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{ "count": 32312, "next": "http://api.gregory-ms.com/articles/?page=2", "previous": null, "results": [ { "article_id": 292205, "title": "Brain‐Wide Neuroregenerative Gene Therapy Improves Cognition in a Mouse Model of Alzheimer's Disease", "summary": "<jats:title>Abstract</jats:title><jats:p>Alzheimer's disease (AD) is a progressive and irreversible brain disorder with extensive neuronal loss in the neocortex and hippocampus. Current therapeutic interventions focus on the early stage of AD but lack effective treatment for the late stage of AD, largely due to the inability to replenish the lost neurons and repair the broken neural circuits. In this study, by using engineered adeno‐associated virus vectors that efficiently cross the blood–brain‐barrier in the mouse brain, a brain‐wide neuroregenerative gene therapy is developed to directly convert endogenous astrocytes into functional neurons in a mouse model of AD. It is found that ≈500 000 new neurons are regenerated and widely distributed in the cerebral cortex and hippocampus. Importantly, it is demonstrated that the converted neurons can integrate into pre‐existing neural networks and improve various cognitive performances in AD mice. Chemogenetic inhibition of the converted neurons abolishes memory enhancement in AD mice, suggesting a pivotal role for the newly converted neurons in cognitive restoration. Together, brain‐wide neuroregenerative gene therapy may provide a viable strategy for the treatment of AD and other brain disorders associated with massive neuronal loss.</jats:p>", "link": "https://pubmed.ncbi.nlm.nih.gov/39951299/?fc=20240608182355&ff=20250215072508&v=2.18.0.post9+e462414", "published_date": "2025-02-14T11:00:00Z", "sources": [ "PubMed CNS Regenerate" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 2, "subject_name": "CNS Regeneration", "description": "https://pubmed.ncbi.nlm.nih.gov/rss/search/1dmEOdK-P_-UBN_co2XahWMyPwt10E-2wAci7qgyqB1wWIwkJY/?limit=100&utm_campaign=pubmed-2&fc=20240608182355\r\n\r\n((\"Central Nervous System Regeneration\" OR \"Neuroregeneration\" OR \"Neural Regeneration\" OR \"Central Nervous System Repair\") \r\nOR (\"Myelination\" OR \"Remyelination\" OR \"Myelin Repair\" OR \"Oligodendrocyte Differentiation\" OR \"Oligodendrocyte Progenitor Cells\" OR \"Myelin Regeneration\") \r\nOR (\"Stem Cells and Myelin Production\" OR \"Neural Stem Cells\" OR \"Growth Factors for Myelin Regeneration\" OR \"Neurotrophic Factors\" OR \"Glial Cell Line-Derived Neurotrophic Factor\") \r\nOR (\"Gene Therapy for CNS Repair\" OR \"Gene Therapy for Myelination\" OR \"Molecular Targets for Myelin Regeneration\" OR \"Epigenetic Regulation of Myelination\") \r\nOR (\"Pharmacological Agents for CNS Regeneration\" OR \"Drugs Promoting Myelination\" OR \"Neuroprotective Agents\" OR \"Remyelinating Drugs\" OR \"Small Molecules for Myelin Repair\") \r\nOR (\"Novel Treatments for CNS Repair\" OR \"Emerging Therapies for Myelin Regeneration\"))", "team_id": 1 } ], "publisher": "Wiley", "container_title": "Advanced Science", "authors": [ { "author_id": 393771, "given_name": "Zheng", "family_name": "Wu", "ORCID": "https://orcid.org/0000-0002-3816-8891", "country": null }, { "author_id": 240115, "given_name": "Liang", "family_name": "Xu", "ORCID": null, "country": null }, { "author_id": 296939, "given_name": "Yu", "family_name": "Xie", "ORCID": null, "country": null }, { "author_id": 393772, "given_name": "Abhijeet", "family_name": "Sambangi", "ORCID": null, "country": null }, { "author_id": 393773, "given_name": "Shreya", "family_name": "Swaminathan", "ORCID": null, "country": null }, { "author_id": 393774, "given_name": "Zifei", "family_name": "Pei", "ORCID": null, "country": null }, { "author_id": 393775, "given_name": "Wenyu", "family_name": "Ji", "ORCID": null, "country": null }, { "author_id": 393776, "given_name": "Zeru", "family_name": "Li", "ORCID": null, "country": null }, { "author_id": 393777, "given_name": "Yaowei", "family_name": "Guo", "ORCID": null, "country": null }, { "author_id": 260831, "given_name": "Zhifei", "family_name": "Li", "ORCID": null, "country": null }, { "author_id": 360883, "given_name": "Gong", "family_name": "Chen", "ORCID": "http://orcid.org/0000-0002-1857-3670", "country": null } ], "discovery_date": "2025-02-15T00:25:21.474007Z", "article_subject_relevances": [], "doi": "10.1002/advs.202410080", "access": "open", "takeaways": "Alzheimer's disease (AD) is a progressive and irreversible brain disorder with extensive neuronal loss in the neocortex and hippocampus. Current therapeutic interventions focus on the early stage of AD but lack effective treatment for the late stage. Brain-wide neuroregenerative gene therapy is developed to directly convert endogenous astrocytes into functional neurons in a mouse model of AD. 500,000 new neurons are regenerated and widely distributed in the", "team_categories": [], "ml_predictions": [] }, { "article_id": 292204, "title": "Roles of Kdm6a and Kdm6b in Regulation of Mammalian Neural Regeneration", "summary": "<jats:title>Abstract</jats:title><jats:p>Epigenetic regulation of neuronal transcriptomic landscape is emerging to be a key coordinator of mammalian neural regeneration. The roles of two histone 3 lysine 27 (H3K27) demethylases, Kdm6a/b, in controlling neuroprotection and axon regeneration are investigated here. Deleting either Kdm6a or Kdm6b leads to enhanced sensory axon regeneration in the peripheral nervous system (PNS), whereas in the central nervous system (CNS), only deleting Kdm6a in retinal ganglion cells (RGCs) significantly enhances optic nerve regeneration. Moreover, both Kdm6a and Kdm6b function to regulate RGC survival but with different mechanisms. Mechanistically, Kdm6a regulates RGC regeneration via distinct pathway from that of Pten, and co‐deleting Kdm6a and Pten results in long distance optic nerve regeneration passing the optic chiasm. In addition, RNA‐seq profiling reveals that Kdm6a deletion switches the RGC transcriptomics into a developmental‐like state and suppresses several known repressors of neural regeneration. Klf4 is identified as a direct downstream target of Kdm6a‐H3K27me3 signaling in both sensory neurons and RGCs to regulate axon regeneration. These findings not only reveal different roles of Kdm6a and Kdm6b in regulation of neural regeneration and their underlying mechanisms, but also identify Kdm6a‐mediated histone demethylation signaling as a novel epigenetic target for supporting CNS neural regeneration.</jats:p>", "link": "https://pubmed.ncbi.nlm.nih.gov/39951327/?fc=20240608182355&ff=20250215072508&v=2.18.0.post9+e462414", "published_date": "2025-02-14T11:00:00Z", "sources": [ "PubMed CNS Regenerate" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 2, "subject_name": "CNS Regeneration", "description": "https://pubmed.ncbi.nlm.nih.gov/rss/search/1dmEOdK-P_-UBN_co2XahWMyPwt10E-2wAci7qgyqB1wWIwkJY/?limit=100&utm_campaign=pubmed-2&fc=20240608182355\r\n\r\n((\"Central Nervous System Regeneration\" OR \"Neuroregeneration\" OR \"Neural Regeneration\" OR \"Central Nervous System Repair\") \r\nOR (\"Myelination\" OR \"Remyelination\" OR \"Myelin Repair\" OR \"Oligodendrocyte Differentiation\" OR \"Oligodendrocyte Progenitor Cells\" OR \"Myelin Regeneration\") \r\nOR (\"Stem Cells and Myelin Production\" OR \"Neural Stem Cells\" OR \"Growth Factors for Myelin Regeneration\" OR \"Neurotrophic Factors\" OR \"Glial Cell Line-Derived Neurotrophic Factor\") \r\nOR (\"Gene Therapy for CNS Repair\" OR \"Gene Therapy for Myelination\" OR \"Molecular Targets for Myelin Regeneration\" OR \"Epigenetic Regulation of Myelination\") \r\nOR (\"Pharmacological Agents for CNS Regeneration\" OR \"Drugs Promoting Myelination\" OR \"Neuroprotective Agents\" OR \"Remyelinating Drugs\" OR \"Small Molecules for Myelin Repair\") \r\nOR (\"Novel Treatments for CNS Repair\" OR \"Emerging Therapies for Myelin Regeneration\"))", "team_id": 1 } ], "publisher": "Wiley", "container_title": "Advanced Science", "authors": [ { "author_id": 393760, "given_name": "Shu‐Guang", "family_name": "Yang", "ORCID": null, "country": null }, { "author_id": 393761, "given_name": "Chang‐Ping", "family_name": "Li", "ORCID": null, "country": null }, { "author_id": 393762, "given_name": "Xue‐Wei", "family_name": "Wang", "ORCID": null, "country": null }, { "author_id": 334137, "given_name": "Tao", "family_name": "Huang", "ORCID": "http://orcid.org/0000-0002-6147-0490", "country": null }, { "author_id": 393763, "given_name": "Cheng", "family_name": "Qian", "ORCID": null, "country": null }, { "author_id": 273763, "given_name": "Qiao", "family_name": "Li", "ORCID": null, "country": null }, { "author_id": 393764, "given_name": "Ling‐Rui", "family_name": "Zhao", "ORCID": null, "country": null }, { "author_id": 393765, "given_name": "Si‐Yu", "family_name": "Zhou", "ORCID": null, "country": null }, { "author_id": 393766, "given_name": "Chen‐Yun", "family_name": "Ding", "ORCID": null, "country": null }, { "author_id": 393767, "given_name": "Rui", "family_name": "Nie", "ORCID": null, "country": null }, { "author_id": 393768, "given_name": "Yu‐Cai", "family_name": "Hong", "ORCID": null, "country": null }, { "author_id": 393769, "given_name": "Chang‐Mei", "family_name": "Liu", "ORCID": "https://orcid.org/0000-0002-2941-4667", "country": null }, { "author_id": 393770, "given_name": "Feng‐Quan", "family_name": "Zhou", "ORCID": "https://orcid.org/0000-0002-1525-9969", "country": null } ], "discovery_date": "2025-02-15T00:25:17.317156Z", "article_subject_relevances": [], "doi": "10.1002/advs.202405537", "access": "open", "takeaways": "Deleting Kdm6a or Km6b leads to enhanced sensory axon regeneration in the peripheral nervous system (PNS) and only deleting Kmm6a in retinal ganglion cells (RGCs) significantly enhances optic nerve regeneration. Deleting the RGC transcriptomics switches the transcriptomics into a developmental state and suppresses repressors of neural regeneration. Klf4 is identified as a direct downstream target of KDM6a's", "team_categories": [], "ml_predictions": [] }, { "article_id": 292203, "title": "The Endocannabinoid System as a Target for Ischemic Stroke Therapy", "summary": "Introduction: Cannabinoids are increasingly being explored as a potential treatment for neurodegenerative diseases. This article aims to provide a narrative review of available data on the treatment of neurological disorders with cannabis constituents, focusing on ischemic stroke. Methods: Selected articles are summarized to describe design, results, limitations, conclusions, and implications about this theme. Results: The growing understanding of the endocannabinoid system and the cannabinoid...", "link": "https://pubmed.ncbi.nlm.nih.gov/39951358/?fc=20240915071900&ff=20250215073107&v=2.18.0.post9+e462414", "published_date": "2025-02-14T11:00:00Z", "sources": [ "PubMed CNS Regenerate", "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 }, { "id": 2, "subject_name": "CNS Regeneration", "description": "https://pubmed.ncbi.nlm.nih.gov/rss/search/1dmEOdK-P_-UBN_co2XahWMyPwt10E-2wAci7qgyqB1wWIwkJY/?limit=100&utm_campaign=pubmed-2&fc=20240608182355\r\n\r\n((\"Central Nervous System Regeneration\" OR \"Neuroregeneration\" OR \"Neural Regeneration\" OR \"Central Nervous System Repair\") \r\nOR (\"Myelination\" OR \"Remyelination\" OR \"Myelin Repair\" OR \"Oligodendrocyte Differentiation\" OR \"Oligodendrocyte Progenitor Cells\" OR \"Myelin Regeneration\") \r\nOR (\"Stem Cells and Myelin Production\" OR \"Neural Stem Cells\" OR \"Growth Factors for Myelin Regeneration\" OR \"Neurotrophic Factors\" OR \"Glial Cell Line-Derived Neurotrophic Factor\") \r\nOR (\"Gene Therapy for CNS Repair\" OR \"Gene Therapy for Myelination\" OR \"Molecular Targets for Myelin Regeneration\" OR \"Epigenetic Regulation of Myelination\") \r\nOR (\"Pharmacological Agents for CNS Regeneration\" OR \"Drugs Promoting Myelination\" OR \"Neuroprotective Agents\" OR \"Remyelinating Drugs\" OR \"Small Molecules for Myelin Repair\") \r\nOR (\"Novel Treatments for CNS Repair\" OR \"Emerging Therapies for Myelin Regeneration\"))", "team_id": 1 } ], "publisher": null, "container_title": null, "authors": [], "discovery_date": "2025-02-15T00:25:16.170023Z", "article_subject_relevances": [], "doi": "10.1089/can.2024.0017", "access": "restricted", "takeaways": "Cannabis is being explored as a potential treatment for neurodegenerative diseases. This article provides a narrative review of available data on", "team_categories": [], "ml_predictions": [] }, { "article_id": 292202, "title": "Detrimental influence of Arginase-1 in infiltrating macrophages on poststroke functional recovery and inflammatory milieu", "summary": "<jats:p>\n Poststroke inflammation critically influences functional outcomes following ischemic stroke. Arginase-1 (Arg1) is considered a marker for anti-inflammatory macrophages, associated with the resolution of inflammation and promotion of tissue repair in various pathological conditions. However, its specific role in poststroke recovery remains to be elucidated. This study investigates the functional impact of Arg1 expressed in macrophages on poststroke recovery and inflammatory milieu. We observed a time-dependent increase in Arg1 expression, peaking at 7 d after photothrombotic stroke in mice. Cellular mapping analysis revealed that Arg1 was predominantly expressed in LysM-positive infiltrating macrophages. Using a conditional knockout (cKO) mouse model, we examined the role of Arg1 expressed in infiltrating macrophages. Contrary to its presumed beneficial effects, Arg1 cKO in LysM-positive macrophages significantly improved skilled forelimb motor function recovery after stroke. Mechanistically, Arg1 cKO attenuated fibrotic scar formation, enhanced peri-infarct remyelination, and increased synaptic density while reducing microglial synaptic elimination in the peri-infarct cortex. Gene expression analysis of fluorescence-activated single cell sorting (FACS)-sorted CD45\n <jats:sup>low</jats:sup>\n microglia revealed decreased transforming growth factor-β (TGF-β) signaling and proinflammatory cytokine activity in peri-infarct microglia from Arg1 cKO animals. In vitro coculture experiments demonstrated that Arg1 activity in macrophages modulates microglial synaptic phagocytosis, providing evidence for macrophage–microglia interaction. These findings present unique insights into the function of Arg1 in central nervous system injury and highlight an interaction between infiltrating macrophages and resident microglia in shaping the poststroke inflammatory milieu. Our study identifies Arg1 in macrophages as a potential therapeutic target for modulating poststroke inflammation and improving functional recovery.\n </jats:p>", "link": "https://pubmed.ncbi.nlm.nih.gov/39951507/?fc=20240608182355&ff=20250215072508&v=2.18.0.post9+e462414", "published_date": "2025-02-14T11:00:00Z", "sources": [ "PubMed CNS Regenerate" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 2, "subject_name": "CNS Regeneration", "description": "https://pubmed.ncbi.nlm.nih.gov/rss/search/1dmEOdK-P_-UBN_co2XahWMyPwt10E-2wAci7qgyqB1wWIwkJY/?limit=100&utm_campaign=pubmed-2&fc=20240608182355\r\n\r\n((\"Central Nervous System Regeneration\" OR \"Neuroregeneration\" OR \"Neural Regeneration\" OR \"Central Nervous System Repair\") \r\nOR (\"Myelination\" OR \"Remyelination\" OR \"Myelin Repair\" OR \"Oligodendrocyte Differentiation\" OR \"Oligodendrocyte Progenitor Cells\" OR \"Myelin Regeneration\") \r\nOR (\"Stem Cells and Myelin Production\" OR \"Neural Stem Cells\" OR \"Growth Factors for Myelin Regeneration\" OR \"Neurotrophic Factors\" OR \"Glial Cell Line-Derived Neurotrophic Factor\") \r\nOR (\"Gene Therapy for CNS Repair\" OR \"Gene Therapy for Myelination\" OR \"Molecular Targets for Myelin Regeneration\" OR \"Epigenetic Regulation of Myelination\") \r\nOR (\"Pharmacological Agents for CNS Regeneration\" OR \"Drugs Promoting Myelination\" OR \"Neuroprotective Agents\" OR \"Remyelinating Drugs\" OR \"Small Molecules for Myelin Repair\") \r\nOR (\"Novel Treatments for CNS Repair\" OR \"Emerging Therapies for Myelin Regeneration\"))", "team_id": 1 } ], "publisher": "Proceedings of the National Academy of Sciences", "container_title": "Proceedings of the National Academy of Sciences", "authors": [ { "author_id": 393778, "given_name": "Hyung Soon", "family_name": "Kim", "ORCID": "https://orcid.org/0000-0001-7765-9696", "country": null }, { "author_id": 393779, "given_name": "Seung Ah", "family_name": "Jee", "ORCID": null, "country": null }, { "author_id": 393780, "given_name": "Ariandokht", "family_name": "Einisadr", "ORCID": "https://orcid.org/0009-0002-6031-7790", "country": null }, { "author_id": 393781, "given_name": "Yeojin", "family_name": "Seo", "ORCID": null, "country": null }, { "author_id": 393782, "given_name": "Hyo Gyeong", "family_name": "Seo", "ORCID": null, "country": null }, { "author_id": 391288, "given_name": "Byeong Seong", "family_name": "Jang", "ORCID": null, "country": null }, { "author_id": 391284, "given_name": "Hee Hwan", "family_name": "Park", "ORCID": null, "country": null }, { "author_id": 393783, "given_name": "Won-Suk", "family_name": "Chung", "ORCID": "https://orcid.org/0000-0003-1060-9007", "country": null }, { "author_id": 391291, "given_name": "Byung Gon", "family_name": "Kim", "ORCID": "https://orcid.org/0000-0003-2233-9569", "country": null } ], "discovery_date": "2025-02-15T00:25:14.847187Z", "article_subject_relevances": [], "doi": "10.1073/pnas.2413484122", "access": "restricted", "takeaways": "Arginase-1 (Arg1) is a marker for anti-inflammatory macrophages. Arg1's specific role in poststroke recovery", "team_categories": [], "ml_predictions": [] }, { "article_id": 292201, "title": "The Recruitment and Immune Suppression Mechanisms of Myeloid‐Derived Suppressor Cells and Their Impact on Bone Metastatic Cancer", "summary": "<jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>MDSCs are immature neutrophils and monocytes with immunosuppressive potentials, involving mononuclear MDSCs (M‐MDSCs) and polymorphonuclear MDSCs (PMN‐MDSCs).</jats:p></jats:sec><jats:sec><jats:title>Recent Findings</jats:title><jats:p>They are significant components of the tumor microenvironment (TME). Besides, recent studies also verified that MDSCs also facilitated the progression of bone metastasis by regulating the network of cytokines and the function of immune cells.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>It is necessary to summarize the mechanisms of MDSC recruitment and immunosuppression, and their impact on bone metastasis.</jats:p></jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/39947253/?fc=20240915071900&ff=20250214073122&v=2.18.0.post9+e462414", "published_date": "2025-02-13T11:00:00Z", "sources": [ "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 } ], "publisher": "Wiley", "container_title": "Cancer Reports", "authors": [ { "author_id": 393718, "given_name": "Chengyuan", "family_name": "Li", "ORCID": "https://orcid.org/0009-0005-5415-3170", "country": null }, { "author_id": 393719, "given_name": "Yucheng", "family_name": "Xue", "ORCID": null, "country": null }, { "author_id": 393720, "given_name": "Eloy", "family_name": "Yinwang", "ORCID": null, "country": null }, { "author_id": 393721, "given_name": "Zhaoming", "family_name": "Ye", "ORCID": "https://orcid.org/0000-0001-5951-5840", "country": null } ], "discovery_date": "2025-02-14T12:32:39.096521Z", "article_subject_relevances": [], "doi": "10.1002/cnr2.70044", "access": "open", "takeaways": "MDSCs are significant components of the tumor microenvironment. They regulate the network of cytokines and the function of immune cells.", "team_categories": [], "ml_predictions": [] }, { "article_id": 292200, "title": "Demography and baseline characteristics of individuals planned for Jack Jumper Ant-specific venom Immunotherapy at the Victorian Insect Venom Allergy Service", "summary": "No abstract", "link": "https://pubmed.ncbi.nlm.nih.gov/39947299/?fc=20240915071900&ff=20250215073107&v=2.18.0.post9+e462414", "published_date": "2025-02-13T11:00:00Z", "sources": [ "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 } ], "publisher": "Elsevier BV", "container_title": "The Journal of Allergy and Clinical Immunology: In Practice", "authors": [ { "author_id": 393713, "given_name": "Kymble", "family_name": "Spriggs", "ORCID": "https://orcid.org/0000-0002-5302-0334", "country": null }, { "author_id": 393714, "given_name": "Elizabeth", "family_name": "Leahy", "ORCID": null, "country": null }, { "author_id": 393715, "given_name": "Nicole", "family_name": "Weibel", "ORCID": null, "country": null }, { "author_id": 393716, "given_name": "Emily", "family_name": "Heke", "ORCID": null, "country": null }, { "author_id": 393717, "given_name": "Sara", "family_name": "Barnes", "ORCID": null, "country": null } ], "discovery_date": "2025-02-14T12:32:37.001695Z", "article_subject_relevances": [], "doi": "10.1016/j.jaip.2025.01.038", "access": "restricted", "takeaways": null, "team_categories": [], "ml_predictions": [] }, { "article_id": 292199, "title": "Protein phosphatase 6 regulates metabolic dysfunction-associated steatohepatitis via the mTORC1 pathway", "summary": "CONCLUSIONS: These results define a fundamental mechanism underlying FGF21 signals in hepatocytes and demonstrate that targeting PPP6C may have therapeutic potential for treating MASH.", "link": "https://pubmed.ncbi.nlm.nih.gov/39947331/?fc=20240915071900&ff=20250215073107&v=2.18.0.post9+e462414", "published_date": "2025-02-13T11:00:00Z", "sources": [ "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 } ], "publisher": "Elsevier BV", "container_title": "Journal of Hepatology", "authors": [ { "author_id": 393702, "given_name": "Zhengshuai", "family_name": "Liu", "ORCID": null, "country": null }, { "author_id": 302508, "given_name": "Shuang", "family_name": "Wei", "ORCID": null, "country": null }, { "author_id": 175007, "given_name": "Yang", "family_name": "Jiang", "ORCID": "http://orcid.org/0000-0002-8697-939X", "country": "CN" }, { "author_id": 393703, "given_name": "Weitong", "family_name": "Su", "ORCID": null, "country": null }, { "author_id": 393704, "given_name": "Fengguang", "family_name": "Ma", "ORCID": null, "country": null }, { "author_id": 393705, "given_name": "Genxiang", "family_name": "Cai", "ORCID": null, "country": null }, { "author_id": 354663, "given_name": "Yuxiao", "family_name": "Liu", "ORCID": null, "country": null }, { "author_id": 393706, "given_name": "Xiaoyang", "family_name": "Sun", "ORCID": null, "country": null }, { "author_id": 393707, "given_name": "Ling", "family_name": "Lu", "ORCID": "https://orcid.org/0000-0002-1670-5027", "country": null }, { "author_id": 393708, "given_name": "Wenguang", "family_name": "Fu", "ORCID": null, "country": null }, { "author_id": 330723, "given_name": "Yong", "family_name": "Xu", "ORCID": "http://orcid.org/0000-0002-4908-1572", "country": null }, { "author_id": 393709, "given_name": "Ruijing", "family_name": "Huang", "ORCID": null, "country": null }, { "author_id": 178946, "given_name": "Jian", "family_name": "Li", "ORCID": "http://orcid.org/0000-0002-7076-3332", "country": null }, { "author_id": 287457, "given_name": "Xu", "family_name": "Lin", "ORCID": null, "country": null }, { "author_id": 393710, "given_name": "Aoyuan", "family_name": "Cui", "ORCID": null, "country": null }, { "author_id": 393711, "given_name": "Mengwei", "family_name": "Zang", "ORCID": null, "country": null }, { "author_id": 245011, "given_name": "Aimin", "family_name": "Xu", "ORCID": null, "country": null }, { "author_id": 393712, "given_name": "Yu", "family_name": "Li", "ORCID": "https://orcid.org/0000-0001-6910-5933", "country": null } ], "discovery_date": "2025-02-14T12:32:30.870469Z", "article_subject_relevances": [], "doi": "10.1016/j.jhep.2025.02.003", "access": "restricted", "takeaways": "", "team_categories": [], "ml_predictions": [] }, { "article_id": 292198, "title": "Oligoclonal bands and kappa free light chains: Competing parameters or complementary biomarkers?", "summary": "CONCLUSION: Both oligoclonal bands and KFLC have unique strengths and limitations that complement each other, potentially serving as complementary markers for evaluating intrathecal Ig synthesis in MS diagnosis. Further evidence is needed to establish the value of KFLC in MS diagnosis, thus multicenter prospective studies are being conducted to compare the diagnostic utility of both markers.", "link": "https://pubmed.ncbi.nlm.nih.gov/39947571/?fc=20240915071900&ff=20250215073107&v=2.18.0.post9+e462414", "published_date": "2025-02-13T11:00:00Z", "sources": [ "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 } ], "publisher": "Elsevier BV", "container_title": "Autoimmunity Reviews", "authors": [ { "author_id": 292103, "given_name": "Marie", "family_name": "Süße", "ORCID": null, "country": null }, { "author_id": 212886, "given_name": "Thomas", "family_name": "Skripuletz", "ORCID": "http://orcid.org/0000-0001-8550-335X", "country": null }, { "author_id": 382961, "given_name": "Markus", "family_name": "Otto", "ORCID": "https://orcid.org/0000-0003-4273-4267", "country": null }, { "author_id": 387457, "given_name": "Thomas", "family_name": "Skripuletz", "ORCID": "https://orcid.org/0000-0001-8550-335X", "country": null }, { "author_id": 393689, "given_name": "Franz F.", "family_name": "Konen", "ORCID": null, "country": null }, { "author_id": 393690, "given_name": "Ulrich", "family_name": "Wurster", "ORCID": null, "country": null }, { "author_id": 220542, "given_name": "Philipp", "family_name": "Schwenkenbecher", "ORCID": "http://orcid.org/0000-0002-1260-1650", "country": "DE" }, { "author_id": 393691, "given_name": "Andreas", "family_name": "Gerritzen", "ORCID": null, "country": null }, { "author_id": 393692, "given_name": "Catharina C.", "family_name": "Groß", "ORCID": null, "country": null }, { "author_id": 261989, "given_name": "Peter", "family_name": "Eichhorn", "ORCID": null, "country": null }, { "author_id": 147548, "given_name": "Andrea", "family_name": "Harrer", "ORCID": "http://orcid.org/0000-0001-7717-6125", "country": "AT" }, { "author_id": 393693, "given_name": "Stefan", "family_name": "Isenmann", "ORCID": null, "country": null }, { "author_id": 393694, "given_name": "Piotr", "family_name": "Lewczuk", "ORCID": null, "country": null }, { "author_id": 197566, "given_name": "Jan", "family_name": "Lewerenz", "ORCID": "http://orcid.org/0000-0002-9272-529X", "country": null }, { "author_id": 197578, "given_name": "Frank", "family_name": "Leypoldt", "ORCID": "http://orcid.org/0000-0002-8972-515X", "country": "DE" }, { "author_id": 155458, "given_name": "Markus", "family_name": "Otto", "ORCID": "http://orcid.org/0000-0003-4273-4267", "country": null }, { "author_id": 383736, "given_name": "Axel", "family_name": "Regeniter", "ORCID": "https://orcid.org/0000-0002-6639-3594", "country": null }, { "author_id": 393695, "given_name": "Martin", "family_name": "Roskos", "ORCID": null, "country": null }, { "author_id": 387139, "given_name": "Klemens", "family_name": "Ruprecht", "ORCID": "https://orcid.org/0000-0003-1962-6014", "country": null }, { "author_id": 393696, "given_name": "Annette", "family_name": "Spreer", "ORCID": null, "country": null }, { "author_id": 393697, "given_name": "Herwig", "family_name": "Strik", "ORCID": null, "country": null }, { "author_id": 393698, "given_name": "Manfred", "family_name": "Uhr", "ORCID": null, "country": null }, { "author_id": 393699, "given_name": "Manfred", "family_name": "Wick", "ORCID": null, "country": null }, { "author_id": 370400, "given_name": "Brigitte", "family_name": "Wildemann", "ORCID": "http://orcid.org/0000-0002-5389-3338", "country": null }, { "author_id": 287584, "given_name": "Jens", "family_name": "Wiltfang", "ORCID": null, "country": null }, { "author_id": 393700, "given_name": "Thomas", "family_name": "Zimmermann", "ORCID": null, "country": null }, { "author_id": 393701, "given_name": "Malte", "family_name": "Hannich", "ORCID": null, "country": null }, { "author_id": 241326, "given_name": "Michael", "family_name": "Khalil", "ORCID": null, "country": null }, { "author_id": 157222, "given_name": "Hayrettin", "family_name": "Tumani", "ORCID": "http://orcid.org/0000-0002-1647-6201", "country": null } ], "discovery_date": "2025-02-14T12:32:23.225395Z", "article_subject_relevances": [], "doi": "10.1016/j.autrev.2025.103765", "access": "open", "takeaways": "Both oligoclonal bands and KFLC have unique strengths and limitations that complement each other. Multicenter prospective", "team_categories": [], "ml_predictions": [] }, { "article_id": 292197, "title": "Oligogenic structure of amyotrophic lateral sclerosis has genetic testing, counselling and therapeutic implications", "summary": "<jats:sec><jats:title>Background</jats:title><jats:p>Despite several studies suggesting a potential oligogenic risk model in amyotrophic lateral sclerosis (ALS), case–control statistical evidence implicating oligogenicity with disease risk or clinical outcomes is limited. Considering its direct clinical and therapeutic implications, we aim to perform a large-scale robust investigation of oligogenicity in ALS risk and in the disease clinical course.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We leveraged Project MinE genome sequencing datasets (6711 cases and 2391 controls) to identify associations between oligogenicity in known ALS genes and disease risk, as well as clinical outcomes.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>In both the discovery and replication cohorts, we observed that the risk imparted from carrying multiple ALS rare variants was significantly greater than the risk associated with carrying only a single rare variant, both in the presence and absence of variants in the most well-established ALS genes. However, in contrast to risk, the relationships between oligogenicity and ALS clinical outcomes, such as age of onset and survival, did not follow the same pattern.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Our findings represent the first large-scale, case–control assessment of oligogenicity in ALS and show that oligogenic events involving known ALS risk genes are relevant for disease risk in ~6% of ALS but not necessarily for disease onset and survival. This must be considered in genetic counselling and testing by ensuring to use comprehensive gene panels even when a pathogenic variant has already been identified. Moreover, in the age of stratified medication and gene therapy, it supports the need for a complete genetic profile for the correct choice of therapy in all ALS patients.</jats:p></jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/39947885/?fc=20240915071900&ff=20250215073107&v=2.18.0.post9+e462414", "published_date": "2025-02-13T11:00:00Z", "sources": [ "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 } ], "publisher": "BMJ", "container_title": "Journal of Neurology, Neurosurgery & Psychiatry", "authors": [ { "author_id": 393670, "given_name": "Alfredo", "family_name": "Iacoangeli", "ORCID": "https://orcid.org/0000-0002-5280-5017", "country": null }, { "author_id": 393671, "given_name": "Allison A", "family_name": "Dilliott", "ORCID": null, "country": null }, { "author_id": 211747, "given_name": "Ahmad", "family_name": "Al Khleifat", "ORCID": "http://orcid.org/0000-0002-7406-9831", "country": "GB" }, { "author_id": 393672, "given_name": "Peter M", "family_name": "Andersen", "ORCID": "https://orcid.org/0000-0003-0094-5429", "country": null }, { "author_id": 393673, "given_name": "Nazlı A", "family_name": "Başak", "ORCID": "https://orcid.org/0000-0001-6977-2517", "country": null }, { "author_id": 393674, "given_name": "Johnathan", "family_name": "Cooper-Knock", "ORCID": "https://orcid.org/0000-0002-0873-8689", "country": null }, { "author_id": 381131, "given_name": "Philippe", "family_name": "Corcia", "ORCID": "https://orcid.org/0000-0002-1625-8845", "country": null }, { "author_id": 393675, "given_name": "Philippe", "family_name": "Couratier", "ORCID": "https://orcid.org/0000-0001-9562-856X", "country": null }, { "author_id": 381756, "given_name": "Mamede", "family_name": "de Carvalho", "ORCID": "https://orcid.org/0000-0001-7556-0158", "country": null }, { "author_id": 393676, "given_name": "Vivian E", "family_name": "Drory", "ORCID": null, "country": null }, { "author_id": 393677, "given_name": "Jonathan D", "family_name": "Glass", "ORCID": null, "country": null }, { "author_id": 393678, "given_name": "Marc", "family_name": "Gotkine", "ORCID": "https://orcid.org/0000-0003-2541-6232", "country": null }, { "author_id": 393679, "given_name": "Yosef M", "family_name": "Lerner", "ORCID": null, "country": null }, { "author_id": 393680, "given_name": "Orla", "family_name": "Hardiman", "ORCID": "https://orcid.org/0000-0003-2610-1291", "country": null }, { "author_id": 393681, "given_name": "John E", "family_name": "Landers", "ORCID": null, "country": null }, { "author_id": 393682, "given_name": "Russell L", "family_name": "McLaughlin", "ORCID": null, "country": null }, { "author_id": 393683, "given_name": "Jesus S Mora", "family_name": "Pardina", "ORCID": null, "country": null }, { "author_id": 393684, "given_name": "Karen", "family_name": "Morrison", "ORCID": null, "country": null }, { "author_id": 393685, "given_name": "Susana", "family_name": "Pinto", "ORCID": "https://orcid.org/0000-0002-0727-5897", "country": null }, { "author_id": 281275, "given_name": "Monica", "family_name": "Povedano", "ORCID": null, "country": null }, { "author_id": 258753, "given_name": "Christopher E", "family_name": "Shaw", "ORCID": null, "country": null }, { "author_id": 379734, "given_name": "Pamela J", "family_name": "Shaw", "ORCID": "https://orcid.org/0000-0002-8925-2567", "country": null }, { "author_id": 393686, "given_name": "Vincenzo", "family_name": "Silani", "ORCID": "https://orcid.org/0000-0002-7698-3854", "country": null }, { "author_id": 211748, "given_name": "Nicola", "family_name": "Ticozzi", "ORCID": "http://orcid.org/0000-0001-5963-7426", "country": "IT" }, { "author_id": 381135, "given_name": "Philip", "family_name": "Van Damme", "ORCID": "https://orcid.org/0000-0002-4010-2357", "country": null }, { "author_id": 227940, "given_name": "Leonard H", "family_name": "van den Berg", "ORCID": "http://orcid.org/0000-0002-5203-9674", "country": null }, { "author_id": 298804, "given_name": "Patrick", "family_name": "Vourc'h", "ORCID": null, "country": null }, { "author_id": 281282, "given_name": "Markus", "family_name": "Weber", "ORCID": null, "country": null }, { "author_id": 381127, "given_name": "Jan H.", "family_name": "Veldink", "ORCID": "https://orcid.org/0000-0001-5572-9657", "country": null }, { "author_id": 337079, "given_name": "Richard", "family_name": "Dobson", "ORCID": null, "country": null }, { "author_id": 381238, "given_name": "Guy A", "family_name": "Rouleau", "ORCID": "https://orcid.org/0000-0001-8403-1418", "country": null }, { "author_id": 393687, "given_name": "Ammar", "family_name": "Al-Chalabi", "ORCID": "https://orcid.org/0000-0002-4924-7712", "country": null }, { "author_id": 393688, "given_name": "Sali M K", "family_name": "Farhan", "ORCID": "https://orcid.org/0000-0001-5936-0957", "country": null } ], "discovery_date": "2025-02-14T12:32:16.897143Z", "article_subject_relevances": [], "doi": "10.1136/jnnp-2024-335364", "access": "open", "takeaways": "Oligogenicity in amyotrophic lateral sclerosis (ALS) is linked to disease risk and clinical outcomes, but not to age of onset and survival. The risk of carrying multiple ALS rare variants is greater than the risk associated with carrying only one rare variant.", "team_categories": [], "ml_predictions": [] }, { "article_id": 292196, "title": "Lifestyle factors associated with benign multiple sclerosis", "summary": "<jats:sec><jats:title>Background</jats:title><jats:p>Benign multiple sclerosis (MS), characterised by minimal disability despite long disease duration, remains poorly understood in terms of its determinants and prognostic implications. While lifestyle factors have been implicated in modifying disease progression, their role in distinguishing benign and non-benign MS remains unclear.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We conducted a comparative analysis of patients with benign (n=2040) and non-benign MS (n=4283) using data from Swedish nationwide case-control studies with long-term follow-up. Logistic regression models were used to analyse associations between a history of infectious mononucleosis (IM) and lifestyle factors (smoking, body mass index, fish consumption and sun exposure habits) and the likelihood of benign MS. Additionally, Cox regression was used to follow patients with benign MS from the 15-year mark onward, identifying factors associated with the transition to non-benign MS over time.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>The odds of having benign MS were reduced in association with a history of IM (OR 0.54, 95% CI 0.45 to 0.65), adolescent overweight and obesity (OR 0.69, 95% CI 0.56 to 0.85 and 0.46, 95% CI 0.32 to 0.66, respectively) and infrequent fish consumption (OR 0.72, 95% CI 0.60 to 0.88). Similar associations were observed for the risk of transitioning from benign to non-benign MS over time.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>A history of IM and modifiable lifestyle factors significantly influence the probability of a benign disease course in MS. These findings underscore the potential for targeted lifestyle interventions to improve MS outcomes. Further research is needed to elucidate the mechanisms by which a past IM infection can continue to influence MS progression long after the initial infection.</jats:p></jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/39947886/?fc=20240915071900&ff=20250215073107&v=2.18.0.post9+e462414", "published_date": "2025-02-13T11:00:00Z", "sources": [ "PubMed for MS" ], "teams": [ { "id": 1, "name": "Team Gregory", "is_active": true, "created": "2024-05-04T18:35:11.961532Z", "modified": "2024-07-04T10:58:33.274216Z", "slug": "team-gregory", "users": [ 3, 1 ] } ], "subjects": [ { "id": 1, "subject_name": "Multiple Sclerosis", "description": null, "team_id": 1 } ], "publisher": "BMJ", "container_title": "Journal of Neurology, Neurosurgery & Psychiatry", "authors": [ { "author_id": 393669, "given_name": "Jie", "family_name": "Guo", "ORCID": "https://orcid.org/0000-0001-6104-9957", "country": null }, { "author_id": 218798, "given_name": "Tomas", "family_name": "Olsson", "ORCID": "http://orcid.org/0000-0002-2938-1877", "country": "SE" }, { "author_id": 380021, "given_name": "Jan", "family_name": "Hillert", "ORCID": "https://orcid.org/0000-0002-7386-6732", "country": null }, { "author_id": 324611, "given_name": "Lars", "family_name": "Alfredsson", "ORCID": "http://orcid.org/0000-0003-1688-6697", "country": null }, { "author_id": 392211, "given_name": "Anna Karin", "family_name": "Hedström", "ORCID": "https://orcid.org/0000-0002-6612-4749", "country": null } ], "discovery_date": "2025-02-14T12:32:13.836511Z", "article_subject_relevances": [], "doi": "10.1136/jnnp-2024-335464", "access": "restricted", "takeaways": "Benign multiple sclerosis (MS) is characterised by minimal disability despite long disease duration. Lifestyle factors have been implicated in modifying disease progression, but their role in distinguishing benign and non-benign MS remains unclear. Logistic regression models were used to analyse associations between a history of infectious mononucleosis (IM) and lifestyle factors (smoking, body mass index, fish consumption and sun exposure habits) and the likelihood of benign MS.", "team_categories": [], "ml_predictions": [] } ] }