论文推荐-08-PD · Jun 11 08:06

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{"output": "1. EBioMedicine. 2026 Jun 9;129:106325. doi: 10.1016/j.ebiom.2026.106325. Online \nahead of print.\n\nThe complement C3-microglial axis in depression of Parkinson's disease: from \nmechanism to therapeutic intervention.\n\nYin Q(1), Ding M(2), Tang Y(3), Qi Y(4), Qin Y(4), Jin H(1), Li Y(5), Bao J(1), \nMa S(1), Li Y(1), Ding H(2), An X(2), Qiao E(1), Tang Y(1), Zhang Q(1), Wang \nL(6), Shao J(7), Feng J(3), Hu LF(8), Wang J(9), Fang P(10), Luo W(11), Cong \nQ(12).\n\nAuthor information:\n(1)Department of Neurology and Clinical Research Center of Neurological Disease, \nThe Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.\n(2)Institute of Molecular Enzymology, School of Life Sciences, Suzhou Medical \nCollege, Soochow University, Suzhou, 215123, China.\n(3)Institute of Science and Technology for Brain-Inspired Intelligence, Fudan \nUniversity, Shanghai, 201203, China.\n(4)Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain \nDiseases, Institute of Neuroscience, Soochow University, Suzhou, 215123, China.\n(5)Department of Neurology, Huzhou Central Hospital, The Fifth School of \nClinical Medicine of Zhejiang Chinese Medical University, Huzhou, 313000, China.\n(6)Lanzhou Biotechnique Development Co., Ltd., Lanzhou, Gansu, 730000, China.\n(7)Department of Neurology, The Third People's Hospital of Zhangjiagang City, \nSuzhou, 215600, Jiangsu, China.\n(8)Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain \nDiseases, Institute of Neuroscience, Soochow University, Suzhou, 215123, China. \nElectronic address: hulifang@suda.edu.cn.\n(9)Institute of Science and Technology for Brain-Inspired Intelligence, Fudan \nUniversity, Shanghai, 201203, China. Electronic address: wangjing_@fudan.edu.cn.\n(10)Institute of Molecular Enzymology, School of Life Sciences, Suzhou Medical \nCollege, Soochow University, Suzhou, 215123, China; State Key Laboratory of \nChemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of \nSciences, Shanghai, 200032, China. Electronic address: panfang@sioc.ac.cn.\n(11)Department of Neurology and Clinical Research Center of Neurological \nDisease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, \nChina. Electronic address: lwfwxx@126.com.\n(12)Department of Neurology and Clinical Research Center of Neurological \nDisease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, \nChina; Jiangsu Key Laboratory of Drug Discovery and Translational Research for \nBrain Diseases, Institute of Neuroscience, Soochow University, Suzhou, 215123, \nChina; Biomedical Basic Research Center (BBRC) of Jiangsu, Soochow University, \nSuzhou, 215123, China; Department of Nephrology, The Second Affiliated Hospital \nof Soochow University, Suzhou, 215004, China; Institute of Neurological \nDiseases, Soochow University-Suzhou Blue Cross Brain Hospital, Soochow \nUniversity, Suzhou, 215123, China; School of Life Sciences, MOE Key Laboratory \nof Geriatric Diseases and Immunology, Suzhou Medical College of Soochow \nUniversity, Soochow University, Suzhou, 215123, China. Electronic address: \nqfcong@suda.edu.cn.\n\nBACKGROUND: Depression is a common and early non-motor symptom of Parkinson's \ndisease (PD) with significant sexual dimorphism, yet its underlying molecular \nmechanisms remain poorly understood. This study aimed to elucidate the \nsex-specific plasma proteomic profiles of depression in patients with PD (DPD) \nand to investigate the role of complement-mediated synaptic pruning in its \npathophysiology.\nMETHODS: Plasma proteomic analysis was performed on data from the Parkinson's \nProgression Markers Initiative (PPMI) and an independent validation cohort, \nstratified by sex. Functional enrichment analyses identified dysregulated \npathways. A chronic MPTP/probenecid-induced mouse model of PD was used to \nvalidate findings. Behavioural tests assessed motor and depressive-like \nphenotypes. Proteomic, biochemical, and imaging techniques were used to evaluate \nprotein expression, synapse density, and microglial phagocytosis. The \ntherapeutic mechanism of Botulinum Neurotoxin A (BoNT/A) on DPD was investigated \nin wild-type, C3-/- and C3aR-/- mice and in microglial cultures.\nFINDINGS: Proteomic profiling revealed both conserved complement-driven immune \ndysfunction and profound sex-divergent molecular perturbations underlying PD and \nDPD. Complement and coagulation cascades were consistently upregulated in both \nsexes. In MPTP-treated male and female mice, hippocampal complement components \n(C1Q, C3, C3aR) and downstream signalling (p-STAT3, p-P65) were elevated, \naccompanied by microglial synapse phagocytosis and depressive-like behaviours. \nGenetic deletion of C3 rescued both MPTP-induced motor and depressive-like \nbehavioural deficits and prevented hippocampal synaptic loss associated with \nmicroglial synaptic engulfment. BoNT/A treatment alleviated depressive-like \nbehaviours and reduced microglial synaptic engulfment in an MPTP model; these \ntherapeutic effects were abolished in C3-/- and C3aR-/- mice. Single-cell RNA \nsequencing and in vitro phagocytosis assay confirmed that BoNT/A modulated \nphagocytosis-related microglial subclusters.\nINTERPRETATION: DPD exhibits distinct sex-specific immune signatures, with \nconvergent complement pathway activation driving microglial synaptic pruning and \ndepressive symptoms. The antidepressant effect of BoNT/A is mediated through \ninhibition of the C3-C3aR signalling axis. These findings highlight the \npotential for sex-stratified diagnostics and complement-targeted therapies for \ndepression in patients with PD. A key limitation is that our clinical analyses \nwere constrained by limited validation cohort sizes, and mechanistic studies \nwere limited to male mice, which may restrict the generalisability of our \nfindings to female populations.\nFUNDING: National Natural Science Foundation of China, Key Project of the \nNatural Science Foundation of Jiangsu Provincial Higher Education Institutions, \nProject of Biomedical Basic Research Center (BBRC) of Jiangsu, Clinical Research \nCenter of Neurological Disease in The Second Affiliated Hospital of Soochow \nUniversity, Project of MOE Key Laboratory of Geriatric Diseases and Immunology, \nJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain \nDiseases; The Lingang Laboratory fund; Shanghai Science and Technology \nInnovation Sailing Special Project, and Shanghai Municipal Science and \nTechnology Major Project; Zhejiang Provincial Natural Science Foundation of \nChina.\n\nCopyright © 2026 The Author(s). Published by Elsevier B.V. All rights reserved.\n\nDOI: 10.1016/j.ebiom.2026.106325\nPMID: 42263400\n\nConflict of interest statement: Declaration of interests Linna Wang is employed \nby Lanzhou Biotechnique Development Co., Ltd. The authors declare no other \ncompeting interests.\n\n\n2. Microsyst Nanoeng. 2026 Jun 10;12(1):225. doi: 10.1038/s41378-026-01209-0.\n\nA microfluidic platform for whole-membrane integrity profiling in live neuronal \ncells.\n\nRyser T(1), Krichene A(1), Marchi N(1), Espinal FR(1), Mahul-Mellier AL(2)(3), \nLashuel HA(4)(5)(6), Guiducci C(7).\n\nAuthor information:\n(1)Laboratory of Life Science Electronics, École polytechnique fédérale de \nLausanne (EPFL), Lausanne, Switzerland.\n(2)Laboratory of Molecular and Chemical Biology of Neurodegeneration, EPFL, \nLausanne, Switzerland.\n(3)Lipid Cell Biology Laboratory, EPFL, Lausanne, Switzerland.\n(4)Laboratory of Molecular and Chemical Biology of Neurodegeneration, EPFL, \nLausanne, Switzerland. halashuel@qf.org.qa.\n(5)Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar. \nhalashuel@qf.org.qa.\n(6)Department of Neurology, Weill Cornell Medicine, New York, NY, USA. \nhalashuel@qf.org.qa.\n(7)Laboratory of Life Science Electronics, École polytechnique fédérale de \nLausanne (EPFL), Lausanne, Switzerland. carlotta.guiducci@epfl.ch.\n\nStructural and functional compromise of the cellular membrane is a central \nmechanism in the pathogenesis of numerous diseases, including neurodegenerative \ndisorders such as Alzheimer's and Parkinson's disease. However, existing \ntechniques for assessing membrane integrity often lack the ability to provide \ndynamic, whole-cell measurements and are limited to localized damage detection \nor population-level analysis. There is a growing need for methods capable of \nmonitoring membrane integrity over time at the single-cell level and across the \nentire membrane surface. In this study, we present a microfluidic platform for \nreal-time, label-free assessment of membrane integrity by analyzing dielectric \nproperties. We apply this system to investigate how different aggregated forms \nof α-Synuclein (aSyn), a protein that plays a central role in the pathogenesis \nof Parkinson's disease and disrupts neuronal membranes. Our platform integrates \nelectrokinetic microdevices with 3D microelectrodes and imaging, enabling \ncontinuous analysis of up to 30 live neuronal cells per hour in flow. By \nmeasuring electrorotation responses, we quantify changes in plasma membrane \ncapacitance in response to monomeric, oligomeric, and fibrillar aSyn. This \napproach allows direct, time-resolved comparison of membrane-disruptive effects \nacross different aSyn conformations with single-cell resolution and \nwhole-membrane sensitivity.\n\n© 2026. The Author(s).\n\nDOI: 10.1038/s41378-026-01209-0\nPMID: 42265078\n\nConflict of interest statement: Conflict of interest: The authors declare no \ncompeting interests.", "exit_code": 0, "error": null}

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{"status": "success", "output": "PMID: 42259820\r\nTitle: Ultrastructural diversity and subcellular organization of nigral Lewy pathology in Parkinson's disease.\r\nJournal: Nat Commun | Date: 2026 Jun 8 | Type: Journal Article\r\nDOI: 10.1038/s41467-026-74083-z\r\n---\r\nPMID: 42234754\r\nTitle: Charting the human-specific properties of gene expression networks in the infant prefrontal cortex.\r\nJournal: Sci Adv | Date: 2026 Jun 5 | Type: Comparative Study, Journal Article\r\nDOI: 10.1126/sciadv.aea3316\r\n---\r\nPMID: 42217054\r\nTitle: GRP78 associates with alpha-synuclein in vulnerable neurons of the Parkinson's disease brain.\r\nJournal: Acta Neuropathol | Date: 2026 May 30 | Type: Letter\r\nDOI: 10.1007/s00401-026-03034-1\r\n---\r\nPMID: 42215465\r\nTitle: Large-scale analysis of temporal gene expression variation in peripheral blood.\r\nJournal: Nat Commun | Date: 2026 May 29 | Type: Journal Article\r\nDOI: 10.1038/s41467-026-73218-6\r\n---\r\nPMID: 42213896\r\nTitle: Clinical markers of disease progression in the prodromal to overt alpha-synucleinopathy continuum.\r\nJournal: Brain | Date: 2026 May 29 | Type: Journal Article\r\nDOI: 10.1093/brain/awag193\r\n---\r\nPMID: 42213789\r\nTitle: Action and rest tremor map to distinct networks within the primary motor cortex.\r\nJournal: Cell Rep | Date: 2026 May 28 | Type: Journal Article\r\nDOI: 10.1016/j.celrep.2026.117404\r\n---\r\nPMID: 42209780\r\nTitle: Gut microbiome screens could identify risk of Parkinson's disease years before symptoms appear.\r\nJournal: Nat Med | Date: 2026 May 28 | Type: Journal Article\r\nDOI: 10.1038/s41591-026-04458-8\r\n---\r\nPMID: 42204590\r\nTitle: Cholesterol metabolism in neurodegenerative diseases: mechanisms and therapeutic advances.\r\nJournal: Mol Neurodegener | Date: 2026 May 28 | Type: Journal Article, Review\r\nDOI: 10.1186/s13024-026-00951-3\r\n---\r\nPMID: 42186854\r\nTitle: Is SORL1 a common genetic target across neurodegenerative diseases? A multi-ancestry biobank study.\r\nJournal: Brain | Date: 2026 May 26 | Type: Journal Article\r\nDOI: 10.1093/brain/awag187\r\n---\r\nPMID: 42166327\r\nTitle: Knockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal autophagy and exacerbates alpha-synuclein aggr\r\nJournal: Cell Rep | Date: 2026 May 21 | Type: Journal Article\r\nDOI: 10.1016/j.celrep.2026.117364\r\n---\r\nPMID: 42161331\r\nTitle: Large-scale antagonistic cerebral networks drive amplitude variability in Parkinson's disease tremor.\r\nJournal: Brain | Date: 2026 May 20 | Type: Journal Article\r\nDOI: 10.1093/brain/awag182\r\n---\r\nPMID: 42161327\r\nTitle: CYP2D6 variants in amyotrophic lateral sclerosis: an association study of risk and survival.\r\nJournal: Brain | Date: 2026 May 20 | Type: Journal Article\r\nDOI: 10.1093/brain/awag178\r\n---\r\nPMID: 42160433\r\nTitle: The immunoproteome and multimorbidity: A Mendelian randomization study.\r\nJournal: Sci Adv | Date: 2026 May 22 | Type: Journal Article\r\nDOI: 10.1126/sciadv.adz7117\r\n---\r\nPMID: 42157002\r\nTitle: A multimodal biomarker strategy to enhance diagnostic precision in neurodegenerative parkinsonism.\r\nJournal: Nat Med | Date: 2026 May 19 | Type: Journal Article\r\nDOI: 10.1038/s41591-026-04398-3\r\n---\r\n", "tool_calls_made": 0, "duration_seconds": 1.22}

{"status": "success", "output": "1. Nat Commun. 2026 Jun 8. doi: 10.1038/s41467-026-74083-z. Online ahead of\r\nprint.\r\n\r\nUltrastructural diversity and subcellular organization of nigral Lewy pathology \r\nin Parkinson's disease.\r\n\r\nLewis AJ(1)(2), van den Heuvel L(3)(4), Di Fabrizio M(3)(4), Bandelier K(3), \r\nProniakova D(3), Burger D(3)(4)(5), Shafiei N(3)(4), Ekundayo K(3)(4), Offringa \r\nS(3), Huisman E(6), Bol JG(6), van de Berg WD(6)(7), Stahlberg H(3)(4).\r\n\r\nAuthor information:\r\n(1)Laboratory of Biological Electron Microscopy, School of Basic Sciences, \r\nFederal Institute of Technology Lausanne (EPFL), Lausanne, Switzerland. \r\namanda.lewis@epfl.ch.\r\n(2)Department of Fundamental Microbiology, University of Lausanne, Lausanne, \r\nSwitzerland. amanda.lewis@epfl.ch.\r\n(3)Laboratory of Biological Electron Microscopy, School of Basic Sciences, \r\nFederal Institute of Technology Lausanne (EPFL), Lausanne, Switzerland.\r\n(4)Department of Fundamental Microbiology, University of Lausanne, Lausanne, \r\nSwitzerland.\r\n(5)F. Hoffmann-La Roche Ltd, Pharma Research and Early Development, \r\nGrenzacherstrasse 124, Basel, Switzerland.\r\n(6)Department of Anatomy and Neurosciences, section Clinical Neuroanatomy and \r\nBiobanking, Amsterdam Neuroscience, Amsterdam University Medical Centre, Vrije \r\nUniversity Amsterdam, Amsterdam, The Netherlands.\r\n(7)Amsterdam Neuroscience program Neurodegeneration, Amsterdam University \r\nMedical Centre, Vrije University Amsterdam, Amsterdam, The Netherlands.\r\n\r\nLewy bodies, the defining pathological feature of Parkinson's disease, are \r\nintraneuronal inclusions enriched in aggregated alpha-synuclein (αSyn). We used \r\ncorrelative light and electron microscopy to selectively investigate \r\nphosphorylated αSyn (αSynpS129)-positive inclusions in the substantia nigra of \r\nend-stage postmortem Parkinson's disease brain. Here we show that somatic \r\nαSynpS129 inclusions in nigral dopaminergic neurons are consistently fibrillar, \r\nwhereas the membranous-type inclusions are restricted to neuritic processes. \r\nThese neuritic inclusions displayed marked ultrastructural heterogeneity, \r\nranging from predominantly membranous to mixed membranous-fibrillar forms. The \r\nselective targeting of defined inclusions enabled detailed structural \r\ncharacterization of Lewy pathology, rather than quantitative or disease-stage \r\ncomparisons. Our findings highlight clear ultrastructural differences between \r\nsomatic and neuritic αSynpS129 pathology and demonstrate the structural \r\ncomplexity and heterogeneity of Lewy pathology in human Parkinson's disease \r\nbrain.\r\n\r\n© 2026. The Author(s).\r\n\r\nDOI: 10.1038/s41467-026-74083-z\r\nPMID: 42259820\r\n\r\nConflict of interest statement: Competing interests: DB is an employee of \r\nF.Hoffman-La Roche Ltd.; the work reported here was conducted prior to the \r\ncommencement of this employment. WVdB is a recipient of ‘ProPARK’, a \r\npublic–private partnership receiving funding from ZonMW (40-46000-98-101), \r\nHersenstichting, Parkinson Vereniging, PHARMO Institute NV, Stichting Woelse \r\nWaard, Stichting Alkemade-Keuls fonds, CHDR, ABBVIE, Hoffman-La Roche and \r\nOccamzRazor. WVdB received funding for a public–private partnership ‘CONCERT’ \r\nand ‘ADAPT-PD’ from Health~Holland, Topsector Life Sciences & Health in \r\ncollaboration with Roche and Genentech. WVdB performed contract research for \r\nRoche Tissue Diagnostics, Discoveric Bio Alpha, AC Immune and Gain Therapeutics. \r\nAll funding has been paid to Amsterdam UMC. WVdB is a member of the scientific \r\nadvisory board of Gain Therapeutics, Alzheimer Nederland and PACE Lundbeck \r\nFoundation Parkinson’s Disease Research Center. WVdB is the president of the \r\nDutch association for Parkinson Scientists and a member of the board of the \r\nParkinsonalliance Netherlands. The remaining authors declare no competing \r\ninterests.\r\n\r\n\r\n2. Acta Neuropathol. 2026 May 30;151(1):64. doi: 10.1007/s00401-026-03034-1.\r\n\r\nGRP78 associates with alpha-synuclein in vulnerable neurons of the Parkinson's \r\ndisease brain.\r\n\r\nHrabos D(1)(2)(3), Mrowiecova A(4), Cicmancova J(4), Ehrmann J(5).\r\n\r\nAuthor information:\r\n(1)Department of Clinical and Molecular Pathology, Palacky University Olomouc \r\nand University Hospital Olomouc, Hněvotínská 3, 779 00, Olomouc, Czech Republic. \r\ndominik.hrabos@upol.cz.\r\n(2)Department of Neurology, Palacky University Olomouc and University Hospital \r\nOlomouc, Olomouc, Czech Republic. dominik.hrabos@upol.cz.\r\n(3)Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech \r\nRepublic. dominik.hrabos@upol.cz.\r\n(4)Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech \r\nRepublic.\r\n(5)Department of Clinical and Molecular Pathology, Palacky University Olomouc \r\nand University Hospital Olomouc, Hněvotínská 3, 779 00, Olomouc, Czech Republic.\r\n\r\nDOI: 10.1007/s00401-026-03034-1\r\nPMID: 42217054\r\n\r\nConflict of interest statement: Declarations. Conflict of interest: The authors \r\ndeclare no competing interests. Ethics statement: This study was approved by the \r\nEthics Committee of University Hospital Olomouc and the Faculty of Medicine and \r\nDentistry, Palacky University Olomouc (reference no. 17/21). Human tissue \r\nsamples were obtained in accordance with Czech legislation (Act No. 373/2011 and \r\nits amendment, Act No. 202/2017).\r\n\r\n\r\n3. Brain. 2026 May 29:awag193. doi: 10.1093/brain/awag193. Online ahead of print.\r\n\r\nClinical markers of disease progression in the prodromal to overt \r\nalpha-synucleinopathy continuum.\r\n\r\nRoascio M(1), Antelmi E(2), Baldelli L(3)(4), Biscarini F(3)(4), Bonanni E(5), \r\nBrunetti V(6)(7), Capriglia E(8), Geromino C(9)(10), Casoni F(11), Cirillo \r\nF(12), Della Marca G(6)(7), Di Laudo F(3), Ferini-Strambi L(13), Fernandes \r\nM(14), Figorilli M(9)(10), Galbiati A(13), Gigli GL(15), Guarnieri B(16)(17), \r\nHoxhaj D(5), Lanza G(18)(19), Liguori C(12)(14)(20), Tassoni MM(5), Maio S(14), \r\nMalomo G(8), Marelli S(13)(21), Mattioli P(22)(23), Mulas M(9)(10), Orso B(22), \r\nPardini M(22)(23), Plazzi G(4)(24), Provini F(3)(4), Pellitteri G(25), \r\nPuligheddu M(9)(10), Terzaghi M(8)(26), Pelletier A(27)(28), Postuma \r\nRB(27)(28)(29), Arnulfo G(1)(30), Arnaldi D(22)(23).\r\n\r\nAuthor information:\r\n(1)Department of Informatics, Bioengineering, Robotics and System Engineering \r\n(DIBRIS), University of Genoa, 16145 Genoa, Italy.\r\n(2)Department of Engineering for Innovative Medicine, University of Verona, \r\n37134 Verona, Italy.\r\n(3)Department of Biomedical and Neuromotor Sciences, University of Bologna, \r\n40138 Bologna, Italy.\r\n(4)IRCCS, Istituto delle Scienze Neurologiche di Bologna, 40124 Bologna, Italy.\r\n(5)Neurology Unit, Department of Clinical and Experimental Medicine, University \r\nof Pisa, 56126 Pisa, Italy.\r\n(6)UOC di Neurologia, Dipartimento di Neuroscienze, Organi di Senso e Torace, \r\nFondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.\r\n(7)Department of Neurosciences, Università Cattolica del Sacro Cuore, 00168 \r\nRome, Italy.\r\n(8)Department of Brain and Behavioral Sciences, University of Pavia, 27100 \r\nPavia, Italy.\r\n(9)Interdepartmental Sleep Medicine Centre, University of Cagliari, Cagliari \r\n09124, Italy.\r\n(10)Neurology Unit, Azienda Ospedaliero-Universitaria, 09042 Cagliari, Italy.\r\n(11)Sleep Disorders Centre, Department of Clinical Neurosciences, IRCCS San \r\nRaffaele Hospital, 20127 Milan, Italy.\r\n(12)Neurology Unit, University Hospital of Rome Tor Vergata, 00133 Rome, Italy.\r\n(13)Vita-Salute San Raffaele University, 20132 Milan, Italy.\r\n(14)Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, \r\nItaly.\r\n(15)Neurology, Department of Medicine (DMED), University of Udine, 33100 Udine, \r\nItaly.\r\n(16)Center of Sleep Medicine, Villa Serena Hospital, Città S. Angelo, 65013 \r\nPescara, Italy.\r\n(17)Fondazione Villaserena per la ricerca, Città S. Angelo, 65013 Pescara, \r\nItaly.\r\n(18)Clinical Neurophysiology Research Unit and Sleep Research Centre, Oasi \r\nResearch Institute-IRCCS, 94018 Troina, Italy.\r\n(19)Department of Surgery and Medical-Surgical Specialties, University of \r\nCatania, 95123 Catania, Italy.\r\n(20)IRCCS Neuromed, 86077 Pozzilli, IS, Italy.\r\n(21)Sleep Disorders Centre, \r\n", "tool_calls_made": 0, "duration_seconds": 0.81}

{"status": "success", "output": "1. Nat Med. 2026 May 28. doi: 10.1038/s41591-026-04458-8. Online ahead of print.\r\n\r\nGut microbiome screens could identify risk of Parkinson's disease years before \r\nsymptoms appear.\r\n\r\n[No authors listed]\r\n\r\nDOI: 10.1038/s41591-026-04458-8\r\nPMID: 42209780\r\n\r\n\r\n2. Cell Rep. 2026 May 21;45(6):117364. doi: 10.1016/j.celrep.2026.117364. Online \r\nahead of print.\r\n\r\nKnockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal \r\nautophagy and exacerbates alpha-synuclein aggregation.\r\n\r\nFricke M(1), Mechel A(1), Evers L(1), Twellsieck B(1), Grein JM(1), Cima-Omori \r\nMS(2), Al-Azzani M(3), Outeiro TF(4), Zweckstetter M(5), Holzbaur ELF(6), \r\nBoecker CA(7).\r\n\r\nAuthor information:\r\n(1)University Medical Center Goettingen, Department of Neurology, 37077 \r\nGoettingen, Germany.\r\n(2)German Center for Neurodegenerative Diseases (DZNE), 37075 Goettingen, \r\nGermany.\r\n(3)University Medical Center Goettingen, Department of Experimental \r\nNeurodegeneration, Center for Biostructural Imaging of Neurodegeneration, 37073 \r\nGoettingen, Germany.\r\n(4)German Center for Neurodegenerative Diseases (DZNE), 37075 Goettingen, \r\nGermany; University Medical Center Goettingen, Department of Experimental \r\nNeurodegeneration, Center for Biostructural Imaging of Neurodegeneration, 37073 \r\nGoettingen, Germany; Faculdade de Medicina e Ciências Biomédicas, Algarve \r\nBiomedical Center Research Institute (ABC-Ri), Universidade do Algarve, 8005-139 \r\nFaro, Portugal; Translational and Clinical Research Institute, Faculty of \r\nMedical Sciences, Newcastle University, NE2 4HH Newcastle upon Tyne, UK.\r\n(5)German Center for Neurodegenerative Diseases (DZNE), 37075 Goettingen, \r\nGermany; Department for NMR-based Structural Biology, Max Planck Institute for \r\nMultidisciplinary Sciences, 37077 Goettingen, Germany.\r\n(6)Department of Physiology, Perelman School of Medicine, University of \r\nPennsylvania, Philadelphia, PA 19104, USA.\r\n(7)University Medical Center Goettingen, Department of Neurology, 37077 \r\nGoettingen, Germany. Electronic address: \r\nalexander.boecker@med.uni-goettingen.de.\r\n\r\nParkinson disease (PD)-associated mutations in the LRRK2 gene hyperactivate \r\nLRRK2 kinase activity, leading to increased phosphorylation of a subset of RAB \r\nGTPases, which are master regulators of intracellular trafficking. In neurons, \r\nprocessive retrograde transport of autophagosomes is essential for autophagosome \r\nmaturation and effective degradation of autophagosomal cargo in the axon. Here, \r\nwe show that knockout of the LRRK2-counteracting RAB phosphatase PPM1H causes a \r\ngene-dose-dependent disruption of the axonal transport of autophagosomes, \r\nleading to impaired degradation of axonal alpha-synuclein (aSyn), a key protein \r\nin PD pathophysiology. Defective autophagosome transport and impaired aSyn \r\ndegradation correlate with increased aSyn aggregation in primary PPM1H knockout \r\nneurons exposed to preformed fibrils of aSyn, an effect that is dependent on \r\nLRRK2 kinase activity. These findings mechanistically link LRRK2-mediated RAB \r\nhyperphosphorylation to defective autophagosomal degradation and enhanced \r\naggregation of aSyn, positioning the LRRK2-RAB axis as a key driver of PD \r\npathophysiology.\r\n\r\nCopyright © 2026 The Author(s). Published by Elsevier Inc. All rights reserved.\r\n\r\nDOI: 10.1016/j.celrep.2026.117364\r\nPMCID: PMC13196427\r\nPMID: 42166327\r\n\r\nConflict of interest statement: Declaration of interests The authors declare no \r\ncompeting interests.\r\n\r\n\r\n3. Nat Med. 2026 May 19. doi: 10.1038/s41591-026-04398-3. Online ahead of print.\r\n\r\nA multimodal biomarker strategy to enhance diagnostic precision in \r\nneurodegenerative parkinsonism.\r\n\r\nMartinez-Valbuena I(1)(2)(3), Emamikhah M(2)(4), Olszewska DA(4)(5), Weber \r\nSK(6)(7), Schnell S(7), Fereshtehnejad SM(4), Reyes NGD(2)(4), Sousa M(4)(8), Di \r\nLuca DG(4)(9), Ta J(1)(3), Anastassiadis C(1)(3)(10), Li J(1), Sasitharan \r\nJ(2)(4), Bhakta P(2)(4), Visanji NP(1)(2)(3)(4)(11), Fox SH(2)(3)(4)(12), \r\nMollenhauer B(6)(7), Tartaglia MC(1)(2)(3)(10)(12), Kovacs GG(1)(2)(3)(4)(11), \r\nLang AE(13)(14)(15)(16)(17).\r\n\r\nAuthor information:\r\n(1)Tanz Centre for Research in Neurodegenerative Diseases, University of \r\nToronto, Toronto, Ontario, Canada.\r\n(2)Rossy Progressive Supranuclear Palsy Centre, Toronto Western Hospital, \r\nToronto, Ontario, Canada.\r\n(3)Krembil Brain Institute, University Health Network, Toronto, Ontario, Canada.\r\n(4)Edmond J. Safra Program in Parkinson's Disease and the Morton and Gloria \r\nShulman Movement Disorders Clinic, Toronto Western Hospital, Toronto, Ontario, \r\nCanada.\r\n(5)Dept of Medicine, University College Cork, Cork, Ireland.\r\n(6)Department of Neurology, University Medical Center Goettingen, Goettingen, \r\nGermany.\r\n(7)Paracelsus-Elena-Klinik, Kassel, Germany.\r\n(8)Department of Neurology, Bern University Hospital and University of Bern, \r\nBern, Switzerland.\r\n(9)Department of Neurology, Washington University in St. Louis, St. Louis, MO, \r\nUSA.\r\n(10)University Health Network Memory Clinic, Toronto Western Hospital, Toronto, \r\nOntario, Canada.\r\n(11)Department of Laboratory Medicine and Pathobiology, University of Toronto, \r\nToronto, Ontario, Canada.\r\n(12)Division of Neurology, Department of Medicine, University of Toronto, \r\nToronto, Ontario, Canada.\r\n(13)Tanz Centre for Research in Neurodegenerative Diseases, University of \r\nToronto, Toronto, Ontario, Canada. anthony.lang@uhn.ca.\r\n(14)Rossy Progressive Supranuclear Palsy Centre, Toronto Western Hospital, \r\nToronto, Ontario, Canada. anthony.lang@uhn.ca.\r\n(15)Krembil Brain Institute, University Health Network, Toronto, Ontario, \r\nCanada. anthony.lang@uhn.ca.\r\n(16)Edmond J. Safra Program in Parkinson's Disease and the Morton and Gloria \r\nShulman Movement Disorders Clinic, Toronto Western Hospital, Toronto, Ontario, \r\nCanada. anthony.lang@uhn.ca.\r\n(17)Division of Neurology, Department of Medicine, University of Toronto, \r\nToronto, Ontario, Canada. anthony.lang@uhn.ca.\r\n\r\nDifferential diagnosis of neurodegenerative parkinsonian syndromes is \r\ncomplicated by overlapping clinical features and frequent co-pathology that \r\nchallenges the interpretation of single-protein biomarkers. We evaluated a \r\nmultimodal, minimally invasive biomarker strategy integrating dermal α-synuclein \r\nand 4-repeat tau seed amplification assays (SAAs) with serum neurofilament light \r\nchain. In a prospective cohort of 166 participants (Parkinson's disease, n = 40; \r\nmultiple system atrophy, n = 29; progressive supranuclear palsy (PSP), n = 77; \r\nhealthy controls, n = 20) with independent external validation (63 \r\nparticipants), α-synuclein SAA identified synucleinopathies with high \r\nsensitivity but was positive in a subset of PSP, which is consistent with \r\nα-synuclein co-pathology. Dermal 4-repeat tau SAA identified PSP with high \r\nsensitivity and specificity. Serum neurofilament light chain distinguished \r\nmultiple system atrophy from Parkinson's disease and correlated with disease \r\nseverity in PSP. Integrating these complementary biomarkers improved diagnostic \r\ndiscrimination compared with individual markers and enabled further \r\nstratification within PSP. These findings support a multimodal biomarker \r\napproach for biologically informed diagnosis of parkinsonian syndromes.\r\n\r\n© 2026. The Author(s), under exclusive licence to Springer Nature America, Inc.\r\n\r\nDOI: 10.1038/s41591-026-04398-3\r\nPMID: 42157002\r\n\r\nConflict of interest statement: Competing interests: I.M.-V., G.G.K. and A.E.L. \r\nshare a pending patent for diagnostic assays for movement disorders \r\n(18/537,455). G.G.K. has a shared patent for the 5G4 synuclein antibody. Outside \r\nthe submitted work, I.M.-V. receives funding from the Michael J. Fox Foundation \r\nfor Parkinson Research and consultancy fees from Ferrer. D.A.O. receives \r\nresearch funding from the Michael J. Fox Foundation for Parkinson Research. \r\nN.G.D.R. is a recipient of the Brain and Behavior Research Foundation Young \r\nInvestigator Award and Ontario Graduate Scholarship. M.S. has received \r\nfellowship funding from the Dystonia Medical Research Foundation of Canada and \r\nis supported by grants from the Swiss National Science Foundation, Parkinson \r\nSchweiz and the Gottfried und Julia Bangerter-Rhyner Foundation. He has also \r\nreceived financial support from Boston Scientific, Medtronic, Zambon and Bial. \r\nS.H.F. receives research Funding from the Michael J. Fox Foundation for \r\nParkinson Research, the NIH (Dystonia Coalition), Parkinson Canada and the \r\nWeston Foundation; honoraria from the International Parkinson and Movement \r\nDisorder Society; consultancy/speaker fees from Abbvie, Lundbeck and Sunovion; \r\nand Royalties from Oxford University Press. B.M. has received honoraria for \r\nconsultancy or educational presentations from GE Healthcare, Bial, Roche, \r\nBiogen, AbbVie, Desitin and Amprion. B.M. is a member of the executive steering \r\ncommittee of the Parkinson Progression Marker Initiative of the Michael J. Fox \r\nFoundation for Parkinson’s Research and has received research funding from \r\nAligning Science Across Parkinson’s disease (Aligning Sciences Across \r\nParkinson’s, Collaborative Research Network). M.C.T. receives funding from the \r\nNIH, the Weston Brain Foundation, the Tanenbaum Institute for Research in \r\nScience of Sport, the Canadian Institutes of Health Research and in-kind funding \r\nfrom Roche; she has served as an advisor to Eisai, Lilly and Novo Nordisk, and \r\nshe conducts clinical trials for Biogen, Anavex, Janssen, Novo Nordisk, Bristol \r\nMyers Squibb, Aribio, Green Valley, UCB and Passage Bio. G.G.K. reports personal \r\nfees from Parexel, Mitsubishi-Tanabe, Ferrer and Treventis, and other funding \r\nfrom the MSA Coalition, the Michael J. Fox Foundation, Parkinson Canada, the \r\nNIH, the Canada Foundation for Innovation and the Ontario Research Fund; in \r\naddition, G.G.K. received royalties from Wiley, Univ. of Cambridge, Taylor & \r\nFrancis and Elsevier. A.E.L. has served as an advisor for AbbVie, Amylyx, \r\nAprinoia, Biogen, BioAdvance, Biohaven, BioVie, BlueRock, Bristol Myers Squibb, \r\nDenali, EG427, Ferrer, Janssen, Lilly, Northera, Pharma 2B, Sun Pharma, UCB and \r\nVentyx Bio; received honoraria from Sun Pharma and AbbVie; received grants from \r\nBrain Canada, the Canadian Institutes of Health Research, the Michael J. Fox \r\nFoundation, the Parkinson Foundation, Parkinson Canada and the Weston \r\nFoundation. A.E.L. is serving as an expert witness in litigation related to \r\nparaquat and PD, and has received publishing royalties from Elsevier, Saunders, \r\nWiley-Blackwell, Johns Hopkins Press and Cambridge Univ. Press. M.E., S.K.W., \r\nS.S., S.-M.F., D.G.D.L., J.T., C.A., J.L., P.B., J.S. and N.P.V. declare no \r\ncompeting interests.\r\n\r\n\r\n4. Brain. 2026 May 20:awag182. doi: 10.1093/brain/awag182. Online ahead of print.\r\n\r\nLarge-scale antagonistic cerebral networks drive amplitude variability in \r\nParkinson's disease tremor.\r\n\r\nvan den Berg KRE(1)(2), Johansson ME(1)(3), Grill F(1)(4), Dirkx MF(1)(2), Bloem \r\nBR(2), Helmich RC(1)(2).\r\n\r\nAuthor information:\r\n(1)Donders Centre for Cognitive Neuroimaging, Donders Institute for Brain, \r\nCognition and Behaviour, Radboud University Nijmegen, 6525 EN Nijmegen, The \r\nNetherlands.\r\n(2)Department of Neurology and Center of Expertise for Parkinson & Movement \r\nDisorders, Donders Institute for Brain, Cognition and Behaviour, Radboud \r\nUniversity Medical Center, 6525 GC Nijmegen, The Netherlands.\r\n(3)Institut du Cerveau - Paris Brain Institute, Movement Investigations and \r\nTherapeutics Team (MOV'IT), Center for NeuroImaging Research (CENIR), Sorbonne \r\nUniversity, Pitié-Salpêtrière Hospital, 75013 Paris, France.\r\n(4)Aging Research Center, Karolinska Institutet and Stockholm University, 171 77 \r\nStockholm, Sweden.\r\n\r\nResting tremor in Parkinson's disease is characterized by considerable \r\nvariability: tremor affects some patients but not others, and its amplitude \r\ntypically fluctuates. Previous research focused primarily on identifying \r\nmechanisms that produce tremor, showing an important role for the basal ganglia \r\nand cerebello-thalamo-cortical circuit. What has been relatively ignored are \r\nmechanisms involved in suppressing tremor. For instance, patients can reduce \r\ntheir tremor by making voluntary movements or by exerting conscious effort. \r\nHere, we aimed to distinguish between brain mechanisms that contribute \r\npositively or negatively to spontaneous fluctuations in Parkinson's tremor. We \r\nleveraged a large sample of 119 tremulous Parkinson patients with concurrent \r\naccelerometry-fMRI. Frame-by-frame fluctuations in accelerometry-derived tremor \r\npower, measured per patient, were used to localize tremor-related brain \r\nactivations and deactivations at a group level. Amplitude-related coupling \r\nbetween tremor-positive and tremor-negative brain networks was examined further \r\nusing physio-physiological interaction analyses. Lastly, whole-brain multiple \r\nregression analyses were used to test the association between tremor-related \r\nactivity and clinically assessed tremor severity. Tremor-related activations \r\nwere found in a lateralized network consisting of contralateral (to tremor) \r\nsensorimotor cortex, ventrolateral thalamus, posterior putamen, and cerebellum \r\n(ipsilateral lobule V, vermis, and bilateral Crus I/II); activity in this \r\nnetwork correlated positively with tremor severity. Tremor-related deactivations \r\nencompassed a bilateral \"anti-tremor\" network, including dorsal premotor cortex, \r\npre-supplementary motor area, somatosensory cortex, posterior parietal cortex, \r\nand insula; activity in this network correlated negatively with tremor severity. \r\nDuring low versus high tremor episodes, functional connectivity between the \r\nanti-tremor and tremor-positive networks increased. This suggests that the \r\nanti-tremor network makes a relevant contribution to modulating tremor amplitude \r\nby connecting to the cerebello-thalamo-cortical circuit in a tremor-dependent \r\nmanner. We conclude that spontaneous fluctuations in Parkinson's tremor \r\namplitude are associated with interactions between a tremor-producing \r\ncerebello-thalamo-cortical circuit and a novel antagonistic anti-tremor network. \r\nFuture intervention studies may investigate whether strengthening of the \r\nanti-tremor network leads to a reduction in tremor, as a potential basis for new \r\ntherapies.\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/awag182\r\nPMID: 42161331\r\n", "tool_calls_made": 0, "duration_seconds": 1.03}

{"todos": [{"id": "1", "content": "Step 1: PubMed search for PD papers (2026/03-2026/06)", "status": "completed"}, {"id": "2", "content": "Step 2: Get full paper details (title, abstract, journal, DOI)", "status": "completed"}, {"id": "3", "content": "Step 3: Initial screening (IF>10 or top journal, 3 months, PD-relevant)", "status": "in_progress"}, {"id": "4", "content": "Step 4: Claude evaluation (5-dimension scoring >=6)", "status": "pending"}, {"id": "5", "content": "Step 5: Generate final recommendation output", "status": "pending"}], "summary": {"total": 5, "pending": 2, "in_progress": 1, "completed": 2, "cancelled": 0}}

{"status": "success", "output": "1. Brain. 2026 May 29:awag193. doi: 10.1093/brain/awag193. Online ahead of print.\r\n\r\nClinical markers of disease progression in the prodromal to overt \r\nalpha-synucleinopathy continuum.\r\n\r\nRoascio M(1), Antelmi E(2), Baldelli L(3)(4), Biscarini F(3)(4), Bonanni E(5), \r\nBrunetti V(6)(7), Capriglia E(8), Geromino C(9)(10), Casoni F(11), Cirillo \r\nF(12), Della Marca G(6)(7), Di Laudo F(3), Ferini-Strambi L(13), Fernandes \r\nM(14), Figorilli M(9)(10), Galbiati A(13), Gigli GL(15), Guarnieri B(16)(17), \r\nHoxhaj D(5), Lanza G(18)(19), Liguori C(12)(14)(20), Tassoni MM(5), Maio S(14), \r\nMalomo G(8), Marelli S(13)(21), Mattioli P(22)(23), Mulas M(9)(10), Orso B(22), \r\nPardini M(22)(23), Plazzi G(4)(24), Provini F(3)(4), Pellitteri G(25), \r\nPuligheddu M(9)(10), Terzaghi M(8)(26), Pelletier A(27)(28), Postuma \r\nRB(27)(28)(29), Arnulfo G(1)(30), Arnaldi D(22)(23).\r\n\r\nAuthor information:\r\n(1)Department of Informatics, Bioengineering, Robotics and System Engineering \r\n(DIBRIS), University of Genoa, 16145 Genoa, Italy.\r\n(2)Department of Engineering for Innovative Medicine, University of Verona, \r\n37134 Verona, Italy.\r\n(3)Department of Biomedical and Neuromotor Sciences, University of Bologna, \r\n40138 Bologna, Italy.\r\n(4)IRCCS, Istituto delle Scienze Neurologiche di Bologna, 40124 Bologna, Italy.\r\n(5)Neurology Unit, Department of Clinical and Experimental Medicine, University \r\nof Pisa, 56126 Pisa, Italy.\r\n(6)UOC di Neurologia, Dipartimento di Neuroscienze, Organi di Senso e Torace, \r\nFondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.\r\n(7)Department of Neurosciences, Università Cattolica del Sacro Cuore, 00168 \r\nRome, Italy.\r\n(8)Department of Brain and Behavioral Sciences, University of Pavia, 27100 \r\nPavia, Italy.\r\n(9)Interdepartmental Sleep Medicine Centre, University of Cagliari, Cagliari \r\n09124, Italy.\r\n(10)Neurology Unit, Azienda Ospedaliero-Universitaria, 09042 Cagliari, Italy.\r\n(11)Sleep Disorders Centre, Department of Clinical Neurosciences, IRCCS San \r\nRaffaele Hospital, 20127 Milan, Italy.\r\n(12)Neurology Unit, University Hospital of Rome Tor Vergata, 00133 Rome, Italy.\r\n(13)Vita-Salute San Raffaele University, 20132 Milan, Italy.\r\n(14)Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, \r\nItaly.\r\n(15)Neurology, Department of Medicine (DMED), University of Udine, 33100 Udine, \r\nItaly.\r\n(16)Center of Sleep Medicine, Villa Serena Hospital, Città S. Angelo, 65013 \r\nPescara, Italy.\r\n(17)Fondazione Villaserena per la ricerca, Città S. Angelo, 65013 Pescara, \r\nItaly.\r\n(18)Clinical Neurophysiology Research Unit and Sleep Research Centre, Oasi \r\nResearch Institute-IRCCS, 94018 Troina, Italy.\r\n(19)Department of Surgery and Medical-Surgical Specialties, University of \r\nCatania, 95123 Catania, Italy.\r\n(20)IRCCS Neuromed, 86077 Pozzilli, IS, Italy.\r\n(21)Sleep Disorders Centre, Neurology, IRCCS San Raffaele Hospital, 20127 Milan, \r\nItaly.\r\n(22)Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, \r\nMaternal and Child Health (DINOGMI), Clinical Neurolog\r\n\r\nNat Med pubtypes: ['Journal Article']\r\nFull journal: Nature medicine\r\nTitle: Gut microbiome screens could identify risk of Parkinson's disease years before symptoms appear.\r\n", "tool_calls_made": 0, "duration_seconds": 1.42}

{"todos": [{"id": "1", "content": "Step 1: PubMed search for PD papers (2026/03-2026/06)", "status": "completed"}, {"id": "2", "content": "Step 2: Get full paper details (title, abstract, journal, DOI)", "status": "completed"}, {"id": "3", "content": "Step 3: Initial screening (IF>10 or top journal, 3 months, PD-relevant)", "status": "completed"}, {"id": "4", "content": "Step 4: Claude evaluation (5-dimension scoring >=6)", "status": "in_progress"}, {"id": "5", "content": "Step 5: Generate final recommendation output", "status": "pending"}], "summary": {"total": 5, "pending": 1, "in_progress": 1, "completed": 3, "cancelled": 0}}

{"todos": [{"id": "1", "content": "Step 1: PubMed search for PD papers (2026/03-2026/06)", "status": "completed"}, {"id": "2", "content": "Step 2: Get full paper details (title, abstract, journal, DOI)", "status": "completed"}, {"id": "3", "content": "Step 3: Initial screening (IF>10 or top journal, 3 months, PD-relevant)", "status": "completed"}, {"id": "4", "content": "Step 4: Claude evaluation (5-dimension scoring >=6)", "status": "completed"}, {"id": "5", "content": "Step 5: Generate final recommendation output (3 papers recommended)", "status": "completed"}], "summary": {"total": 5, "pending": 0, "in_progress": 0, "completed": 5, "cancelled": 0}}