Core Insights - Researchers from institutions including the University of California, Los Angeles, published a paper in the journal E-Biomedicine, revealing that Alzheimer's disease has a discernible development trajectory rather than being random [1] Group 1 - The study utilized advanced algorithms such as dynamic time warping and machine learning clustering to analyze electronic health records of nearly 25,000 Alzheimer's patients from the University of California health database [1] - The findings suggest that the occurrence of Alzheimer's disease is not coincidental, indicating a pattern in its progression [1]

Core Insights - The research conducted by the team led by Yao Yonggang and Zhang Dengfeng from the Kunming Institute of Zoology, Chinese Academy of Sciences, provides new insights into the cellular and molecular pathological changes in the choroid plexus of Alzheimer's disease mice during the early stages of the disease, potentially aiding in the development of early intervention strategies for Alzheimer's disease [1][2] Group 1: Research Findings - The study constructed a single-cell transcriptome map related to the choroid plexus in Alzheimer's disease for the first time, elucidating the cellular and molecular pathological changes in the early stages of the disease [2] - The choroid plexus is composed of various cell types, with epithelial cells accounting for approximately 75% of the total cell population [2] - The permeability of choroid plexus epithelial cells in Alzheimer's disease mice was found to be increased, indicating a compromised barrier function [2] Group 2: Immune Response - The choroid plexus contains multiple myeloid and lymphoid immune cell subpopulations, with some lymphocytes, macrophages, and dendritic cell subpopulations expressing proliferation signals, suggesting a "lymph node-like" proliferation of immune cells in situ [2] - Downregulation of macrophage migration inhibitory factor expression in the choroid plexus epithelial cells of Alzheimer's disease mice leads to disrupted immune cell communication and macrophage activation [2] Group 3: Gender Differences - The study identified significant gender differences in the gene expression profile of the choroid plexus, providing data support for future research on the pathological mechanisms and interventions related to gender differences in Alzheimer's disease [2]

Core Viewpoint - The article discusses a shocking discovery that microplastics and nanoplastics have been found in human brain tissue, raising concerns about their potential impact on health, particularly in relation to neurodegenerative diseases [5][7][9]. Group 1: Research Findings - A study published in Nature Medicine revealed that all tested human brain samples contained microplastics and nanoplastics, with the highest concentration reaching 7 grams, equivalent to the weight of a plastic spoon [5][6]. - The concentration of microplastics in the brains of individuals with Alzheimer's disease and vascular dementia was found to be 3 to 5 times higher than in healthy individuals, suggesting a possible link between plastic exposure and cognitive decline [7]. - Between 2016 and 2024, the concentration of microplastics in brain tissue increased by 50%, paralleling the trend of plastic production doubling every 10 to 15 years [9]. Group 2: Sources of Microplastics - Microplastics enter the human body primarily through food and drink, as they have infiltrated the marine food chain, affecting seafood and salt consumption [10][11]. - Airborne microplastics, including synthetic fibers and particles from tire wear, also contribute to human exposure, with urban residents potentially inhaling up to 74,000 microplastic particles annually [13]. Group 3: Implications and Recommendations - The pervasive presence of microplastics in daily life necessitates a reduction in unnecessary plastic exposure, such as minimizing the use of single-use takeaway containers and opting for glass or stainless steel products [14]. - The article emphasizes that the concern has shifted from plastic pollution in oceans to its infiltration into human bodies, highlighting the urgent need for awareness and action [15].

Core Viewpoint - A recent study published in Nature Medicine reveals the presence of microplastics and nanoplastics in human brain tissue, raising concerns about their potential impact on neurological health [2][4]. Group 1: Research Findings - All tested human brain samples contained microplastics, with the highest concentration reaching 7 grams, equivalent to the weight of a plastic spoon [3]. - Individuals with Alzheimer's disease and vascular dementia exhibited 3 to 5 times higher concentrations of microplastics in their brains compared to healthy individuals [4][6]. - Over the past eight years, the concentration of microplastics in the brain has increased by 50%, paralleling the trend of plastic production doubling every 10 to 15 years [7]. Group 2: Sources of Microplastics - Microplastics enter the human body primarily through food and drink, with seafood, salt, and bottled water being significant sources [9][12]. - Airborne microplastics, including synthetic fibers and particles from tire wear, contribute to inhalation exposure, with urban residents potentially inhaling up to 74,000 microplastic particles annually [13][14]. Group 3: Implications and Recommendations - The pervasive presence of microplastics necessitates a reduction in unnecessary plastic exposure, such as minimizing takeout food and opting for glass or stainless steel containers [17]. - The shift in focus from ocean plastic pollution to human health underscores the urgent need for awareness and action regarding plastic consumption [18].

Core Viewpoint - A recent study published in Nature Medicine reveals the presence of microplastics and nanoplastics in human brain tissue, raising concerns about their potential impact on neurological health [2][4]. Group 1: Research Findings - All tested human brain samples contained microplastics, with the highest concentration reaching 7 grams, equivalent to the weight of a plastic spoon [3]. - Individuals with Alzheimer's disease and vascular dementia exhibited 3 to 5 times higher concentrations of microplastics in their brains compared to healthy individuals [4][6]. - Over the past eight years, the concentration of microplastics in the brain has increased by 50%, paralleling the trend of plastic production doubling every 10 to 15 years [7]. Group 2: Sources of Microplastics - Microplastics enter the human body primarily through food and drink, with seafood, salt, and bottled water being significant sources [9][12]. - Airborne microplastics, including synthetic fibers and tire wear particles, also contribute to human exposure, with urban residents potentially inhaling up to 74,000 microplastic particles annually [13][14]. Group 3: Implications and Recommendations - The pervasive presence of microplastics suggests that complete avoidance is impossible, but reducing unnecessary plastic exposure is advisable, such as minimizing takeout and opting for glass or stainless steel containers [17]. - The shift in concern from ocean plastic pollution to human health implications underscores the urgency of addressing plastic contamination [18].

人物小传 田金洲，1956年生，湖北天门人，中国工程院院士，北京中医药大学东直门医院脑病科主任医师、教 授。致力于用中医药防治阿尔茨海默病及其他神经系统疾病研究，将最新的阿尔茨海默病诊疗技术与我 国古代的临床经验、当今的应用场景紧密结合，创建阿尔茨海默病序贯疗法，辨证施治，更好地发挥中 医药作用。 每周四早晨7点半，田金洲会准时出现在北京中医药大学东直门医院脑病科诊室，近69岁的他乌发间仍 透着精气神。来就诊的是一群特殊的患者——他们沉默地坐着，记忆的碎片正悄然流逝，全靠家属帮他 们描述病情。 "最近他起夜次数比以前少了""现在不乱跑了，但最近肠胃不太好"……家属们轻声细语地介绍着病情， 田金洲的笔尖在病历本上沙沙作响，记录着患者的情况。 阿尔茨海默病是一种进行性神经系统退行性疾病，迄今为止病因尚不明确，没有世界公认的特效药。田 金洲说："现代医学现有的治疗措施均不能逆转病情发展，中医药为疾病的诊治提供了新的方式。" 1 一套"组合拳" 设计序贯疗法，结合病情发展进行分阶段治疗 遗忘、混乱、妄想……疾病的骤然来临会全然改变一个人、一个家庭的命运。无论患者的一生是跌宕起 伏还是平平淡淡，人生下一幕都会起始于这个 ...

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].