Core Insights - The establishment of the first comprehensive dementia prevention and care center in Jinan, which integrates prevention, screening, rehabilitation, and care services [2][3][4] - The center has quickly reached full capacity, indicating a high demand for specialized dementia care services [3][4] - The center employs a multidisciplinary team to provide personalized care plans and incorporates advanced cognitive rehabilitation techniques [3][4] Group 1: Center Features - The dementia care center includes various sensory and cognitive stimulation areas, such as a multi-sensory room and cognitive activity room, designed to aid memory and recognition [3] - Unique interventions like the "doll therapy" have been developed to alleviate behavioral issues in dementia patients [4] - The center has been recognized as a designated institution for promoting dementia care in Jinan, participating in community health screenings [5] Group 2: Community Impact - The aging population is leading to increased cases of dementia, creating significant challenges for families [5] - A dedicated expert advisory group has been formed to guide dementia care initiatives across the city, focusing on knowledge dissemination and community rehabilitation [5] - The center's efforts align with the 2025 municipal project aimed at enhancing care services for elderly individuals with dementia [5]

Core Viewpoint - The article highlights the significant contributions of Professor Danyang in the field of sleep research and her recent affiliation with Shenzhen Medical Academy, where she will establish a Sleep and Consciousness Laboratory [1][4]. Group 1: Professor Danyang's Background - Professor Danyang graduated from Peking University with a degree in Physics and later pursued a PhD in Biology at Columbia University, followed by postdoctoral research at Rockefeller University and Harvard Medical School [4]. - She has been a faculty member at the University of California, Berkeley since 1997, focusing on the neural circuits that control sleep and the functions of the prefrontal cortex [4][21]. Group 2: Recent Research Contributions - On December 8, 2023, Professor Danyang's team published a study in Cell, revealing that frontal cortical ignition, related to consciousness awareness, is strongly suppressed during NREM sleep in mice due to cholinergic modulation [7][10]. - On January 18, 2024, a study published in Nature Neuroscience demonstrated that microglia can promote sleep through calcium-dependent modulation of norepinephrine transmission, suggesting a protective role for microglia in brain health [12][13]. - On January 17, 2025, a study in Science Advances explored how activation of locus coeruleus noradrenergic neurons rapidly increases homeostatic sleep pressure, indicating a mechanism for sleep regulation [15][17]. Group 3: Implications for Sleep Research - The findings from Professor Danyang's research suggest that understanding the mechanisms of sleep regulation could have implications for addressing sleep disruptions associated with neurodegenerative diseases like Alzheimer's [13]. - The research emphasizes the importance of microglial function in maintaining sleep and brain homeostasis, potentially offering insights into therapeutic strategies for sleep-related disorders [13]. - The studies collectively indicate that the functional fatigue of locus coeruleus neurons may lead to increased sleep pressure, providing a new perspective on the relationship between wakefulness and sleep [17].

编译丨王聪 编辑丨王多鱼 排版丨水成文 人们越来越认识到睡眠作为大脑健康的重要生理过程所具有的重要意义。在人的整个生命周期中，睡眠时长和模式的紊乱现象屡见不鲜，无论是在正常衰老还是 病理性衰老中都存在这种情况。 这些睡眠紊乱会增加认知缺陷和阿尔茨海默病的风险。全球脑健康理事会建议成年人每晚睡 7-8 小时以保持大脑健康。多项研究表明，相对于建议的睡眠时长， 睡眠过多或过少都与认知相关能力受损有关，包括记忆力、注意力以及管理、引导其他心理过程的能力 （例如规划、解决问题和控制冲动) 。 然而，这些研究证据因所考察的寿命阶段以及诸如抑郁等健康差异而存在不一致之处。抑郁是认知能力下降的一个可改变的风险因素，它常常与睡眠障碍同时出 现。睡眠障碍与抑郁之间的关联已得到充分证实，约 90% 的抑郁症患者都报告存在睡眠问题。 近日 ， 德克萨斯大学圣安东尼奥健康科学中心的研究人员在 Alzheimer's & Dementia: The Journal of the Alzheimer's Association 期刊发表了题为： Long sleep duration, cognitive performance, an ...

Core Viewpoint - The article discusses the potential neuroprotective effects of GLP-1 receptor agonists (GLP-1RAs) like semaglutide and tirzepatide in reducing the risk of Alzheimer's disease (AD) in patients with type 2 diabetes, highlighting a recent study that elucidates the underlying molecular mechanisms [2][3][8]. Group 1: Research Findings - GLP-1RAs activate the AMPK signaling pathway, significantly reducing core pathological features of Alzheimer's disease and effectively improving cognitive dysfunction [3][5]. - In Alzheimer's disease model mice, plasma GLP-1 levels were found to be decreased, and in AD patients, GLP-1 levels were negatively correlated with β-amyloid (Aβ) burden [6]. - The study demonstrated that enhancing GLP-1 signaling through GLP-1RAs (using exenatide or tirzepatide) increases CaMKK2-AMPK signaling, thereby reducing the generation of Aβ through the inhibition of β-secretase 1 (BACE1) [6][8]. Group 2: Implications for Treatment - The findings provide critical experimental evidence for the clinical application of GLP-1RAs in the prevention and treatment of Alzheimer's disease, potentially leading to expanded clinical trials and indications [8].

Core Viewpoint - The research highlights the critical role of TMEM119 in maintaining microglial homeostasis and regulating the progression of Alzheimer's disease (AD), suggesting innovative therapeutic strategies targeting this pathway [2][3][4]. Group 1: Research Findings - The study published in the journal Immunity elucidates the mechanism by which TMEM119 interacts with amyloid-β (Aβ) to promote its clearance in a mouse model of AD [2][3]. - TMEM119 expression decreases with Aβ deposition, correlating positively with the progression of AD in mice, and its absence accelerates the transition of microglia to a disease-associated state [4][5]. - Overexpression of TMEM119 enhances microglial phagocytic activity, and two small molecules, Kartogenin and SRI-011381, can improve cognitive function in mid-stage AD mice by enhancing TMEM119 expression [4][5]. Group 2: Comparison with Other Receptors - The study compares TMEM119 with another important Aβ receptor, TREM2, noting that TREM2 deficiency blocks the transition of microglia from homeostasis to a disease-associated state, while TMEM119 deficiency leads to a loss of homeostasis and accelerates the transition to an earlier disease-associated state [4][5]. Group 3: Implications for Treatment - The research indicates that restoring microglial homeostasis through TMEM119 presents a promising therapeutic avenue for AD, with significant clinical translation potential despite the need for further optimization of the candidate compounds [5].

阿尔茨海默病主要表现除了典型的认知能力以及记忆力下降之外，还表现为非典型的语言和视空间障 碍，并可伴有精神症状。 近日，一名87岁的老人不慎跌入黄浦江后获救。据民警称，老人患有阿尔茨海默病，在被救起后，身上 多处骨折，老人已记不起自己是在哪里失足跌落以及如何跌落的过程。 这一事件引发了社会对阿尔茨海默病患者如何照护的关注。阿尔茨海默病是一种神经退行性疾病，早期 症状隐匿，诊断不足的情况严重，患者就医时往往病程已处于中重度阶段，无特效药可用。 相关数据显示，在60岁以上老年人中，阿尔茨海默痴呆的发病率在5%以上，而85岁以上老年人中，阿 尔茨海默痴呆的发病率更是高达30%。阿尔茨海默病的主要表现除了典型的认知能力以及记忆力下降之 外，还有非典型的语言和视空间障碍，并可伴有精神症状。 此外，目前已经在国内获批的两款阿尔茨海默特效药，也仅针对延缓早期阿尔茨海默疾病进展显示出效 果，尚无法满足中国大量阿尔茨海默病患者的临床需求。 在这一背景下，专家呼吁一方面亟需开发更多我国自主研发的阿尔茨海默病新靶点和新疗法；另一方 面，也需要提升痴呆症的早诊、早筛，加强疾病预防阶段的技术投入。 "阿尔茨海默新靶点的发现离不开对基础 ...

据悉，上海交通大学医学院附属精神卫生中心肖世富/岳玲教授团队联合上海科技大学沈定刚/潘永生教 授团队获得的研究成果在知名期刊《阿尔茨海默病预防杂志》(Journal of Prevention of Alzheimer's Disease)上刊登。据悉，轻度认知损害(Mild Cognitive Impairment, MCI)被视为阿尔茨海默病等认知障碍 的前期风险状态。这项研究对认知障碍的早期预测工作显得尤为关键：不仅有助于识别潜在患者，还能 为及时实施有效治疗提供可能，从而延缓疾病进展，改善患者预后。 来源：中国新闻网 中新网上海5月7日电 (记者 陈静) 当下，随着疾病修饰治疗药物(如仑卡奈单抗、多奈单抗)的获批并投 入临床使用，轻度认知损害(MCI)和轻度痴呆阶段成为阿尔茨海默病患者干预的黄金窗口期。记者7日 获悉，中国医学专家获得最新研究成果：成功构建 MCI预测模型，为认知障碍的早期识别提供新方 法。 据介绍，该模型基于结构磁共振图像(MRI)数据，建立了一套深度学习训练框架；通过基于多个感兴趣 区域的网络(MRNet)筛选并整合包括海马体、杏仁核、小脑等10个高区分度脑区特征，并进一步构建了 ...

PHGDH是一种参与丝氨酸合成的代谢酶，过去的研究发现，PHGDH在神经胶质细胞（如星形胶质细胞）中高表达，其代谢产物D-丝氨酸对 于神经传递至关重要。不过，近年来的队列研究逐渐揭开了PHGDH的另一面——PHGDH及其RNA表达水平在晚发型AD患者的血液和脑组织 中显著升高，并与疾病严重程度正相关。这一现象提示，PHGDH还可能通过未知的机制直接参与AD的病理进程。 作为最常见的痴呆症形式，阿尔茨海默病（AD）占所有痴呆病例的60%~70%，会给患者带来认知功能衰退、记忆丧失和行为改变等多种症 状。AD典型的病理特征包括β-淀粉样蛋白（Aβ）沉积形成的斑块，以及过度磷酸化的Tau蛋白形成的神经纤维缠结。随着人类寿命增长以及 人口老龄化，AD的发病率不断上升，已成为影响老年人生活质量的重大健康挑战。 在AD中，早发型AD主要与致病基因突变相关，具有家族遗传倾向；相比之下，多发生于65岁以后的晚发型AD有着截然不同的致病机制—— 他们通常并未携带家族性和原发性AD致病突变，并且只有不到半数的患者携带APOE4或TREM2风险等位基因。因此，晚发型AD往往缺乏明 确的遗传生物标记物。为了实现晚发型AD的早期诊断， ...

在致病机制未明确的背景下，大量新药研发在中途折戟。据美国药物生产与研发协会数据，全球累计在阿尔茨海默病上的研发投入超过6000亿美元，失败的 临床药物超过300种，失败率高达99.6%。近年来，随着两款单抗新药前后上市，阿尔茨海默病的主流假说淀粉样蛋白（Aβ）级联瀑布假说得到进一步印 证。今年3月，礼来旗下的多奈单抗在国内商业化上市。 近日，四川大学华西医院神经内科副主任、教授商慧芳在接受《每日经济新闻》记者专访时表示，这些清除淀粉样蛋白斑块新药的上市意味着阿尔茨海默病 从对症治疗进入了疾病修饰治疗的新阶段。随着更多阿尔茨海默病新药成功上市，未来针对阿尔茨海默病的治疗可能是非单一靶点的治疗，而是采用针对多 靶点的鸡尾酒疗法，以实现更好的治疗获益。 早期阿尔茨海默病治疗迎来药物突破，实现疾病修饰治疗 每经记者 陈星 每经编辑 董兴生 作为一种常见的神经退化性疾病，阿尔茨海默病（AD）困扰着大量患者及家庭，严重影响患者生存质量的同时，也造成沉重照护负担和庞大社会经济成 本。 记者注意到，今年1月，强生已经宣布其在研靶向Tau蛋白的单抗Posdinemab获美国食品药品监督管理局（FDA）快速通道资格，用于治疗早期 ...