协会成员、临床医生和研究人员组成的全球 AD 多领域专家团队，就以下目标达成共识： ①为个人、家庭、社区、协会和组织提供专家指导意见；②介绍用于认知障碍和痴呆居家筛查的数字工具和可用资源，并为AD高危人群或疑似患者制定下一步应对策略；③讨论现有可用或将来可能的居家筛查适宜AD生物标志物；④为未来的改进和全球应用建立可行性框架。专家组对于当前可用的证据、工具和资源进行综述，并进一步考量其在AD 居家筛查中的价值。

The cognitive impairment patterns and the association with Alzheimer's disease (AD) in mental disorders remain poorly understood.We analyzed data from 486,297 UK Biobank participants, categorizing them by mental disorder history to identify the risk of AD and the cognitive impairment characteristics. Causation was further assessed using Mendelian randomization (MR).AD risk was higher in individuals with bipolar disorder (BD; hazard ratio [HR] = 2.37, P < 0.01) and major depressive disorder (MDD; HR = 1.63, P < 0.001). MR confirmed a causal link between BD and AD (OR= 1.098), as well as obsessive-compulsive disorder (OCD) and AD (OR= 1.050). Cognitive impairments varied, with BD and schizophrenia showing widespread deficits, and OCD affecting complex task performance.Observational study and MR provide consistent evidence that mental disorders are independent risk factors for AD. Mental disorders exhibit distinct cognitive impairment prior to dementia, indicating the potential different mechanisms in AD pathogenesis. Early detection of these impairments in mental disorders is crucial for AD prevention.This is the most comprehensive study that investigates the risk and causal relationships between a history of mental disorders and the development of Alzheimer's disease (AD), alongside exploring the cognitive impairment characteristics associated with different mental disorders. Individuals with bipolar disorder (BD) exhibited the highest risk of developing AD (hazard ratio [HR] = 2.37, P < 0.01), followed by those with major depressive disorder (MDD; HR = 1.63, P < 0.001). Individuals with schizophrenia (SCZ) showed a borderline higher risk of AD (HR = 2.36, P = 0.056). Two-sample Mendelian randomization (MR) confirmed a causal association between BD and AD (OR= 1.098, P < 0.05), as well as AD family history (proxy-AD, OR= 1.098, P < 0.001), and kept significant after false discovery rate correction. MR also identified a nominal significant causal relationship between the obsessive-compulsive disorder (OCD) spectrum and AD (OR= 1.050, P < 0.05). Individuals with SCZ, BD, and MDD exhibited impairments in multiple cognitive domains with distinct patterns, whereas those with OCD showed only slight declines in complex tasks.© 2024 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.

阿尔茨海默病是一种病因复杂的严重智力致残疾病，目前尚无有效的治疗方法。我国是世界上老年人口最多、增长最快的国家之一,也是阿尔茨海默病发病率较高的国家。因此，如何早期预防阿尔茨海默病的发生，是现今健康领域最重要的课题之一。我们在国内外相关研究的基础上，通过文献循证、干预研究实践、案例分析、经验总结和专家咨询，结合中国老年健康和社会文化特点，体现中国传统医学、武术、养生以及社区组织优势，制订出具有中国特色的阿尔茨海默病早期预防指南，涵盖了个人、家庭和社会三个层面的预防策略，从积极生活态度、社会活动参与、认知训练、体育锻炼、戒烟限酒、营养、睡眠，血压、血糖、血脂管理，体重和其他慢病管理以及中医开展针对阿尔茨海默病的一级预防。本指南仅供个人、家庭和社会开展阿尔茨海默病预防时参考。

Subjective Cognitive Decline (SCD) in older adults has been identified as a risk factor for dementia, although the literature is inconsistent, and it is unclear which factors moderate progression from SCD to dementia. Through separate meta-analyses, we aimed to determine if SCD increased the risk of developing dementia or mild cognitive impairment (MCI). Furthermore, we examined several possible moderators. Longitudinal studies of participants with SCD at baseline, with data regarding incident dementia or MCI, were extracted from MEDLINE and PsycINFO. Articles were excluded if SCD occurred solely in the context of dementia, MCI, or as part of a specific disease. Pooled estimates were calculated using a random-effects model, with moderator analyses examining whether risk varied according to SCD definition, demographics, genetics, recruitment source, and follow-up duration. Risk of study bias was assessed using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS)-2 tool. 46 studies with more than 74,000 unique participants were included. SCD was associated with increased risk of developing dementia (HR = 1.90, 95% CI 1.52-2.36; OR = 2.48, 95% CI 1.97-3.14) and MCI (HR = 1.73, 95% CI 1.18-2.52; OR = 1.83, 95% CI 1.56-2.16). None of the potential moderating factors examined influenced the HR or OR of developing dementia. In contrast, including worry in the definition of SCD, younger age, and recruitment source impacted the OR of developing MCI, with clinic samples demonstrating highest risk. SCD thus represents an at-risk phase, ideal for early intervention, with further research required to identify effective interventions for risk reduction, and cognitive-behavioural interventions for cognitive management. PROSPERO, protocol number: CRD42016037993.© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

背景 主观认知下降（SCD）是阿尔茨海默病（AD）早期预防的目标阶段，AD与慢性病共病关系密切，但二者间相关性尚不十分明确。 目的 探究老年人SCD与慢性病共病的相关性，为AD早期预防和干预提供理论依据。 方法 于2021年1月至2022年6月，在广州市城市生活小区和养老机构以便利抽样法抽取≥60岁的老年人612例。采用基础版蒙特利尔认知评估量表（MoCA-B）、临床痴呆量表（CDR）、Hachinski缺血指数量表（HIS）评定客观认知功能水平，通过SCD标准诊断框架和SCD问卷（SCD-Q9）进行分组，将整体客观认知水平无异常、符合SCD标准诊断框架和SCD-Q9≥5分的老年人分入SCD组，将整体客观认知功能无异常和SCD-Q9&lt;5分的老年人为认知无异常（CN）组。采用一般资料问卷收集老年人的社会人口学（性别、年龄、居住地、受教育年限、婚姻状况、退休前职业类型、月收入）和健康相关资料〔体质指数、腰围、吸烟习惯、饮酒习惯、饮茶习惯、锻炼频率、午觉习惯及平均时长、睡眠质量、抑郁及焦虑症状、日常生活活动能力（ADL）〕，其中睡眠质量、抑郁症状、焦虑症状及ADL分别采用匹兹堡睡眠指数量表（PSQI）、病人健康问卷抑郁自评量表（PHQ-9）、广泛性焦虑障碍量表（GAD-7）、ADL量表评估；收集老年人的慢性病史，按照疾病种数分为无慢性病共病水平（0~1种疾病）、低慢性病共病水平（2~4种疾病）和高慢性病共病水平（≥5种疾病）。采用二元Logistic回归探讨老年人慢性病共病对SCD的影响。 结果 本次调查的612例老年人中，SCD-Q9平均得分为（4.20±1.95）分，SCD组者250例（40.8%），CN组者362例（59.2%）。SCD组和CN组的性别、年龄、受教育年限、退休前职业类型、月收入、饮茶习惯、睡眠质量、抑郁症状、焦虑症状及ADL得分比较，差异有统计学意义（P&lt;0.05）。本次调查中患有慢性病者574例（93.8%），存在慢性病共病者475例（77.6%）；低慢性病共病水平者352例（57.5%），高慢性病共病水平者123例（20.1%）。SCD组和CN组共病情况的比较中，慢性病共病状态、慢性病共病水平及糖尿病、关节炎、骨质疏松的检出率比较，差异均有统计学意义（P&lt;0.05）。二元Logistic回归分析显示：年龄增长、睡眠质量差、有焦虑症状、ADL差、高慢性病共病水平为SCD的危险因素（P&lt;0.05），其中，高慢性病共病水平的SCD发生风险是无慢性病共病水平的1.826〔95%CI为（1.037，3.216）〕倍；受教育年限长为SCD的保护因素（P&lt;0.05）。 结论 高慢性病共病水平与SCD相关，是导致SCD的危险因素。社区和养老机构医护人员可将慢性病共病纳为认知功能下降的评估指标，协同实施慢性病共病及相关因素的管理，积极识别和干预SCD，以延缓老年人AD发生发展，推进健康老龄化。

轻度认知功能障碍（MCI）是介于正常衰老和痴呆之间的一种过渡状态，MCI作为痴呆的前驱阶段，进展为痴呆的风险是正常中老年人的10倍。本文通过对国内外MCI与抑郁、焦虑症状相关性的研究进展进行综述，发现MCI患者的抑郁、焦虑症状检出率高，抑郁、焦虑症状可促使MCI向痴呆转化。因此，重视MCI患者的抑郁、焦虑症状的评估及早期干预，对于防止MCI恶化、预防痴呆具有非常重要的意义。

轻度认知障碍（ mild cognitive impairment,MCI）是一种介于正常衰老与痴呆的认知障碍综合征［1］，其认知功能可进一步加重变为痴呆，也可保持稳定或者恢复正常，即使一些MCI 患者认知功能能够恢复正常，但和其他健康老年人相比，MCI进展为痴呆的风险仍然增高。MCI 患病率随年龄增高呈递增趋势，其发病率可从60岁的6.7%上升到80岁的25.2%［2］。鉴于痴呆治疗方法的局限性，对MCI的早期识别和干预最有重要的意义。一项研究显示，如果能将阿尔茨海默病（Alzheimer disease,AD）的发病延迟5 y，将可使AD的患者数目减少57%，将医疗费用从6270亿美元减少到3440亿美元，而AD的最佳干预窗口期就是患者出现轻度认知功能损害时［3］。尽管目前关于MCI和睡眠结构的研究较多，也有研究发现MCI患者在夜间总的睡眠时间存在不同程度的减少，睡眠结构也有不同程度的紊乱，睡眠效率和睡眠质量相比正常老年人也有所下降［4］。但针对MCI睡眠结构的研究样本量少且结果并不一致。因此，本研究拟通过Meta分析探讨MCI患者睡眠结构的变化，旨在为MCI患者的早期识别和管理提供循证依据。

阿尔茨海默病(Alzheimer's disease, AD)和骨质疏松症(osteoporosis, OP)是老年人群中最常见的退行性疾病。AD和OP表面上看是两种截然不同的疾病,但越来越多的研究表明两者存在一些共有的致病因素、发病机制和信号通路。一些体内外的研究支持了这一观点。AD患者脑内淀粉样蛋白过多,病变可延伸至外周器官,引起骨骼淀粉样沉积,这将增强核因子NF-&#x003ba;B受体活化体配体信号,导致破骨细胞活性增强。OP患者可能缺乏维生素D或维生素D结合蛋白水平较低,维生素D结合蛋白可以防止淀粉样蛋白聚集,从而将维生素D缺乏与AD和OP联系起来。Wnt信号拮抗剂DKK1可能是连接AD和OP的一个共同风险分子。

Both Alzheimer's disease and osteoporosis occur mainly in persons aged over 60. Both diseases are often seen to co-occur in clinical practice, yet very few investigators have addressed this problem. They have demonstrated that several different clinical factors can lead to a higher incidence of osteoporosis in persons with Alzheimer's disease. Serum concentrations of vitamins D and K, calcium and PTH; the duration of sunlight exposure; dietary calcium intake; genetic factors as well as the effect of oestrogens on mineral bone density in patients with and without dementia have been studied. Furthermore, the effects of vitamin D and calcium preparations with or without bisphosphonates (risedronate) have also been assessed. The authors concertedly emphasise that the treatment of patients with dementia needs to include the prophylaxis of osteoporosis, falls and fractures.

Longitudinal clinical-pathological studies have increasingly recognized the importance of mixed pathologies (the coexistence of one or more neurodegenerative and cerebrovascular disease pathologies) as important factors in the development of Alzheimer's disease (AD) and other forms of dementia. Older persons with AD pathology, often have concomitant cerebrovascular disease pathologies (macroinfarcts, microinfarcts, atherosclerosis, arteriolosclerosis, cerebral amyloid angiopathy) as well as other concomitant neurodegenerative disease pathologies (Lewy bodies, TDP-43, hippocampal sclerosis). These additional pathologies lower the threshold for clinical diagnosis of AD. Many of these findings from pathologic studies, especially for CVD, have been confirmed using sophisticated neuroimaging technologies. In vivo biomarker studies are necessary to provide an understanding of specific pathologic contributions and time course relationships along the spectrum of accumulating pathologies. In this review, we provide a clinical-pathological perspective on the role of multiple brain pathologies in dementia followed by a review of the available clinical and biomarker data on some of the mixed pathologies.

Delirium and dementia are two of the most common causes of cognitive impairment in older populations, yet their interrelation remains poorly understood. Previous studies have shown that dementia is the leading risk factor for delirium and that delirium is an independent risk factor for subsequent development of dementia. However, a major area of controversy is whether delirium is simply a marker of vulnerability to dementia, whether the effect of delirium is solely related to its precipitating factors, or whether delirium itself can cause permanent neuronal damage and lead to dementia. Ultimately, all of these hypotheses are likely to be true. Emerging evidence from epidemiological, clinicopathological, neuroimaging, biomarker, and experimental studies lends support to a strong relation between delirium and dementia, and to both shared and distinct pathological mechanisms. New preventive and therapeutic approaches that target delirium might offer a sought-after opportunity for early intervention, preservation of cognitive reserve, and prevention of irreversible cognitive decline in ageing. Copyright © 2015 Elsevier Ltd. All rights reserved.

Behavioral and psychological symptoms of dementia (BPSD) are common in the clinical manifestation of dementia. Although most patients with dementia exhibit some BPSD during the course of the illness, the association of BPSD with the stage of dementia remains unclear. It was the aim of this study to evaluate the impact of severity of dementia on the expression of BPSD in patients with dementia with Lewy bodies (DLB) and Alzheimer's disease (AD).Ninety-seven patients with DLB and 393 patients with AD were recruited from 8 dementia clinics across Japan. BPSD were assessed by the Neuropsychiatric Inventory (NPI). A relationship between BPSD and dementia stage classified by the Clinical Dementia Rating (CDR) in each type of dementia was assessed.No significant difference was seen in NPI total score across CDR staging in the DLB group. On the other hand, the NPI total score significantly increased with dementia stage in the AD group.The relationship of dementia stage with the expression of BPSD was different according to the type of dementia. BPSD and dementia stage were correlated in AD subjects, in whom psychiatric symptoms increase as the disease progresses, but not in DLB subjects.

The history of Alzheimer's disease (AD) started in 1907, but we needed to wait until the end of the century to identify the components of pathological hallmarks and genetic subtypes and to formulate the first pathogenic hypothesis. Thanks to biomarkers and new technologies, the concept of AD then rapidly changed from a static view of an amnestic dementia of the presenium to a biological entity that could be clinically manifested as normal cognition or dementia of different types. What is clearly emerging from studies is that AD is heterogeneous in each aspect, such as amyloid composition, tau distribution, relation between amyloid and tau, clinical symptoms, and genetic background, and thus it is probably impossible to explain AD with a single pathological process. The scientific approach to AD suffers from chronological mismatches between clinical, pathological, and technological data, causing difficulty in conceiving diagnostic gold standards and in creating models for drug discovery and screening. A recent mathematical computer-based approach offers the opportunity to study AD in real life and to provide a new point of view and the final missing pieces of the AD puzzle.