论文推荐-11-神经炎症 · Jun 11 11:04

{"success": true, "name": "paper-recommender", "file": "references/pubmed-API-patterns.md", "content": "# PubMed E-utilities API 实战笔记\n\n## 搜索API (esearch)\n\n### 基础结构\n```\nbase: https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi\nparams:\n db=pubmed\n term=<查询表达式>\n mindate/maxdate — 日期范围\n datetype=pdat (publication date)\n retmax=N — 最大返回数\n retmode=json\n```\n\n### 已验证的关键查询模式\n\n**1. 主题搜索 + 高影响因子期刊过滤**\n```python\nquery = 'Parkinson AND (\"Nat Neurosci\"[Journal] OR \"Neuron\"[Journal] OR \"Nat Med\"[Journal])'\n```\n- 期刊名必须用 `\"全称\"[Journal]` 格式\n- 不加 `[Journal]` 标签时，`Neuron` 被翻译为 MeSH 的 neurons（神经元）\n- `Brain` 被翻译为 MeSH 的 brain（大脑解剖结构）\n\n**2. 已测试的有效期刊标签**\n| 期刊 | 标签 |\n|------|------|\n| Nature Communications | `\"Nat Commun\"[Journal]` |\n| Nature Medicine | `\"Nat Med\"[Journal]` |\n| Neuron | `\"Neuron\"[Journal]` |\n| Nature Neuroscience | `\"Nat Neurosci\"[Journal]` |\n| Science Advances | `\"Sci Adv\"[Journal]` |\n| EBioMedicine | `\"EBioMedicine\"[Journal]` |\n| Acta Neuropathologica | `\"Acta Neuropathol\"[Journal]` |\n| Brain | `\"Brain\"[Journal]` |\n| Cell Reports | `\"Cell Rep\"[Journal]` |\n| Molecular Neurodegeneration | `\"Mol Neurodegener\"[Journal]` |\n| Lancet Neurology | `\"Lancet Neurol\"[Journal]` |\n\n### 已验证无用的参数\n- `sort=date` — 返回 warning \"Unknown sort schema 'date' ignored\"，无效果\n\n## 获取详情API (esummary)\n\n```python\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&id=<PMID列表>&retmode=json'\n```\n\n关键字段：\n- `pubtype` — 文章类型（含 \"Review\" 则为综述）\n- `source` — 期刊缩写名\n- `articleids[].idtype == 'doi'` — DOI\n- `attributes` — 包含 \"Has Abstract\" 则有摘要\n- `pubdate` — 发表日期\n- `title` — 标题\n\n## 获取摘要API (efetch)\n\n```python\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=<PMID列表>&retmode=text&rettype=abstract'\n```\n\n返回纯文本，包含标题、作者、机构、摘要正文、DOI、PMID、利益冲突声明。\n\n## 已知环境陷阱\n\n### 1. SSL连接失败（exit code 35）\n某些环境（git-bash/MSYS2）的 curl SSL 版本与 NCBI 服务器不兼容。\n- 修复1：`curl -k`（跳过证书验证）\n- 修复2：改用 Python 的 `urllib.request`（在本环境中工作可靠）\n- 修复3：更新 curl CA bundle\n\n### 2. URL编码问题\ncurl 命令行中包含 `()\"[]` 等特殊字符时容易解析失败（exit code 3）。\n- 修复：用 Python 的 `urllib.parse.urlencode(params)` 构建查询串\n\n## 搜索策略（两阶段工作流）\n\n### 阶段A：主题搜索\n```python\nquery = 'Parkinson disease AND (dopamine neuron OR synuclein OR MPTP)'\nparams = {\n 'db': 'pubmed', 'term': query,\n 'mindate': '2026/03/01', 'maxdate': '2026/06/10',\n 'datetype': 'pdat', 'retmax': 8, 'retmode': 'json'\n}\n```\n目的：快速了解该时间段的总论文数和热门方向，获取基础 PMID 列表。\n\n### 阶段B：高影响力期刊过滤\n```python\njournal_tags = '\"Nat Neurosci\"[Journal] OR \"Neuron\"[Journal] OR \"Nat Med\"[Journal] OR \"Lancet Neurol\"[Journal] OR \"Nat Commun\"[Journal] OR \"Sci Adv\"[Journal] OR \"Cell Rep\"[Journal] OR \"Acta Neuropathol\"[Journal] OR \"Brain\"[Journal] OR \"Mol Neurodegener\"[Journal] OR \"EBioMedicine\"[Journal]'\nquery = f'Parkinson AND ({journal_tags})'\n```\n目的：直接命中 IF>10 或领域顶刊的高质量论文。\n注意：`count` 字段显示总命中数，通常 100+。\n\n### 初筛要点（esummary 检查）\n1. `pubtype` 不含 \"Review\" → 原创研究\n2. `attributes` 含 \"Has Abstract\" → 有可用摘要\n3. 检查 DOI 是否存在 → 正式发表\n4. 排除 \"No authors listed\" → 通常是 News & Views / 编辑评论\n\n## 评分标准（5维度）\n\n| 维度 | 评分要点 | 满分 |\n|------|---------|------|\n| 逻辑完整性 | gain+loss of function, KO/KI, 药理抑制, 正反验证 | 10 |\n| 方法学水平 | 单细胞测序, 蛋白组学, CLEM, 空间转录组, 活细胞成像 | 10 |\n| 创新性 | 新概念/新机制/新方法, 首次报道 | 10 |\n| 可借鉴性 | 实验设计可迁移, 技术平台可复现 | 10 |\n| 临床转化潜力 | 体内验证, 治疗靶点, 生物标志物 | 10 |\n\n总分 ≥ 6/10 且与用户方向高度相关 → 推送。\n", "file_type": ".md"}

{"todos": [{"id": "search", "content": "PubMed Phase A + B search for neuroinflammation/glial papers", "status": "in_progress"}, {"id": "fetch", "content": "Fetch esummary + abstracts for candidate papers", "status": "pending"}, {"id": "screen", "content": "Screen papers: high-IF journals, original research, recent (3mo)", "status": "pending"}, {"id": "evaluate", "content": "5-dimension quality scoring (logic, methods, innovation, transferability, clinical translation)", "status": "pending"}, {"id": "output", "content": "Produce recommendation or [SILENT]", "status": "pending"}], "summary": {"total": 5, "pending": 4, "in_progress": 1, "completed": 0, "cancelled": 0}}

{"status": "success", "output": "=== PHASE A: Topic Search ===\r\nURL: https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=%28neuroinflammation+OR+microglia+OR+astrocyte\r\nTotal count: 4758\r\nPMIDs: ['42268521', '42268517', '42268435', '42268366', '42267908', '42267754', '42267516', '42267401']\r\n\r\n=== PHASE B: High-Impact Journals ===\r\nURL length: 739\r\nTotal count: 168\r\nPMIDs: ['42267908', '42265101', '42265098', '42263678', '42263400', '42259289', '42248891', '42242217', '42237401', '42237024', '42236496', '42235487', '42230793', '42230582', '42228568']\r\n\r\nTotal unique PMIDs to fetch: 22\r\nAll: ['42268521', '42268517', '42268435', '42268366', '42267908', '42267754', '42267516', '42267401', '42265101', '42265098', '42263678', '42263400', '42259289', '42248891', '42242217', '42237401', '42237024', '42236496', '42235487', '42230793', '42230582', '42228568']\r\n", "tool_calls_made": 0, "duration_seconds": 3.42}

{"status": "success", "output": "=== ESUMMARY RESULTS ===\r\n\r\nPMID 42268521:\r\n Title: Mitochondrial Dysfunction as a Driver of Neurodegeneration in Parkinson's and Huntington's Disease: Molecular Insights a\r\n Journal: Mol Neurobiol\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article', 'Review']\r\n DOI: 10.1007/s12035-026-05991-w\r\n Has Abstract: True\r\n Authors: Kuwar OK, Khan S, Maloo A\r\n\r\nPMID 42268517:\r\n Title: Ischemic Stroke Induces Ferroptosis and Neuroinflammation via Activation of the Microglial Tbp-Lpl Transcriptional Axis.\r\n Journal: Neurochem Res\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article']\r\n DOI: 10.1007/s11064-026-04812-9\r\n Has Abstract: True\r\n Authors: Wang Z, Xiong J, Lv R\r\n\r\nPMID 42268435:\r\n Title: Comparison between molecular and histological IDH-wild-type glioblastoma and extensive subgroup analysis of IDH-wild-typ\r\n Journal: J Neurooncol\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article']\r\n DOI: 10.1007/s11060-026-05637-w\r\n Has Abstract: True\r\n Authors: Seifert AM, Richter S, Sagerer A\r\n\r\nPMID 42268366:\r\n Title: Unlocking Neuroprotection: Exercise-Induced Muscle Secretome (Myokines) as a Therapeutic Avenue Against Alzheimer's Dise\r\n Journal: J Mol Neurosci\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article', 'Review']\r\n DOI: 10.1007/s12031-026-02556-3\r\n Has Abstract: True\r\n Authors: Shirvani H, Pescatello LS, Eftekhari Moghadam AR\r\n\r\nPMID 42267908:\r\n Title: Developmental circuit instability in amyotrophic lateral sclerosis: from hyperexcitability to network collapse.\r\n Journal: Brain\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article']\r\n DOI: 10.1093/brain/awag185\r\n Has Abstract: True\r\n Authors: Donati Della Lunga I, Cerutti L, Barabino V\r\n\r\nPMID 42267754:\r\n Title: Therapeutic Potential of Stearylamine-Conjugated Phenylboronic Acid-Modified Nanocarriers of 4-Allyl Pyrocatechol in Mod\r\n Journal: Mol Pharm\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article']\r\n DOI: 10.1021/acs.molpharmaceut.5c01768\r\n Has Abstract: True\r\n Authors: Katti VB, Kolusu AS, Madhana RM\r\n\r\nPMID 42267516:\r\n Title: RNF138-Mediated Ubiquitination and Degradation of NS5 Restricts Tick-Borne Encephalitis Virus Infection.\r\n Journal: Adv Sci (Weinh)\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article']\r\n DOI: 10.1002/advs.75991\r\n Has Abstract: True\r\n Authors: Sun J, Yang W, Zhou H\r\n\r\nPMID 42267401:\r\n Title: An Astrocyte-Targeted Nanoplatform with Ultrasound-Responsive Fluorescence Switch for Synergistic Chemo-Sonothermal Ther\r\n Journal: ACS Appl Mater Interfaces\r\n Date: 2026 Jun 10\r\n Types: ['Journal Article']\r\n DOI: 10.1021/acsami.6c03192\r\n Has Abstract: True\r\n Authors: Wang Z, Gao P, Song X\r\n\r\nPMID 42265101:\r\n Title: Scg2 drives corticospinal circuit reorganization with spinal premotor interneurons and astrocytes for motor recovery aft\r\n Journal: Nat Commun\r\n Date: 2026 Jun 9\r\n Types: ['Journal Article']\r\n DOI: 10.1038/s41467-026-73518-x\r\n Has Abstract: True\r\n Authors: Sato T, Nakamura Y, Hoshina K\r\n\r\nPMID 42265098:\r\n Title: Semaglutide attenuates neuroinflammation in male mice.\r\n Journal: Nat Commun\r\n Date: 2026 Jun 9\r\n Types: ['Journal Article']\r\n DOI: 10.1038/s41467-026-74038-4\r\n Has Abstract: True\r\n Authors: Belmont-Rausch DM, Ludwig MQ, Bentsen MA\r\n\r\nPMID 42263678:\r\n Title: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer's disease pathogenesis.\r\n Journal: Neuron\r\n Date: 2026 Jun 9\r\n Types: ['Journal Article']\r\n DOI: 10.1016/j.neuron.2026.05.015\r\n Has Abstract: True\r\n Authors: Liu Y, Ye Y, Fan M\r\n\r\nPMID 42263400:\r\n Title: The complement C3-microglial axis in depression of Parkinson's disease: from mechanism to therapeutic intervention.\r\n Journal: EBioMedicine\r\n Date: 2026 Jun 9\r\n Types: ['Journal Article']\r\n DOI: 10.1016/j.ebiom.2026.106325\r\n Has Abstract: True\r\n Authors: Yin Q, Ding M, Tang Y\r\n\r\nPMID 42259289:\r\n Title: Developmental and age-related synapse elimination is mediated by glial Croquemort.\r\n Journal: Neuron\r\n Date: 2026 Jun 8\r\n Types: ['Journal Article']\r\n DOI: 10.1016/j.neuron.2026.04.046\r\n Has Abstract: True\r\n Authors: Jay TR, Kang Y, Ouellet-Massicotte V\r\n\r\nPMID 42248891:\r\n Title: Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in 5×FAD mice.\r\n Journal: Nat Commun\r\n Date: 2026 Jun 5\r\n Types: ['Journal Article']\r\n DOI: 10.1038/s41467-026-74037-5\r\n Has Abstract: True\r\n Authors: Zhou Q, Sun F, Zhang Y\r\n\r\nPMID 42242217:\r\n Title: A specialized population of hair afferents dedicated to transmitting mechanical itch.\r\n Journal: Neuron\r\n Date: 2026 Jun 4\r\n Types: ['Journal Article']\r\n DOI: 10.1016/j.neuron.2026.05.017\r\n Has Abstract: True\r\n Authors: Fatima M, Lee H, Cha H\r\n\r\nPMID 42237401:\r\n Title: Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.\r\n Journal: Mol Neurodegener\r\n Date: 2026 Jun 3\r\n Types: ['Journal Article']\r\n DOI: 10.1186/s13024-026-00946-0\r\n Has Abstract: True\r\n Authors: Nicholson L, Tang SJ, Karra T\r\n\r\nPMID 42237024:\r\n Title: AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction.\r\n Journal: Acta Neuropathol\r\n Date: 2026 Jun 3\r\n Types: ['Journal Article', \"Research Support, Non-U.S. Gov't\"]\r\n DOI: 10.1007/s00401-026-03033-2\r\n Has Abstract: True\r\n Authors: Dunot J, Gandin C, Truchi M\r\n\r\nPMID 42236496:\r\n Title: Genetic architecture of white matter microstructure captured by unsupervised deep representation learning of fractional \r\n Journal: Nat Commun\r\n Date: 2026 Jun 3\r\n Types: ['Journal Article']\r\n DOI: 10.1038/s41467-026-73996-z\r\n Has Abstract: True\r\n Authors: Zhao X, Xie Z, He W\r\n\r\nPMID 42235487:\r\n Title: Who sets the brakes on anxiety? A role for astrocytic histamine 3 receptors.\r\n Journal: Neuron\r\n Date: 2026 Jun 3\r\n Types: ['Journal Article']\r\n DOI: 10.1016/j.neuron.2026.05.011\r\n Has Abstract: True\r\n Authors: Gómez-Sotres P, Mederos S\r\n\r\nPMID 42230793:\r\n Title: Author Correction: CHIT1-positive microglia drive motor neuron ageing in the primate spinal cord.\r\n Journal: Nature\r\n Date: 2026 Jun 2\r\n Types: ['Published Erratum']\r\n DOI: 10.1038/s41586-026-10728-9\r\n Has Abstract: False\r\n Authors: Sun S, Li J, Wang S\r\n\r\nPMID 42230582:\r\n Title: Cross-species transcriptomic analysis of rodent model fidelity to human mesial temporal lobe epilepsy.\r\n Journal: Nat Commun\r\n Date: 2026 Jun 2\r\n Types: ['Journal Article']\r\n DOI: 10.1038/s41467-026-73796-5\r\n Has Abstract: True\r\n Authors: Kim J, Lee S, Kim B\r\n\r\nPMID 42228568:\r\n Title: Nociceptive neurons inhibit neutrophil extracellular trap formation via MLKL-licensed histone release.\r\n Journal: Cell Rep\r\n Date: 2026 Jun 1\r\n Types: ['Journal Article']\r\n DOI: 10.1016/j.celrep.2026.117457\r\n Has Abstract: True\r\n Authors: Meng H, Hu W, Kang E\r\n\r\n\r\n=== ABSTRACTS (split by PMID) ===\r\n", "tool_calls_made": 0, "duration_seconds": 2.62}

{"status": "success", "output": "1. Brain. 2026 Jun 10:awag185. doi: 10.1093/brain/awag185. Online ahead of print.\r\n\r\nDevelopmental circuit instability in amyotrophic lateral sclerosis: from \r\nhyperexcitability to network collapse.\r\n\r\nDonati Della Lunga I(1), Cerutti L(1)(2), Barabino V(1), Figus GG(1)(3), \r\nCallegari F(1), Oneto L(1), Tedesco M(1), Bacchetti F(4), Milanese M(4)(5), \r\nMassobrio P(1), Brofiga M(1)(2)(6).\r\n\r\nAuthor information:\r\n(1)Department of Informatics, Bioengineering, Robotics and System Engineering \r\n(DIBRIS), Università of Genova, 16145, Genova, Italy.\r\n(2)Neurofacility, Istituto Italiano di Tecnologia (IIT), 16163, Genova, Italy.\r\n(3)Genoa Instruments, 16152, Genova, Italy.\r\n(4)Department of Pharmacy (DIFAR), Università of Genova, 16147, Genova, Italy.\r\n(5)IRCCS Ospedale Policlinico San Martino, 16132, Genova, Italia.\r\n(6)Inter-University Center for the Promotion of the 3Rs Principles in Teaching & \r\nResearch (Centro 3R), 16145, Genova, Italy.\r\n\r\nAmyotrophic lateral sclerosis (ALS) is traditionally viewed as a late-onset \r\nmotor neuron disease, yet how cortical dysfunction originates and contributes to \r\npathogenesis remains unresolved. In this study, we reconstruct the developmental \r\ntrajectory of cultured cortical networks derived from SOD1G93A mouse embryos \r\nusing a multimodal approach, by combining morphometric, electrophysiological, \r\npharmacological, molecular, computational, and machine-learning techniques. We \r\nprove that ALS neurons fail to acquire mature polarization and connectivity, \r\ndisplaying a transient phase of hyperexcitability that precedes a progressive \r\ncollapse of network organization. Astrocytic dysfunction emerges early and \r\nimpairs synchronization, establishing a causal link between glial dysfunction \r\nand neuronal instability. The analysis of synaptic transmission reveals an \r\nexcitatory bias followed by maladaptive inhibitory recruitment and \r\nGABA/glutamate co-release, causing fragmented and inefficient network \r\ntopologies. Finally, in silico modelling identified deficient intrinsic \r\nadaptation as a key driver of hyperexcitability. Together, our findings position \r\nALS as a developmentally rooted disorder of cultured cortical network \r\nhomeostasis, driven by glial, synaptic, and intrinsic adaptation failures. By \r\ndemonstrating that cortical dysfunction is embedded before degeneration, this \r\nwork provides a unifying framework connecting early network instability to \r\ndisease progression and establishes electrophysiological network signatures, \r\ndetected by machine learning classifiers, as candidate biomarkers for early \r\ndiagnosis and therapeutic screening.\r\n\r\n© The Author(s) 2026. Published by Oxford University Press on behalf of the \r\nGuarantors of Brain.\r\n\r\nDOI: 10.1093/brain/awag185\r\nPMID: 42267908\r\n\r\n\r\n2. Nat Commun. 2026 Jun 9;17(1):4880. doi: 10.1038/s41467-026-73518-x.\r\n\r\nScg2 drives corticospinal circuit reorganization with spinal premotor \r\ninterneurons and astrocytes for motor recovery after stroke in mice.\r\n\r\nSato T(1)(2), Nakamura Y(1)(2), Hoshina K(1)(2), Inoue KI(3)(4), Takada M(3)(5), \r\nYano M(6)(7), Matsuzawa H(8)(9), Ueno M(10)(11).\r\n\r\nAuthor information:\r\n(1)Department of System Pathology for Neurological Disorders, Brain Research \r\nInstitute, Niigata University, Niigata, Niigata, Japan.\r\n(2)Department of Systems Neuropathology and Neural Repair, Brain Research \r\nInstitute, Niigata University, Niigata, Niigata, Japan.\r\n(3)Institute for the Evolutionary Origins of Human Behavior, Kyoto University, \r\nInuyama, Aichi, Japan.\r\n(4)Department of Integrative Anatomy, Graduate School of Medical Sciences and \r\nMedical School, Nagoya City University, Nagoya, Aichi, Japan.\r\n(5)Department of Neurology, Graduate School of Medicine, The University of \r\nOsaka, Suita, Osaka, Japan.\r\n(6)Division of Neurobiology and Anatomy, Graduate School of Medical and Dental \r\nSciences, Niigata University, Niigata, Niigata, Japan.\r\n(7)Core Research Facilities for Basic Science Research Center for Medical \r\nScience, The Jikei University School of Medicine, Minato-ku, Tokyo, Japan.\r\n(8)Center for Integrated Human Brain Science, Niigata University, Niigata, \r\nNiigata, Japan.\r\n(9)Center for Advanced Medicine and Clinical Research, Sapporo Hakuyokai \r\nHospital, Sapporo, Hokkaido, Japan.\r\n(10)Department of System Pathology for Neurological Disorders, Brain Research \r\nInstitute, Niigata University, Niigata, Niigata, Japan. \r\nms-ueno@bri.niigata-u.ac.jp.\r\n(11)Department of Systems Neuropathology and Neural Repair, Brain Research \r\nInstitute, Niigata University, Niigata, Niigata, Japan. \r\nms-ueno@bri.niigata-u.ac.jp.\r\n\r\nBrain injuries such as stroke damage neural circuitry and lead to functional \r\ndeficits. Spared motor pathways are often reorganized for recovery; however, the \r\nconnectivity and mechanisms that drive the reorganization are largely unknown. \r\nHere, we demonstrate structural and functional connectivity reformed by \r\ncorticospinal axons after stroke in male mice and determine a secretory protein \r\nthat drives the reorganization. We first find that corticospinal axons innervate \r\nthe denervated cervical cord and reconnect to premotor V2a interneurons after \r\nstroke. Kinematic analyses and chemogenetic silencing reveal their contribution \r\nto motor recovery. Translated mRNA expression analyses identify a secretory \r\nprotein secretogranin II (Scg2), which is upregulated in astrocytes by \r\ninjury-induced ATP and in V2a neurons by rehabilitation-induced neural activity. \r\nScg2 promotes axon growth via cAMP and S6 and enhances axon rewiring, while its \r\nknockdown attenuates it. Our data reveal the neural substrate and molecular \r\nmechanism to induce reorganization and recovery, providing therapeutic targets \r\nfor central nervous system (CNS) injuries.\r\n\r\n© 2026. The Author(s).\r\n\r\nDOI: 10.1038/s41467-026-73518-x\r\nPMID: 42265101\r\n\r\nConflict of interest statement: Competing interests: The authors declare no \r\ncompeting interests.\r\n\r\n\r\n3. Nat Commun. 2026 Jun 9. doi: 10.1038/s41467-026-74038-4. Online ahead of\r\nprint.\r\n\r\nSemaglutide attenuates neuroinflammation in male mice.\r\n\r\nBelmont-Rausch DM(#)(1)(2)(3), Ludwig MQ(#)(1)(3), Bentsen MA(#)(4), Hansen \r\nSN(3), Secher A(3), Holst D(3), Moreno J(3), Das V(4), Egerod KL(1), Bjerregaard \r\nAM(4), Niss K(3), Bau S(3), Pyke C(3), Dalgaard K(3), Merkestein M(3), Wichern \r\nF(5), Hansen CT(4), Polex-Wolf J(4), Knudsen LB(6), Pers TH(7)(8).\r\n\r\nAuthor information:\r\n(1)Novo Nordisk Foundation Center for Basic Metabolic Research, University of \r\nCopenhagen, Copenhagen, Denmark.\r\n(2)Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad \r\nInstitute of MIT and Harvard, Cambridge, MA, USA.\r\n(3)Research and Development, Novo Nordisk A/S, Måløv, Denmark.\r\n(4)Research and Development, Novo Nordisk A/S, Søborg, Denmark.\r\n(5)Gubra A/S, Hørsholm, Denmark.\r\n(6)Research and Development, Novo Nordisk A/S, Måløv, Denmark. \r\nlottebjerreknudsen@icloud.com.\r\n(7)Novo Nordisk Foundation Center for Basic Metabolic Research, University of \r\nCopenhagen, Copenhagen, Denmark. tune.pers@sund.ku.dk.\r\n(8)Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad \r\nInstitute of MIT and Harvard, Cambridge, MA, USA. tune.pers@sund.ku.dk.\r\n(#)Contributed equally\r\n\r\nGlucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in \r\npreclinical models of neurodegeneration, with emerging evidence suggesting these \r\neffects may be driven by modulation of neuroinflammation. However, the cellular \r\nmechanisms underlying GLP-1RA effects on neuroinflammation remain poorly \r\nunderstood. Here we show, using a mouse model of lipopolysaccharide-induced \r\nneuroinflammation, how semaglutide coordinates cellular responses to resolve \r\nneuroinflammation. We find that semaglutide in male mice prevents brain \r\ninfiltration of neutrophils, excessive cytokine release, and suppresses \r\nneuroinflammation-associated transcriptional signatures specifically in \r\nmicroglia, endothelial cells, and a subset of pericytes. Mechanistically, we \r\nidentify a subset of Glp1r-expressing neurons in the dorsal vagal complex that, \r\nupon semaglutide treatment, regulate genes involved in anti-inflammatory \r\nsignaling. Semaglutide-modulated pathways overlap with inflammatory signatures \r\nfound in human neurodegenerative diseases, including Alzheimer's disease, \r\nsuggesting broad relevance for conditions involving neuroinflammation. Together, \r\nthese findings reveal how GLP-1R signaling in male mice orchestrates resolution \r\nof neuroinflammation through coordinated multi-cellular programs.\r\n\r\n© 2026. The Author(s).\r\n\r\nDOI: 10.1038/s41467-026-74038-4\r\nPMID: 42265098\r\n\r\nConflict of interest statement: Competing interests: THP receives research \r\nsupport from the Novo Nordisk A/S, his household holds stocks in Novo Nordisk \r\nA/S and he has received counseling fees from Eli Lilly and Zealand Pharma. \r\nDuring completion of this study, DMR, MAB and MQL have become employed at Novo \r\nNordisk A/S; K.D. has become employed at the Lundbeck Foundation; and F.W. at \r\nLundbeck A/S. S.N.H., A.S., D.H., J.M., V.D., A.M.B., K.N., S.B., C.P., M.M., \r\nC.T.H., J.P.W., L.B.K. are employees at Novo Nordisk A/S. All other authors have \r\nno competing interests to declare. Declaration of generative AI and AI-assisted \r\ntechnologies in the writing process: During the preparation of this work the \r\nauthors used generative AI tools to improve readability and language of the \r\nmanuscript. After using these services, the authors reviewed and edited the \r\ncontent as needed and take full responsibility for the content of the published \r\narticle.\r\n\r\n\r\n4. Neuron. 2026 Jun 9:S0896-6273(26)00386-7. doi: 10.1016/j.neuron.2026.05.015. \r\nOnline ahead of print.\r\n\r\nEpigenetic control of microglial mitochondrial immunity by KAT7 drives \r\nAlzheimer's disease pathogenesis.\r\n\r\nLiu Y(1), Ye Y(1), Fan M(2), Cheng HY(1), Sun S(3), Qiu Z(4).\r\n\r\nAuthor information:\r\n(1)Department of Physiology, Pharmacology and Therapeutics, Johns Hopkins \r\nUniversity School of Medicine, Baltimore, MD 21205, USA.\r\n(2)Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School \r\nof Medicine, Baltimore, MD 21205, USA.\r\n(3)Department of Physiology, Pharmacology and Therapeutics, Johns Hopkins \r\nUniversity School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder \r\nDepartment of Neuroscience, Johns Hopkins University School of Medicine, \r\nBaltimore, MD 21205, USA; Brain Science Institute, Johns Hopkins University \r\nSchool of Medicine, Baltimore, MD, USA.\r\n(4)Department of Physiology, Pharmacology and Therapeutics, Johns Hopkins \r\nUniversity School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder \r\nDepartment of Neuroscience, Johns Hopkins University School of Medicine, \r\nBaltimore, MD 21205, USA; Department of Neurosurgery, Johns Hopkins University \r\nSchool of Medicine, Baltimore, MD 21205, USA. Electronic address: \r\nzhaozhu@jhmi.edu.\r\n\r\nMitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic \r\nneuroinflammation in neurological diseases such as Alzheimer's disease (AD), yet \r\nhow this pathway is regulated in microglia remains poorly understood. Here, we \r\nidentify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic \r\nregulator that links chromatin remodeling to mitochondrial immune activation. \r\nKAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and \r\nhuman AD brains. Integrative transcriptomic and epigenomic analyses reveal that \r\nKAT7 activates transcription of cytidine/uridine monophosphate kinase 2 (Cmpk2), \r\na mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 \r\nexpression, impairs mtDNA replication and release, and consequently suppresses \r\ncyclic guanosine monophosphate-AMP synthase (cGAS)-stimulator of interferon \r\ngenes (STING) and NLRP3 signaling. Importantly, both microglia-specific deletion \r\nand pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced \r\nneuroinflammation, decrease β-amyloid burden, restore synaptic plasticity, and \r\nimprove cognitive function in 5×FAD mice. Together, these findings uncover an \r\nepigenetic-mitochondrial axis sustaining microglial pathogenicity and establish \r\nKAT7 as a potential therapeutic target for AD.\r\n\r\nCopyright © 2026 The Author(s). Published by Elsevier Inc. All rights reserved.\r\n\r\nDOI: 10.1016/j.neuron.2026.05.015\r\nPMID: 42263678\r\n\r\nConflict of interest statement: Declaration of interests The authors declare no \r\ncompeting interests.\r\n\r\n\r\n5. EBioMedicine. 2026 Jun 9;129:106325. doi: 10.1016/j.ebiom.2026.106325. Online \r\nahead of print.\r\n\r\nThe complement C3-microglial axis in depression of Parkinson's disease: from \r\nmechanism to therapeutic intervention.\r\n\r\nYin Q(1), Ding M(2), Tang Y(3), Qi Y(4), Qin Y(4), Jin H(1), Li Y(5), Bao J(1), \r\nMa S(1), Li Y(1), Ding H(2), An X(2), Qiao E(1), Tang Y(1), Zhang Q(1), Wang \r\nL(6), Shao J(7), Feng J(3), Hu LF(8), Wang J(9), Fang P(10), Luo W(11), Cong \r\nQ(12).\r\n\r\nAuthor information:\r\n(1)Department of Neurology and Clinical Research Center of Neurological Disease, \r\nThe Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.\r\n(2)Institute of Molecular Enzymology, School of Life Sciences, Suzhou Medical \r\nCollege, Soochow University, Suzhou, 215123, China.\r\n(3)Institute of Science and Technology for Brain-Inspired Intelligence, Fudan \r\nUniversity, Shanghai, 201203, China.\r\n(4)Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain \r\nDiseases, Institute of Neuroscience, Soochow University, Suzhou, 215123, China.\r\n(5)Department of Neurology, Huzhou Central Hospital, The Fifth School of \r\nClinical Medicine of Zhejiang Chinese Medical University, Huzhou, 313000, China.\r\n(6)Lanzhou Biotechnique Development Co., Ltd., Lanzhou, Gansu, 730000, China.\r\n(7)Department of Neurology, The Third People's Hospital of Zhangjiagang City, \r\nSuzhou, 215600, Jiangsu, China.\r\n(8)Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain \r\nDiseases, Institute of Neuroscience, Soochow University, Suzhou, 215123, China. \r\nElectronic address: hulifang@suda.edu.cn.\r\n(9)Institute of Science and Technology for Brain-Inspired Intelligence, Fudan \r\nUniversity, Shanghai, 201203, China. Electronic address: wangjing_@fudan.edu.cn.\r\n(10)Institute of Molecular Enzymology, School of Life Sciences, Suzhou Medical \r\nCollege, Soochow University, Suzhou, 215123, China; State Key Laboratory of \r\nChemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of \r\nSciences, Shanghai, 200032, China. Electronic address: panfang@sioc.ac.cn.\r\n(11)Department of Neurology and Clinical Research Center of Neurological \r\nDisease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, \r\nChina. Electronic address: lwfwxx@126.com.\r\n(12)Department of Neurology and Clinical Research Center of Neurological \r\nDisease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, \r\nChina; Jiangsu Key Laboratory of Drug Discovery and Translational Research for \r\nBrain Diseases, Institute of Neuroscience, Soochow University, Suzhou, 215123, \r\nChina; Biomedical Basic Research Center (BBRC) of Jiangsu, Soochow University, \r\nSuzhou, 215123, China; Department of Nephrology, The Second Affiliated Hospital \r\nof Soochow University, Suzhou, 215004, China; Institute of Neurological \r\nDiseases, Soochow University-Suzhou Blue Cross Brain Hospital, Soochow \r\nUniversity, Suzhou, 215123, China; School of Life Sciences, MOE Key Laboratory \r\nof Geriatric Diseases and Immunology, Suzhou Medical College of Soochow \r\nUniversity, Soochow University, Suzhou, 215123, China. Electronic address: \r\nqfcong@suda.edu.cn.\r\n\r\nBACKGROUND: Depression is a common and early non-motor symptom of Parkinson's \r\ndisease (PD) with significant sexual dimorphism, yet its underlying molecular \r\nmechanisms remain poorly understood. This study aimed to elucidate the \r\nsex-specific plasma proteomic profiles of depression in patients with PD (DPD) \r\nand to investigate the role of complement-mediated synaptic pruning in its \r\npathophysiology.\r\nMETHODS: Plasma proteomic analysis was performed on data from the Parkinson's \r\nProgression Markers Initiative (PPMI) and an independent validation cohort, \r\nstratified by sex. Functional enrichment analyses identified dysregulated \r\npathways. A chronic MPTP/probenecid-induced mouse model of PD was used to \r\nvalidate findings. Behavioural tests assessed motor and depressive-like \r\nphenotypes. Proteomic, biochemical, and imaging techniques were used to evaluate \r\nprotein expression, synapse density, and microglial phagocytosis. The \r\ntherapeutic mechanism of Botulinum Neurotoxin A (BoNT/A) on DPD was investigated \r\nin wild-type, C3-/- and C3aR-/- mice and in microglial cultures.\r\nFINDINGS: Proteomic profiling revealed both conserved complement-driven immune \r\ndysfunction and profound sex-divergent molecular perturbations underlying PD and \r\nDPD. Complement and coagulation cascades were consistently upregulated in both \r\nsexes. In MPTP-treated male and female mice, hippocampal complement components \r\n(C1Q, C3, C3aR) and downstream signalling (p-STAT3, p-P65) were elevated, \r\naccompanied by microglial synapse phagocytosis and depressive-like behaviours. \r\nGenetic deletion of C3 rescued both MPTP-induced motor and depressive-like \r\nbehavioural deficits and prevented hippocampal synaptic loss associated with \r\nmicroglial synaptic engulfment. BoNT/A treatment alleviated depressive-like \r\nbehaviours and reduced microglial synaptic engulfment in an MPTP model; these \r\ntherapeutic effects were abolished in C3-/- and C3aR-/- mice. Single-cell RNA \r\nsequencing and in vitro phagocytosis assay confirmed that BoNT/A modulated \r\nphagocytosis-related microglial subclusters.\r\nINTERPRETATION: DPD exhibits distinct sex-specific immune signatures, with \r\nconvergent complement pathway activation driving microglial synaptic pruning and \r\ndepressive symptoms. The antidepressant effect of BoNT/A is mediated through \r\ninhibition of the C3-C3aR signalling axis. These findings highlight the \r\npotential for sex-stratified diagnostics and complement-targeted therapies for \r\ndepression in patients with PD. A key limitation is that our clinical analyses \r\nwere constrained by limited validation cohort sizes, and mechanistic studies \r\nwere limited to male mice, which may restrict the generalisability of our \r\nfindings to female populations.\r\nFUNDING: National Natural Science Foundation of China, Key Project of the \r\nNatural Science Foundation of Jiangsu Provincial Higher Education Institutions, \r\nProject of Biomedical Basic Research Center (BBRC) of Jiangsu, Clinical Research \r\nCenter of Neurological Disease in The Second Affiliated Hospital of Soochow \r\nUniversity, Project of MOE Key Laboratory of Geriatric Diseases and Immunology, \r\nJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain \r\nDiseases; The Lingang Laboratory fund; Shanghai Science and Technology \r\nInnovation Sailing Special Project, and Shanghai Municipal Science and \r\nTechnology Major Project; Zhejiang Provincial Natural Science Foundation of \r\nChina.\r\n\r\nCopyright © 2026 The Author(s). Published by Elsevier B.V. All rights reserved.\r\n\r\nDOI: 10.1016/j.ebiom.2026.106325\r\nPMID: 42263400\r\n\r\nConflict of interest statement: Declaration of interests Linna Wang is employed \r\nby Lanzhou Biotechnique Development Co., Ltd. The authors declare no other \r\ncompeting interests.\r\n\r\n\r\n6. Neuron. 2026 Jun 8:S0896-6273(26)00369-7. doi: 10.1016/j.neuron.2026.04.046. \r\nOnline ahead of print.\r\n\r\nDevelopmental and age-related synapse elimination is mediated by glial \r\nCroquemort.\r\n\r\nJay TR(1), Kang Y(2), Ouellet-Massicotte V(2), Micael MKB(2), Kacouros-Perkins \r\nVL(2), Chen J(2), Sheehan A(2), Freeman MR(3).\r\n\r\nAuthor information:\r\n(1)Vollum Institute, Oregon Health & Science University, Portland, OR 97239, \r\nUSA. Electronic address: taylor-jay@uiowa.edu.\r\n(2)Vollum Institute, Oregon Health & Science University, Portland, OR 97239, \r\nUSA.\r\n(3)Vollum Institute, Oregon Health & Science University, Portland, OR 97239, \r\nUSA. Electronic address: freemmar@ohsu.edu.\r\n\r\nNeurons and glia work together to dynamically regulate neural circuit assembly \r\nand maintenance. In this study, we show that Drosophila exhibit large-scale \r\nsynapse formation and elimination as part of normal CNS circuit maturation and \r\nthat glia use conserved molecules to regulate these processes. Using a \r\nhigh-throughput ELISA-based in vivo screening assay, we identify new glial genes \r\nthat regulate synapse numbers in Drosophila in vivo, including the scavenger \r\nreceptor ortholog Croquemort (Crq). Crq acts as an essential regulator of \r\nglial-dependent synapse elimination during development, with glial Crq loss \r\nleading to excess CNS synapses and progressive seizure susceptibility in adults. \r\nLoss of Crq in glia also prevents age-related synaptic, but not neuronal, loss \r\nin the adult brain. This work provides new insights into the cellular and \r\nmolecular mechanisms that underlie synapse development and maintenance across \r\nthe lifespan and identifies glial Crq as a key regulator of these processes.\r\n\r\nCopyright © 2026 The Authors. Published by Elsevier Inc. All rights reserved.\r\n\r\nDOI: 10.1016/j.neuron.2026.04.046\r\nPMID: 42259289\r\n\r\nConflict of interest statement: Declaration of interests The authors declare no \r\ncompeting interests.\r\n\r\n\r\n7. Nat Commun. 2026 Jun 5. doi: 10.1038/s41467-026-74037-5. Online ahead of\r\nprint.\r\n\r\nMicroglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in \r\n5×FAD mice.\r\n\r\nZhou Q(#)(1)(2)(3), Sun F(#)(1), Zhang Y(4), Cao X(2)(3), Li M(1)(5), Yu H(1), \r\nJiang T(1), Li S(1), Wang W(1), Xie J(1), He T(1), Liu Y(1)(6), Ke D(1), Wang \r\nXC(1), Xu P(7), Liu E(8), Chen H(9)(10), Wang JZ(11)(12).\r\n\r\nAuthor information:\r\n(1)Key Laboratory of Education Ministry of China/Hubei Province for Neurological \r\nDisorders, Department of Pathophysiology, School of Basic Medicine, Tongji \r\nMedical College, Huazhong University of Science and Technology, Wuhan, China.\r\n(2)Department of Rehabilitation, Tongji Hospital, Tongji Medical College, \r\nHuazhong University of Science and Technology, Wuhan, China.\r\n(3)Stem Cell Research Center, Tongji Hospital, Tongji Medical College, Huazhong \r\nUniversity of Science and Technology, Wuhan, China.\r\n(4)Department of Endocrinology, Key Laboratory of Ministry of Education for \r\nNeurological Disorders, Li Yuan Hospital, Tongji Medical College, Huazhong \r\nUniversity of Science and Technology, Wuhan, China.\r\n(5)Department of Neurosurgery, The Central Hospital of Wuhan, Tongji Medical \r\nCollege, Huazhong University of Science and Technology, Wuhan, China.\r\n(6)Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong \r\nUniversity of Science and Technology, Wuhan, China.\r\n(7)Center of Clinical Laboratory Medicine, Zhongda Hospital, School of Medicine, \r\nAdvanced Institute for Life and Health, Southeast University, Nanjing, China.\r\n(8)Department of Pathology, The First Affiliated Hospital of Zhengzhou \r\nUniversity, Zhengzhou, China. liuenjie01@163.com.\r\n(9)Department of Rehabilitation, Tongji Hospital, Tongji Medical College, \r\nHuazhong University of Science and Technology, Wuhan, China. \r\nchenhong1129@hotmail.com.\r\n(10)Stem Cell Research Center, Tongji Hospital, Tongji Medical College, Huazhong \r\nUniversity of Science and Technology, Wuhan, China. chenhong1129@hotmail.com.\r\n(11)Key Laboratory of Education Ministry of China/Hubei Province for \r\nNeurological Disorders, Department of Pathophysiology, School of Basic Medicine, \r\nTongji Medical College, Huazhong University of Science and Technology, Wuhan, \r\nChina. wangjz@mail.hust.edu.cn.\r\n(12)Hubei Key Laboratory of Cognitive and Affective Disorders, Jianghan \r\nUniversity, Wuhan, China. wangjz@mail.hust.edu.cn.\r\n(#)Contributed equally\r\n\r\nMicroglia play crucial roles in Alzheimer's disease (AD), yet the molecular \r\nmechanisms are unclear. Here, we show that CD31, a recognized endothelial \r\nmarker, is predominantly expressed in microglia but not in neurons or \r\nastrocytes, and it is significantly elevated in the brains of AD patients and \r\nmouse models. Microglia-specific CD31 knockdown in 5xFAD mice substantially \r\nattenuated the dysregulated transcription networks, suppressed microglia \r\nhyperactivation and the disease-associated microglia (DAM), mitigated Aβ \r\ndeposition and inflammation, and eventually improved cognitive functions in \r\nmice. Mechanistically, CD31 knockdown damaged the simultaneous recruitment of \r\nSrc homology phosphatase 2 (SHP2) and STAT3, leading to a reduced \r\ndephosphorylation and enhanced activation of STAT3, a transcription factor. \r\nSTAT3 activation increased transcription of membrane metalloendopeptidase (MME) \r\nand promoted Aβ clearance. Collectively, this study identifies microglial CD31, \r\nby regulating SHP2-STAT3-MME axis, plays a role in AD pathogenesis and targeting \r\nCD31 is promising in AD drug development.\r\n\r\n© 2026. The Author(s).\r\n\r\nDOI: 10.1038/s41467-026-74037-5\r\nPMID: 42248891\r\n\r\nConflict of interest statement: Competing interests: The authors declare no \r\ncompeting interests.\r\n\r\n\r\n8. Mol Neurodegener. 2026 Jun 3. doi: 10.1186/s13024-026-00946-0. Online ahead of\r\n print.\r\n\r\nInsulin resistance alters cortical inhibitory neurons and microglia to \r\nexacerbate Alzheimer's knock-in mouse phenotypes.\r\n\r\nNicholson L(1)(2), Tang SJ(1)(2)(3), Karra T(1)(2)(4), Abouelatta H(1)(2)(5), \r\nStrittmatter SM(6)(7).\r\n\r\nAuthor information:\r\n(1)Departments of Neuroscience and Neurology, Yale School of Medicine, New \r\nHaven, CT, USA.\r\n(2)Program in Cellular Neuroscience, Neurodegeneration, and Repair, Yale School \r\nof Medicine, New Haven, CT, USA.\r\n(3)School of Medicine, University of California Davis Medical Center, \r\nSacramento, CA, USA.\r\n(4)Institute of Neuropathology, University Medical Centre Göttingen, 37077, \r\nGöttingen, Germany.\r\n(5)Department of Neuroscience and Behavior, Mount Holyoke College, South Hadley, \r\nMA, USA.\r\n(6)Departments of Neuroscience and Neurology, Yale School of Medicine, New \r\nHaven, CT, USA. stephen.strittmatter@yale.edu.\r\n(7)Program in Cellular Neuroscience, Neurodegeneration, and Repair, Yale School \r\nof Medicine, New Haven, CT, USA. stephen.strittmatter@yale.edu.\r\n\r\nUpdate of\r\n bioRxiv. 2025 Sep 10:2025.09.05.674487. doi: 10.1101/2025.09.05.674487.\r\n\r\nBACKGROUND: Metabolic dysfunction contributes to the risk and progression of \r\nAlzheimer's disease (AD), yet the cellular mechanisms linking impaired insulin \r\nsignaling and systemic metabolic stress to brain dysfunction remain incompletely \r\ndefined.\r\nMETHODS: We examined the impact of chronic high-fat, high-sugar (HFHS)-induced \r\ninsulin resistance on metabolic parameters, spatial learning and memory, and in \r\nvivo glial activation and neuropathology in Alzheimer's disease knock-in mice \r\nexpressing human mutant APP and wild-type (WT) tau. Single-nucleus RNA \r\nsequencing was performed to resolve cell-type-specific transcriptional \r\nresponses.\r\nRESULTS: HFHS-diet induced weight gain, hyperglycemia, and glucose intolerance \r\nin WT and AD knock-in mice as compared to control diet-fed mice. However, \r\nimpaired spatial learning was observed only in AD knock-in mice on the HFHS \r\ndiet, even though there was no greater amyloid-β deposition or tau \r\nphosphorylation than in control diet AD knock-in mice. Transcriptomic profiling \r\nrevealed that HFHS-fed AD mice engaged a distinct glial program, which we termed \r\nthe metabolic impairment in neurodegeneration (MinD) state, characterized by \r\nupregulation of genes involved in synaptic targeting and trans-synaptic \r\nsignaling shared across microglia, astrocytes, and oligodendrocytes. In \r\nparallel, we identified selective induction of the transcription factor Meis2 in \r\ncortical Layer 2 inhibitory neurons, which exhibited HFHS-diet transcriptional \r\nremodeling enriched for pathways regulating vesicle release, synaptic \r\norganization, and membrane excitability. These coordinated glial and neuronal \r\ntranscriptional changes were associated with reduced inhibitory synapse density \r\nin HFHS-fed AD mice.\r\nCONCLUSION: Diet-induced insulin resistance in AD knock-in mice is associated \r\nwith coordinated glial and inhibitory neuron transcriptional remodeling and \r\ncognitive impairment, without alteration of the classical amyloid and tau \r\npathology present in the AD mice fed a lean diet. These findings define cellular \r\nprograms linking systemic insulin metabolic dysfunction to cortical circuity \r\nvulnerability in AD.\r\n\r\n© 2026. The Author(s).\r\n\r\nDOI: 10.1186/s13024-026-00946-0\r\nPMID: 42237401\r\n\r\nConflict of interest statement: Declarations. Ethics approval and consent to \r\nparticipate: Not applicable. Consent for publication: Not applicable. Competing \r\ninterests: The authors declare no competing interests.\r\n\r\n\r\n9. Neuron. 2026 Jun 3;114(11):1884-1886. doi: 10.1016/j.neuron.2026.05.011.\r\n\r\nWho sets the brakes on anxiety? A role for astrocytic histamine 3 receptors.\r\n\r\nGómez-Sotres P(1), Mederos S(2).\r\n\r\nAuthor information:\r\n(1)Hospital del Mar Research Institute Barcelona (HMRIB), Barcelona, Spain.\r\n(2)Hospital del Mar Research Institute Barcelona (HMRIB), Barcelona, Spain. \r\nElectronic address: smederos@researchmar.net.\r\n\r\nHistamine has long been linked to anxiety, yet its effects vary across brain \r\nregions and conditions, indicating that its site of action remains unresolved. \r\nIn this issue of Neuron, Li et al. 1 identify astrocytic H3 receptors in ventral \r\nCA1 as key cellular mechanisms, where histaminergic input triggers glial GABA \r\nrelease to suppress anxiety-like behavior.\r\n\r\nCopyright © 2026 Elsevier Inc. All rights reserved.\r\n\r\nDOI: 10.1016/j.neuron.2026.05.011\r\nPMID: 42235487\r\n\r\nConflict of interest statement: Declaration of interests The authors declare no \r\ncompeting interests.\r\n", "tool_calls_made": 0, "duration_seconds": 0.81}

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