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{ "count": 24395, "next": "http://api.gregory-ms.com/articles/?format=api&page=4", "previous": "http://api.gregory-ms.com/articles/?format=api&page=2", "results": [ { "article_id": 283212, "title": "Adaptive immune changes associate with clinical progression of Alzheimer’s disease", "summary": "<jats:title>Abstract</jats:title><jats:sec>\n <jats:title>Background</jats:title>\n <jats:p>Alzheimer’s disease (AD) is the most frequent cause of dementia. Recent evidence suggests the involvement of peripheral immune cells in the disease, but the underlying mechanisms remain unclear.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Methods</jats:title>\n <jats:p>We comprehensively mapped peripheral immune changes in AD patients with mild cognitive impairment (MCI) or dementia compared to controls, using cytometry by time-of-flight (CyTOF).</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Results</jats:title>\n <jats:p>We found an adaptive immune signature in AD, and specifically highlight the accumulation of PD1<jats:sup>+</jats:sup> CD57<jats:sup>+</jats:sup> CD8<jats:sup>+</jats:sup> T effector memory cells re-expressing CD45RA in the MCI stage of AD. In addition, several innate and adaptive immune cell subsets correlated to cerebrospinal fluid (CSF) biomarkers of AD neuropathology and measures for cognitive decline. Intriguingly, subsets of memory T and B cells were negatively associated with CSF biomarkers for tau pathology, neurodegeneration and neuroinflammation in AD patients. Lastly, we established the influence of the APOE ε4 allele on peripheral immunity.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Conclusions</jats:title>\n <jats:p>Our findings illustrate significant peripheral immune alterations associated with both early and late clinical stages of AD, emphasizing the necessity for further investigation into how these changes influence underlying brain pathology.</jats:p>\n </jats:sec>", "link": "https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-024-00726-8", "published_date": "2024-04-23T23:00:00Z", "source": "BioMedCentral", "publisher": "Springer Science and Business Media LLC", "container_title": "Molecular Neurodegeneration", "authors": [ { "author_id": 175989, "given_name": "Lynn", "family_name": "van Olst", "ORCID": "http://orcid.org/0000-0001-7569-0470", "country": null }, { "author_id": 175991, "given_name": "Alwin", "family_name": "Kamermans", "ORCID": "http://orcid.org/0000-0002-3601-395X", "country": null }, { "author_id": 348825, "given_name": "Sem", "family_name": "Halters", "ORCID": null, "country": null }, { "author_id": 295782, "given_name": "Susanne M. A.", "family_name": "van der Pol", "ORCID": null, "country": null }, { "author_id": 321155, "given_name": "Ernesto", "family_name": "Rodriguez", "ORCID": null, "country": null }, { "author_id": 344258, "given_name": "Inge M. W.", "family_name": "Verberk", "ORCID": null, "country": null }, { "author_id": 254954, "given_name": "Sanne G. S.", "family_name": "Verberk", "ORCID": null, "country": null }, { "author_id": 348826, "given_name": "Danielle W. R.", "family_name": "Wessels", "ORCID": null, "country": null }, { "author_id": 348827, "given_name": "Jan", "family_name": "Verhoeff", "ORCID": null, "country": null }, { "author_id": 330931, "given_name": "Dorine", "family_name": "Wouters", "ORCID": null, "country": null }, { "author_id": 254970, "given_name": "Jan", "family_name": "Van den Bossche", "ORCID": null, "country": null }, { "author_id": 348828, "given_name": "Juan J.", "family_name": "Garcia-Vallejo", "ORCID": null, "country": null }, { "author_id": 329115, "given_name": "Afina W.", "family_name": "Lemstra", "ORCID": null, "country": null }, { "author_id": 200460, "given_name": "Maarten E.", "family_name": "Witte", "ORCID": "http://orcid.org/0000-0002-1407-6220", "country": "NL" }, { "author_id": 269759, "given_name": "Wiesje M.", "family_name": "van der Flier", "ORCID": null, "country": null }, { "author_id": 237158, "given_name": "Charlotte E.", "family_name": "Teunissen", "ORCID": null, "country": null }, { "author_id": 254964, "given_name": "Helga E.", "family_name": "de Vries", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T20:27:18.366573Z", "noun_phrases": null, "doi": "10.1186/s13024-024-00726-8", "access": "restricted", "takeaways": "Alzheimer’s disease (AD) is the most frequent cause of dementia. Recent evidence suggests the involvement of peripheral immune cells in the disease. We comprehensively mapped immune changes in AD patients with mild cognitive impairment (MCI) or dementia compared to controls.", "categories": [] }, { "article_id": 283211, "title": "The Study of Remyelinating Therapies in Multiple Sclerosis: Visual Outcomes as a Window Into Repair", "summary": "<jats:sec>\n<jats:title>Introduction:</jats:title>\n<jats:p>Amelioration of disability in multiple sclerosis requires the development of complementary therapies that target neurodegeneration and promote repair. Remyelination is a promising neuroprotective strategy that may protect axons from damage and subsequent neurodegeneration.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Methods:</jats:title>\n<jats:p>A review of key literature plus additional targeted search of PubMed and Google Scholar was conducted.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Results:</jats:title>\n<jats:p>There has been a rapid expansion of clinical trials studying putative remyelinating candidates, but further growth of the field is limited by the lack of consensus on key aspects of trial design. We have not yet defined the ideal study population, duration of therapy, or the appropriate outcome measures to detect remyelination in humans. The varied natural history of multiple sclerosis, coupled with the short time frame of phase II clinical trials, requires that we develop and validate biomarkers of remyelination that can serve as surrogate endpoints in clinical trials.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Conclusions:</jats:title>\n<jats:p>We propose that the visual system may be the most well-suited and validated model for the study potential remyelinating agents. In this review, we discuss the pathophysiology of demyelination and summarize the current clinical trial landscape of remyelinating agents. We present some of the challenges in the study of remyelinating agents and discuss current potential biomarkers of remyelination and repair, emphasizing both established and emerging visual outcome measures.</jats:p>\n</jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/38654413/?fc=20210216052009&ff=20240425062541&v=2.18.0.post9+e462414", "published_date": "2024-04-24T10:00:00Z", "source": "PubMed", "publisher": "Ovid Technologies (Wolters Kluwer Health)", "container_title": "Journal of Neuro-Ophthalmology", "authors": [ { "author_id": 348851, "given_name": "Leah R.", "family_name": "Zuroff", "ORCID": null, "country": null }, { "author_id": 329872, "given_name": "Ari J.", "family_name": "Green", "ORCID": "http://orcid.org/0000-0001-9275-3066", "country": null } ], "relevant": null, "ml_prediction_gnb": true, "ml_prediction_lr": false, "ml_prediction_lsvc": true, "discovery_date": "2024-04-24T18:25:38.772204Z", "noun_phrases": null, "doi": "10.1097/WNO.0000000000002149", "access": "restricted", "takeaways": "The visual system may be the most well-suited and validated model for the study potential remyelinating agents.", "categories": [] }, { "article_id": 283210, "title": "Shifting patterns of multiple sclerosis treatment in a highly prevalent United States population", "summary": "<jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Our objectives were to (1) obtain the prevalence and demography of people with multiple sclerosis (MS) in a representative Colorado population, and (2) to assess the utilization of disease‐modifying therapy within this prevalent cohort.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>This is a retrospective, observational study of patients that had contact with the University of Colorado Health System from 2012 to 2020. We queried Health Data Compass, a data warehouse, for patient data and applied the MS Prevalence Workgroup Algorithm to generate a prevalent cohort. We calculated prevalence as of 31 December 2020, and stratified by age, sex, race, and ethnicity. Payer information and treatment exposure were obtained from linked claims from the Colorado All Payers Claim Database. Disease‐modifying therapies were classified as highly effective and moderately effective based on the clinical trial, TREAT‐MS (NCT03500328).</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>From a population of 1,382,821 individuals, 8557 people with MS were captured. Age‐adjusted prevalence of MS as of 31 December 2020 was 572.3 per 100,000 with a mean age of 47.36. Prevalence varied between demographic subgroups, with the lowest prevalence in Hispanic men (215.6) and highest in White (824.1) and Black women (820.1). Overall disease‐modifying therapy exposure was 62.4%, with increased highly effective therapy use and a corresponding decrease in moderately effective therapy use on a yearly basis.</jats:p></jats:sec><jats:sec><jats:title>Interpretation</jats:title><jats:p>MS is highly prevalent in a representative Colorado cohort. Overall treatment and proportion of highly effective therapy exposure increased significantly during a critical period of MS therapeutic advances, indicating a shift in disease management driven sharply by the availability of on‐label anti‐CD20 therapy.</jats:p></jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/38654416/?fc=20210216052009&ff=20240425062541&v=2.18.0.post9+e462414", "published_date": "2024-04-24T10:00:00Z", "source": "PubMed", "publisher": "Wiley", "container_title": "Annals of Clinical and Translational Neurology", "authors": [ { "author_id": 348829, "given_name": "Sue", "family_name": "Kwon", "ORCID": "http://orcid.org/0000-0002-3694-2855", "country": null }, { "author_id": 265383, "given_name": "Stefan", "family_name": "Sillau", "ORCID": null, "country": null }, { "author_id": 331945, "given_name": "John R.", "family_name": "Corboy", "ORCID": "http://orcid.org/0000-0003-4169-1461", "country": null }, { "author_id": 265380, "given_name": "Kavita V.", "family_name": "Nair", "ORCID": null, "country": null }, { "author_id": 348830, "given_name": "Aaron M.", "family_name": "Carlson", "ORCID": "http://orcid.org/0000-0001-7520-7864", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T18:25:37.887218Z", "noun_phrases": null, "doi": "10.1002/acn3.52069", "access": "restricted", "takeaways": "", "categories": [] }, { "article_id": 283209, "title": "A rapid review of differences in cerebrospinal neurofilament light levels in clinical subtypes of progressive multiple sclerosis", "summary": "<jats:sec><jats:title>Background</jats:title><jats:p>Multiple sclerosis (MS) is divided into three clinical phenotypes: relapsing–remitting MS (RRMS), secondary progressive MS (SPMS), and primary progressive MS (PPMS). It is unknown to what extent SPMS and PPMS pathophysiology share inflammatory or neurodegenerative pathological processes. Cerebrospinal (CSF) neurofilament light (NfL) has been broadly studied in different MS phenotypes and is a candidate biomarker for comparing MS subtypes.</jats:p></jats:sec><jats:sec><jats:title>Research question</jats:title><jats:p>Are CSF NfL levels different among clinical subtypes of progressive MS?</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>A search strategy identifying original research investigating fluid neurodegenerative biomarkers in progressive forms of MS between 2010 and 2022 was applied to Medline. Identified articles underwent title and abstract screen and full text review against pre-specified criteria. Data abstraction was limited to studies that measured NfL levels in the CSF. Reported statistical comparisons of NfL levels between clinical phenotypes were abstracted qualitatively.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>18 studies that focused on investigating direct comparisons of CSF NfL from people with MS were included in the final report. We found NfL levels were typically reported to be higher in relapsing and progressive MS compared to healthy controls. Notably, higher NfL levels were not clearly associated with progressive MS subtypes when compared to relapsing MS, and there was no observed difference in NfL levels between PPMS and SPMS in articles that separately assessed these phenotypes.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>CSF NfL levels distinguish individuals with MS from healthy controls but do not differentiate MS subtypes. Broad biological phenotyping is needed to overcome limitations of current clinical phenotyping and improve biomarker translatability to decision-making in the clinic.</jats:p></jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/38654736/?fc=20210216052009&ff=20240425062541&v=2.18.0.post9+e462414", "published_date": "2024-04-24T10:00:00Z", "source": "PubMed", "publisher": "Frontiers Media SA", "container_title": "Frontiers in Neurology", "authors": [ { "author_id": 291952, "given_name": "Haritha L.", "family_name": "Desu", "ORCID": null, "country": null }, { "author_id": 348715, "given_name": "Katherine M.", "family_name": "Sawicka", "ORCID": null, "country": null }, { "author_id": 273448, "given_name": "Emily", "family_name": "Wuerch", "ORCID": null, "country": null }, { "author_id": 348716, "given_name": "Vanessa", "family_name": "Kitchin", "ORCID": null, "country": null }, { "author_id": 272355, "given_name": "Jacqueline A.", "family_name": "Quandt", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T18:25:36.807917Z", "noun_phrases": null, "doi": "10.3389/fneur.2024.1382468", "access": "open", "takeaways": "Cerebrospinal (CSF) neurofilament light (NfL) has been studied in different MS phenotypes and is a candidate biomarker for comparing MS subtypes. CSF NfL levels are higher in relapsing and progressive MS compared to healthy controls, but not in PPMS or SPMS.", "categories": [] }, { "article_id": 283208, "title": "Editorial: Pediatric multiple sclerosis - from bench to bedside", "summary": "No abstract", "link": "https://pubmed.ncbi.nlm.nih.gov/38655108/?fc=20210216052009&ff=20240425062541&v=2.18.0.post9+e462414", "published_date": "2024-04-24T10:00:00Z", "source": "PubMed", "publisher": "Frontiers Media SA", "container_title": "Frontiers in Neuroscience", "authors": [ { "author_id": 155107, "given_name": "Ethel", "family_name": "Ciampi", "ORCID": "http://orcid.org/0000-0002-7330-5433", "country": null }, { "author_id": 191028, "given_name": "Filipe", "family_name": "Palavra", "ORCID": "http://orcid.org/0000-0002-2165-130X", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T18:25:35.716913Z", "noun_phrases": null, "doi": "10.3389/fnins.2024.1381189", "access": "open", "takeaways": null, "categories": [] }, { "article_id": 283207, "title": "BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair", "summary": "<jats:title>Abstract</jats:title><jats:p>In multiple sclerosis (MS), persisting disability can occur independent of relapse activity or development of new central nervous system (CNS) inflammatory lesions, termed chronic progression. This process occurs early and it is mostly driven by cells within the CNS. One promising strategy to control progression of MS is the inhibition of the enzyme Bruton's tyrosine kinase (BTK), which is centrally involved in the activation of both B cells and myeloid cells, such as macrophages and microglia. The benefit of BTK inhibition by evobrutinib was shown as we observed reduced pro-inflammatory activation of microglia when treating chronic experimental autoimmune encephalomyelitis (EAE) or following the adoptive transfer of activated T cells. Additionally, in a model of toxic demyelination, evobrutinib-mediated BTK inhibition promoted the clearance of myelin debris by microglia, leading to an accelerated remyelination. These findings highlight that BTK inhibition has the potential to counteract underlying chronic progression of MS.</jats:p>", "link": "https://pubmed.ncbi.nlm.nih.gov/38656399/?fc=20210216052009&ff=20240425062541&v=2.18.0.post9+e462414", "published_date": "2024-04-24T10:00:00Z", "source": "PubMed", "publisher": "Springer Science and Business Media LLC", "container_title": "Acta Neuropathologica", "authors": [ { "author_id": 275240, "given_name": "Anastasia", "family_name": "Geladaris", "ORCID": null, "country": null }, { "author_id": 167999, "given_name": "Sebastian", "family_name": "Torke", "ORCID": "http://orcid.org/0000-0002-1029-3623", "country": null }, { "author_id": 325863, "given_name": "Darius", "family_name": "Saberi", "ORCID": "http://orcid.org/0000-0002-0004-4578", "country": null }, { "author_id": 348831, "given_name": "Yasemin B.", "family_name": "Alankus", "ORCID": null, "country": null }, { "author_id": 348832, "given_name": "Frank", "family_name": "Streit", "ORCID": null, "country": null }, { "author_id": 348833, "given_name": "Sabrina", "family_name": "Zechel", "ORCID": null, "country": null }, { "author_id": 309281, "given_name": "Christine", "family_name": "Stadelmann-Nessler", "ORCID": null, "country": null }, { "author_id": 348834, "given_name": "Andreas", "family_name": "Fischer", "ORCID": null, "country": null }, { "author_id": 326609, "given_name": "Ursula", "family_name": "Boschert", "ORCID": "http://orcid.org/0000-0001-7541-5284", "country": null }, { "author_id": 253883, "given_name": "Darius", "family_name": "Häusler", "ORCID": null, "country": null }, { "author_id": 168008, "given_name": "Martin S.", "family_name": "Weber", "ORCID": "http://orcid.org/0000-0001-8409-0389", "country": null } ], "relevant": true, "ml_prediction_gnb": true, "ml_prediction_lr": true, "ml_prediction_lsvc": true, "discovery_date": "2024-04-24T18:25:34.821522Z", "noun_phrases": null, "doi": "10.1007/s00401-024-02730-0", "access": "restricted", "takeaways": "In MS, persisting disability can occur independent of relapse activity or development of new central nervous system (CNS) inflammatory lesions. One promising strategy to control progression of MS is", "categories": [] }, { "article_id": 283205, "title": "Mendelian randomization and colocalization analysis reveal novel drug targets for myasthenia gravis", "summary": "<jats:title>Abstract</jats:title><jats:sec>\n <jats:title>Objective</jats:title>\n <jats:p>Myasthenia gravis (MG) is a complex autoimmune disease affecting the neuromuscular junction with limited drug options, but the field of MG treatment recently benefits from novel biological agents. We performed a drug-targeted Mendelian randomization (MR) study to identify novel therapeutic targets of MG.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Methods</jats:title>\n <jats:p>Cis-expression quantitative loci (cis-eQTL), which proxy expression levels for 2176 druggable genes, were used for MR analysis. Causal relationships between genes and disease, identified by eQTL MR analysis, were verified by comprehensive sensitivity, colocalization, and protein quantitative loci (pQTL) MR analyses. The protein-protein interaction (PPI) analysis was also performed to extend targets, followed by enzyme-linked immunosorbent assay (ELISA) to explore the serum level of drug targets in MG patients. A phenome-wide MR analysis was then performed to assess side effects with a clinical trial review assessing druggability.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Results</jats:title>\n <jats:p>The eQTL MR analysis has identified eight potential targets for MG, one for early-onset MG and seven for late-onset MG. Further colocalization analyses indicated that CD226, CDC42BPB, PRSS36, and TNFSF12 possess evidence for colocalization with MG or late-onset MG. pQTL MR analyses identified the causal relations of TNFSF12 and CD226 with MG and late-onset MG. Furthermore, PPI analysis has revealed the protein interaction between TNFSF12-TNFSF13(APRIL) and TNFSF12-TNFSF13B(BLyS). Elevated TNFSF13 serum level of MG patients was also identified by ELISA experiments. This study has ultimately proposed three promising therapeutic targets (TNFSF12, TNFSF13, TNFSF13B) of MG.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Conclusions</jats:title>\n <jats:p>Three drug targets associated with the BLyS/APRIL pathway have been identified. Multiple biological agents, including telitacicept and belimumab, are promising for MG therapy.</jats:p>\n </jats:sec>", "link": "https://humgenomics.biomedcentral.com/articles/10.1186/s40246-024-00607-7", "published_date": "2024-04-23T23:00:00Z", "source": "BioMedCentral", "publisher": "Springer Science and Business Media LLC", "container_title": "Human Genomics", "authors": [ { "author_id": 324861, "given_name": "Yuzhen", "family_name": "Ouyang", "ORCID": null, "country": null }, { "author_id": 158328, "given_name": "Yu", "family_name": "Chen", "ORCID": "http://orcid.org/0000-0001-9767-4797", "country": null }, { "author_id": 348836, "given_name": "Kangzhi", "family_name": "Chen", "ORCID": null, "country": null }, { "author_id": 348837, "given_name": "Zhenwei", "family_name": "Tang", "ORCID": null, "country": null }, { "author_id": 348838, "given_name": "Guanzhong", "family_name": "Shi", "ORCID": null, "country": null }, { "author_id": 348839, "given_name": "Chunrun", "family_name": "Qu", "ORCID": null, "country": null }, { "author_id": 348840, "given_name": "Kaiyue", "family_name": "Zhang", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T16:27:08.631470Z", "noun_phrases": null, "doi": "10.1186/s40246-024-00607-7", "access": "restricted", "takeaways": "Myasthenia gravis (MG) is a complex autoimmune disease affecting the neuromuscular junction with limited drug options. We performed a drug-targeted Mendelian randomization study to identify novel therapeutic targets of MG. Three drug targets associated with the BLyS/APRIL pathway have been identified. Telitacicept and belimumab are promising for MG therapy.", "categories": [] }, { "article_id": 283204, "title": "Evolving insights into the improvement of adoptive T-cell immunotherapy through PD-1/PD-L1 blockade in the clinical spectrum of lung cancer", "summary": "<jats:title>Abstract</jats:title><jats:p>Undeniably, cancer immunotherapies have expanded the spectrum of cancer treatment, however, some patients do not respond to immunotherapies. This scenario is no different for lung cancer, whose two main types, non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), still pose a serious clinical challenge. Adoptive T-cell therapies (ATC), which primarily include cytokine-induced killer (CIK) cell therapy, chimeric antigen receptor T-cell (CAR T-cell) therapy and γδ-T-cell therapy, strengthen the patient’s immune system in combating cancer. Combining ATC with immune checkpoint inhibitors (ICI) further enhances the effectiveness of this approach to eradicate cancer. With a particular emphasis on CIK cell therapy, which recently completed 30 years, we highlight the role of the PD-1/PD-L1 axis in NSCLC and SCLC. Besides, we provide insights into the potential synergies of PD-1/PD-L1 inhibitors with adoptive T-cell immunotherapy in reshaping the treatment paradigm for lung cancer.</jats:p>", "link": "https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-023-01926-4", "published_date": "2024-04-23T23:00:00Z", "source": "BioMedCentral", "publisher": "Springer Science and Business Media LLC", "container_title": "Molecular Cancer", "authors": [ { "author_id": 348835, "given_name": "Yutao", "family_name": "Li", "ORCID": null, "country": null }, { "author_id": 235009, "given_name": "Amit", "family_name": "Sharma", "ORCID": "http://orcid.org/0000-0002-2216-5389", "country": "DE" }, { "author_id": 345623, "given_name": "Ingo G.H.", "family_name": "Schmidt-Wolf", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T16:26:48.668266Z", "noun_phrases": null, "doi": "10.1186/s12943-023-01926-4", "access": "restricted", "takeaways": "Some cancer patients do not respond to immunotherapies. Adoptive T-cell therapies strengthen the patient’s immune system in combating cancer. Combining ATC with immune checkpoint inhibitors (ICI) further enhances the effectiveness of this approach to eradicate cancer.", "categories": [] }, { "article_id": 283202, "title": "Fatigue in children using motor imagery and P300 brain-computer interfaces", "summary": "<jats:title>Abstract</jats:title><jats:sec>\n <jats:title>Background</jats:title>\n <jats:p>Brain-computer interface (BCI) technology offers children with quadriplegic cerebral palsy unique opportunities for communication, environmental exploration, learning, and game play. Research in adults demonstrates a negative impact of fatigue on BCI enjoyment, while effects on BCI performance are variable. To date, there have been no pediatric studies of BCI fatigue. The purpose of this study was to assess the effects of two different BCI paradigms, motor imagery and visual P300, on the development of self-reported fatigue and an electroencephalography (EEG) biomarker of fatigue in typically developing children.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Methods</jats:title>\n <jats:p>Thirty-seven typically-developing school-aged children were recruited to a prospective, crossover study. Participants attended three sessions: (A) motor imagery-BCI, (B) visual P300-BCI, and (C) video viewing (control). The motor imagery task involved an imagined left- or right-hand squeeze. The P300 task involved attending to one square on a 3 × 3 grid during a random single flash sequence. Each paradigm had respective calibration periods and a similar visual counting game. Primary outcomes were self-reported fatigue and the power of the EEG alpha band both collected during resting-state periods pre- and post-task. Self-reported fatigue was measured using a 10-point visual analog scale. EEG alpha band power was calculated as the integrated power spectral density from 8 to 12 Hz of the EEG spectrum.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Results</jats:title>\n <jats:p>Thirty-two children completed the protocol (age range 7–16, 63% female). Self-reported fatigue and EEG alpha band power increased across all sessions (<jats:italic>F</jats:italic><jats:sub>(1,155)</jats:sub> = 33.9, <jats:italic>p</jats:italic> < 0.001; <jats:italic>F</jats:italic> = 5.0<jats:sub>(1,149)</jats:sub>, <jats:italic>p</jats:italic> = 0.027 respectively). No differences in fatigue development were observed between session types. There was no correlation between self-reported fatigue and EEG alpha band power change. BCI performance varied between participants and paradigms as expected but was not associated with self-reported fatigue or EEG alpha band power.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Conclusion</jats:title>\n <jats:p>Short periods (30-mintues) of BCI use can increase self-reported fatigue and EEG alpha band power to a similar degree in children performing motor imagery and P300 BCI paradigms. Performance was not associated with our measures of fatigue; the impact of fatigue on useability and enjoyment is unclear. Our results reflect the variability of fatigue and the BCI experience more broadly in children and warrant further investigation.</jats:p>\n </jats:sec>", "link": "https://jneuroengrehab.biomedcentral.com/articles/10.1186/s12984-024-01349-2", "published_date": "2024-04-23T23:00:00Z", "source": "BioMedCentral", "publisher": "Springer Science and Business Media LLC", "container_title": "Journal of NeuroEngineering and Rehabilitation", "authors": [ { "author_id": 348852, "given_name": "Joanna RG.", "family_name": "Keough", "ORCID": null, "country": null }, { "author_id": 348853, "given_name": "Brian", "family_name": "Irvine", "ORCID": null, "country": null }, { "author_id": 348854, "given_name": "Dion", "family_name": "Kelly", "ORCID": null, "country": null }, { "author_id": 348855, "given_name": "James", "family_name": "Wrightson", "ORCID": null, "country": null }, { "author_id": 348856, "given_name": "Daniel", "family_name": "Comaduran Marquez", "ORCID": null, "country": null }, { "author_id": 348857, "given_name": "Eli", "family_name": "Kinney-Lang", "ORCID": null, "country": null }, { "author_id": 348858, "given_name": "Adam", "family_name": "Kirton", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T10:26:48.567543Z", "noun_phrases": null, "doi": "10.1186/s12984-024-01349-2", "access": "restricted", "takeaways": null, "categories": [] }, { "article_id": 283199, "title": "Regulation of human microglial gene expression and function via RNAase-H active antisense oligonucleotides in vivo in Alzheimer’s disease", "summary": "<jats:title>Abstract</jats:title><jats:sec>\n <jats:title>Background</jats:title>\n <jats:p>Microglia play important roles in maintaining brain homeostasis and neurodegeneration. The discovery of genetic variants in genes predominately or exclusively expressed in myeloid cells, such as Apolipoprotein E (<jats:italic>APOE</jats:italic>) and triggering receptor expressed on myeloid cells 2 (<jats:italic>TREM2</jats:italic>), as the strongest risk factors for Alzheimer’s disease (AD) highlights the importance of microglial biology in the brain. The sequence, structure and function of several microglial proteins are poorly conserved across species, which has hampered the development of strategies aiming to modulate the expression of specific microglial genes. One way to target <jats:italic>APOE</jats:italic> and <jats:italic>TREM2</jats:italic> is to modulate their expression using antisense oligonucleotides (ASOs).</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Methods</jats:title>\n <jats:p>In this study, we identified, produced, and tested novel, selective and potent ASOs for human <jats:italic>APOE</jats:italic> and <jats:italic>TREM2</jats:italic>. We used a combination of in vitro iPSC-microglia models, as well as microglial xenotransplanted mice to provide proof of activity in human microglial in vivo.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Results</jats:title>\n <jats:p>We proved their efficacy in human iPSC microglia in vitro, as well as their pharmacological activity in vivo in a xenografted microglia model. We demonstrate ASOs targeting human microglia can modify their transcriptional profile and their response to amyloid-β plaques in vivo in a model of AD.</jats:p>\n </jats:sec><jats:sec>\n <jats:title>Conclusions</jats:title>\n <jats:p>This study is the first proof-of-concept that human microglial can be modulated using ASOs in a dose-dependent manner to manipulate microglia phenotypes and response to neurodegeneration in vivo<jats:italic>.</jats:italic></jats:p>\n </jats:sec>", "link": "https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-024-00725-9", "published_date": "2024-04-23T23:00:00Z", "source": "BioMedCentral", "publisher": "Springer Science and Business Media LLC", "container_title": "Molecular Neurodegeneration", "authors": [ { "author_id": 348859, "given_name": "Lina", "family_name": "Vandermeulen", "ORCID": null, "country": null }, { "author_id": 348860, "given_name": "Ivana", "family_name": "Geric", "ORCID": null, "country": null }, { "author_id": 319889, "given_name": "Laura", "family_name": "Fumagalli", "ORCID": "http://orcid.org/0000-0002-9333-926X", "country": null }, { "author_id": 348861, "given_name": "Mohamed", "family_name": "Kreir", "ORCID": null, "country": null }, { "author_id": 348862, "given_name": "Ashley", "family_name": "Lu", "ORCID": null, "country": null }, { "author_id": 348863, "given_name": "Annelies", "family_name": "Nonneman", "ORCID": null, "country": null }, { "author_id": 348864, "given_name": "Jessie", "family_name": "Premereur", "ORCID": null, "country": null }, { "author_id": 348865, "given_name": "Leen", "family_name": "Wolfs", "ORCID": null, "country": null }, { "author_id": 348866, "given_name": "Rafaela", "family_name": "Policarpo", "ORCID": null, "country": null }, { "author_id": 348867, "given_name": "Nicola", "family_name": "Fattorelli", "ORCID": null, "country": null }, { "author_id": 348868, "given_name": "An", "family_name": "De Bondt", "ORCID": null, "country": null }, { "author_id": 348869, "given_name": "Ilse", "family_name": "Van Den Wyngaert", "ORCID": null, "country": null }, { "author_id": 348870, "given_name": "Bob", "family_name": "Asselbergh", "ORCID": null, "country": null }, { "author_id": 348871, "given_name": "Mark", "family_name": "Fiers", "ORCID": null, "country": null }, { "author_id": 265440, "given_name": "Bart", "family_name": "De Strooper", "ORCID": null, "country": null }, { "author_id": 348872, "given_name": "Constantin", "family_name": "d’Ydewalle", "ORCID": null, "country": null }, { "author_id": 319893, "given_name": "Renzo", "family_name": "Mancuso", "ORCID": "http://orcid.org/0000-0002-7046-3348", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2024-04-24T06:26:48.496143Z", "noun_phrases": null, "doi": "10.1186/s13024-024-00725-9", "access": "restricted", "takeaways": "Microglia play important roles in maintaining brain homeostasis and neurodegeneration. APOE and TREM2 are risk factors for Alzheimer's disease. Antisense oligonucleotides (ASOs) can be used to target microglia expression using selective and potent ASOs.", "categories": [] } ] }