近一个月内，宁波大学附属第一医院感染科已连续收治8例脑膜炎患者，他们的平 均年龄仅26岁，最小的患者甚至只有16岁。 来源：国家应急广播微信公众号 "熬夜刷手机""作息昼夜颠倒"，正悄悄击垮许多年轻人。 日前，话题"30岁小伙长期熬夜智力退回3岁"登上社交平台热搜，频发的年轻患者 病例为我们敲响警钟。 熬夜刷手机 25岁夜猫子"刷"出脑膜炎 25岁的小李(化名)每天刷手机视频到凌晨三四点。今年10月，她出现发热症状，体 温最高达38℃，还伴随持续头胀。有时候明明没温度，但头依然很胀。起初，小 李以为没休息好，直到发热持续超过一周，才来到医院。 脑部磁共振报告显示其"双侧额颞部脑膜稍增厚伴强化"，提示脑膜炎。经5天抗病 毒治疗，小李病情好转出院。 习惯性熬夜患"脑膜炎伴脑炎" 智力退至3岁水平 与小李相比，30岁的宁波小伙小张(化名)病情更为凶险。他平时晚上没事喜欢打游 戏，有时一玩就到了凌晨。 直到有一天小张因没去上班，被发现在宿舍高烧不退、言语不清，随即被送往医 院。 送医途中，小张病情急剧恶化，转至宁波大学附属第一医院时已陷入昏迷。经检 查，小张确诊"病毒性脑膜炎伴脑炎"，这意味着他不仅脑膜发炎，脑实质也 ...

Core Viewpoint - Alzheimer's disease (AD) is characterized by the accumulation of β-amyloid protein and hyperphosphorylated tau protein, leading to neuronal dysfunction and cognitive decline. Current treatments only alleviate symptoms without altering disease progression, while emerging therapies face significant challenges [2]. Group 1: Current Treatments and Limitations - Approved therapies for Alzheimer's, such as acetylcholinesterase inhibitors and NMDA receptor antagonists, only provide symptomatic relief and do not modify disease progression [2]. - Anti-Aβ monoclonal antibodies can reduce Aβ plaque burden and slow cognitive decline but have limitations, including low blood-brain barrier (BBB) permeability and ineffectiveness against newly generated Aβ [2]. - Emerging anti-tau therapies also face challenges, including off-target toxicity and poor clinical efficacy [2]. Group 2: Recent Research Developments - A study published by researchers from Sichuan University developed a method called Microglia-Liposome Fusion Extrusion (MiLi-FE) to create microglia-derived nanovesicles that can cross the BBB and co-deliver rapamycin and AR7 to treat Alzheimer's disease [3][4]. - The study confirmed that both macroautophagy and chaperone-mediated autophagy are impaired in Alzheimer's disease model mice, which precedes Aβ accumulation and drives disease progression [4]. Group 3: Mechanism and Efficacy of New Approach - The AR@ENV nanovesicles can effectively penetrate the BBB and target inflammatory sites in the brains of Alzheimer's patients, activating both autophagy pathways to enhance the clearance of Aβ and other toxic protein aggregates [5]. - This dual activation restores protein homeostasis and provides significant neuroprotection, improving neuroinflammation and cognitive deficits in two different Alzheimer's mouse models [5]. Group 4: Future Implications - The combination of synchronized dual autophagy activation and targeted biomimetic delivery positions AR@ENV as a promising candidate for Alzheimer's treatment. The MiLi-FE platform offers a flexible and scalable method for delivering various therapeutic agents to the central nervous system, potentially expanding its applicability to a range of neurological diseases [7].

Core Viewpoint - Sleep deprivation activates the body's inflammatory response, leading to cognitive impairment and increased risk of various diseases [2][3][6]. Group 1: Impact of Sleep Deprivation - A study involving 2,641 participants found that sleeping less than 6 hours triggers systemic inflammation and increases the risk of cognitive impairment [3]. - Sleep deprivation causes a series of inflammatory responses in the brain, releasing pro-inflammatory factors that adversely affect neurons and cognitive functions [3]. - Chronic sleep deprivation leads to oxidative stress and cellular damage, further exacerbating cognitive decline [3][6]. Group 2: Health Risks Associated with Sleep Deprivation - Insufficient sleep and chronic inflammation are linked to various diseases, including metabolic disorders, cancer, and mental health issues [6]. - Research indicates that sleeping less than 6 hours per night for a week can negatively impact metabolism, inflammation, immunity, and stress response [6]. - Prolonged sleep deprivation keeps the body in a state of stress, lowering immune function and increasing disease risk [6]. Group 3: Recommendations for Mitigating Damage - Adults typically need 7-8 hours of sleep per night, while older adults may require 5-7 hours [11]. - To combat sleep deprivation, lifestyle adjustments and medical interventions are recommended, such as increasing sunlight exposure and regular exercise [13]. - A balanced diet rich in anti-inflammatory foods, such as whole grains, deep-sea fish, cruciferous vegetables, and berries, can help reduce inflammation [14][15].

Core Viewpoint - Alzheimer's disease (AD) is a severe neurodegenerative disorder with significant impacts on individuals and society, yet drug development has faced numerous failures despite substantial investments from major pharmaceutical companies [2][3]. Drug Development and FDA Approvals - In June 2021, the FDA accelerated the approval of Aducanumab, developed by Eisai and Biogen, marking the first new drug for Alzheimer's since 2003, although its approval was controversial due to associated risks like ARIA (Amyloid-related Imaging Abnormalities) [3][6]. - Following Aducanumab, the FDA approved two additional antibody drugs targeting Aβ: Donanemab by Eli Lilly and Lecanemab by Eisai and Biogen, both of which also present ARIA-related side effects [3][6]. Denali Therapeutics' Research - Denali Therapeutics published a study in August 2025 on a new antibody transport carrier, ATV cisLALA, which utilizes transferrin receptor (TfR) to enhance brain delivery of anti-Aβ antibodies while mitigating ARIA risks [4][9]. - The ATV cisLALA carrier shows improved distribution in brain tissue compared to traditional Aβ antibodies, which tend to accumulate around blood vessels, potentially triggering inflammatory responses and ARIA [9][11]. Mechanism of Action - Traditional Aβ antibodies enter the brain through cerebrospinal fluid and perivascular spaces, where amyloid deposits are located, leading to inflammation and ARIA. In contrast, the ATV carrier enhances delivery through capillaries, reducing ARIA side effects [11][12]. - Denali's TfR-based approach is not limited to Aβ; the company is also developing therapies targeting tau protein using the same delivery mechanism, aiming to address two key toxic proteins in Alzheimer's simultaneously [11].

Core Viewpoint - The research published by Yale University confirms the presence of T cells in the healthy brains of mice and humans, specifically in the subfornical organ (SFO), indicating that T cells can reside in the brain under normal conditions, contrary to previous beliefs about the blood-brain barrier and immune cell isolation [3][11]. Group 1: Research Findings - The study reveals that T cells in the SFO are enriched and play a crucial role in monitoring gut and fat tissue information, which is essential for regulating feeding and behavior [3][11]. - T cells in the SFO are distinct from those in the meninges, as they express proteins like CXCR6 that allow them to remain in brain tissue and secrete immune signaling proteins such as IFNγ [8][11]. - The research indicates a relationship between dietary habits and the quantity of T cells in the brain, with high-fat diets leading to an increase in T cells in both fat tissue and the brain [8][9]. Group 2: Mechanisms of Interaction - The study demonstrates that fasting increases T cell numbers in the brain while decreasing them in fat tissue, suggesting that dietary intake can dynamically regulate T cell migration to the central nervous system [9][11]. - Antibiotic intervention to deplete gut microbiota resulted in a significant reduction of T cells in the brain, indicating that gut microbiota may influence immune cell homeostasis in the central nervous system [9][11]. - The presence of T cells in the brain is linked to feeding behavior, as T cell-deficient mice took longer to find food when hungry compared to normal mice, highlighting their role in foraging and eating behaviors [9][11].

Core Viewpoint - The research reveals the developmental control mechanism of the meningeal lymphatic system in the brain, highlighting the dynamic regulation by neural activity through specific glial cell subtypes, which provides new insights into the interaction between the nervous and immune systems [3][6][9]. Group 1: Research Findings - The study identifies that neural activity regulates the expression of Vegfc in slc6a11b+ radial astrocytes, which in turn controls the development of mural lymphatic endothelial cells (muLEC) in the meninges [3][5]. - It demonstrates that slc6a11b+ radial astrocytes are the primary source of Vegfc, essential for muLEC development, and that this process is modulated by neural activity [7][9]. - The collaboration between slc6a11b+ radial astrocytes and ccbe1+ fibroblasts ensures that muLEC is restricted to the brain surface, preventing invasion into the brain parenchyma [5][9]. Group 2: Implications for Future Research - The findings suggest that the brain not only processes neural information but also coordinates its microenvironment, providing a new framework for understanding brain-immune interactions [9]. - The research opens avenues for interventions targeting this regulatory network, potentially offering new perspectives on the role of the meningeal lymphatic system in neurodegenerative diseases [9][14]. - It emphasizes the importance of a functional lymphatic network for brain health, indicating that targeting the external lymphatic pathways may enhance treatment efficacy for neurological disorders [14].