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{ "count": 24302, "next": "http://api.gregory-ms.com/articles/?format=api&page=2", "previous": null, "results": [ { "article_id": 283097, "title": "Astrocytes ACLYmate to chronic neuroinflammation", "summary": "Astrocytes are essential cells of the mammalian central nervous system (CNS), with key roles in development, homeostasis, and disease. Lee and colleagues recently showed that astrocytes can develop epigenetic memory, which enhances proinflammatory responses to subsequent stimulation, potentially driving sustained neurological disease pathology, such as in multiple sclerosis (MS).", "link": "https://pubmed.ncbi.nlm.nih.gov/38632002/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": "Elsevier BV", "container_title": "Trends in Immunology", "authors": [ { "author_id": 348395, "given_name": "Kevin", "family_name": "Champagne-Jorgensen", "ORCID": "http://orcid.org/0000-0002-1445-1449", "country": null }, { "author_id": 174752, "given_name": "Jennifer L.", "family_name": "Gommerman", "ORCID": "http://orcid.org/0000-0003-4576-6168", "country": "CA" } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-18T05:25:37.896705Z", "noun_phrases": null, "doi": "10.1016/j.it.2024.04.003", "access": "restricted", "takeaways": null, "categories": [] }, { "article_id": 283096, "title": "Effect of siponimod on lymphocyte subsets in active secondary progressive multiple sclerosis and clinical implications", "summary": "<jats:title>Abstract</jats:title><jats:sec>\n<jats:title>Background</jats:title>\n<jats:p>Circulating immune cells play a pathogenic role in multiple sclerosis (MS). However, the role of specific lymphocyte subpopulations is not unveiled yet, especially in progressive stages. We aimed to investigate lymphocyte changes during siponimod treatment in active secondary progressive MS (aSPMS) and their associations with clinical outcomes.</jats:p>\n</jats:sec><jats:sec>\n<jats:title>Methods</jats:title>\n<jats:p>We enrolled 46 aSPMS patients starting on siponimod treatment with at least 6 months of follow-up and two visits within the scheduled timeframes and 14 sex- and age-matched healthy controls (HCs). Clinical and laboratory data were collected retrospectively at baseline, 3rd, 6th, 12th, and 24th month for MS patients, and at baseline for HCs.</jats:p>\n</jats:sec><jats:sec>\n<jats:title>Results</jats:title>\n<jats:p>At baseline SPMS patients presented with increased naïve regulatory T lymphocytes (<jats:italic>p</jats:italic> = 0.02) vs. HCs. Over time, SPMS patients showed decreased T CD4+ (coeff. range = −24/−17, 95% CI range = −31.60 to −10.40), B lymphocyte (coeff. range = −3.77/−2.54, 95% CI range = −6.02 to −0.35), memory regulatory B cells (coeff. range = −0.78/−0.57, 95% CI range = −1.24 to −0.17) and CD4/CD8 ratio (coeff. range = −4.44/−0.67, 95% CI range = −1.61 to −0.17) from month 3 thereafter vs. baseline, and reduced CD3+CD20+ lymphocytes from month 12 thereafter (coeff. range = −0.32/−0.24, 95% CI range = −0.59 to −0.03). Patients not experiencing disability progression while on siponimod treatment showed B lymphocyte reduction from month 3 (coeff. range = −4.23/−2.32, 95% CI range = −7.53 to −0.15) and CD3+CD20+ lymphocyte reduction from month 12 (coeff. range = −0.32/−0.24, 95% CI range = −0.59 to −0.03) vs. patients experiencing progression.</jats:p>\n</jats:sec><jats:sec>\n<jats:title>Conclusions</jats:title>\n<jats:p>Patients treated with siponimod showed a T and B lymphocyte reduction, especially CD4+, CD3+CD20+ and naïve regulatory T cells and memory regulatory B cells. Disability progression while on siponimod treatment was associated with a less pronounced effect on B and CD3+CD20+ lymphocytes.</jats:p>\n</jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/38632126/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": "Springer Science and Business Media LLC", "container_title": "Journal of Neurology", "authors": [ { "author_id": 221216, "given_name": "Antonio Luca", "family_name": "Spiezia", "ORCID": "http://orcid.org/0000-0003-3287-3247", "country": "IT" }, { "author_id": 286450, "given_name": "Giulia", "family_name": "Scalia", "ORCID": null, "country": null }, { "author_id": 168446, "given_name": "Maria", "family_name": "Petracca", "ORCID": "http://orcid.org/0000-0001-9429-2769", "country": "IT" }, { "author_id": 319909, "given_name": "Daniele", "family_name": "Caliendo", "ORCID": "http://orcid.org/0000-0001-9280-8477", "country": null }, { "author_id": 167240, "given_name": "Marcello", "family_name": "Moccia", "ORCID": "http://orcid.org/0000-0003-2613-3090", "country": "IT" }, { "author_id": 295070, "given_name": "Antonia", "family_name": "Fiore", "ORCID": null, "country": null }, { "author_id": 286443, "given_name": "Vincenza", "family_name": "Cerbone", "ORCID": null, "country": null }, { "author_id": 143716, "given_name": "Roberta", "family_name": "Lanzillo", "ORCID": "http://orcid.org/0000-0001-6388-8180", "country": null }, { "author_id": 217509, "given_name": "Vincenzo", "family_name": "Brescia Morra", "ORCID": "http://orcid.org/0000-0002-2807-6483", "country": null }, { "author_id": 148586, "given_name": "Antonio", "family_name": "Carotenuto", "ORCID": "http://orcid.org/0000-0002-1574-9693", "country": "IT" } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-18T05:25:36.518005Z", "noun_phrases": null, "doi": "10.1007/s00415-024-12362-9", "access": "open", "takeaways": null, "categories": [] }, { "article_id": 283095, "title": "Robotic Biliary Stricturoplasty and Roux-en-Y Hepaticojejunostomy After Hepatic Artery Infusion Pump Injury", "summary": "CONCLUSIONS: Robotic biliary stricturoplasty with RY hepaticojejunostomy for treatment of biliary sclerosis after HAIP chemotherapy is safe and feasible. Appropriate experience in minimally invasive hepatobiliary surgery is necessary to achieve this goal.", "link": "https://pubmed.ncbi.nlm.nih.gov/38632219/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": "Springer Science and Business Media LLC", "container_title": "Annals of Surgical Oncology", "authors": [ { "author_id": 348390, "given_name": "Emanuel", "family_name": "Shapera", "ORCID": null, "country": null }, { "author_id": 348391, "given_name": "Sharona", "family_name": "Ross", "ORCID": null, "country": null }, { "author_id": 348392, "given_name": "Tara", "family_name": "Pattilachan", "ORCID": null, "country": null }, { "author_id": 348393, "given_name": "Maria", "family_name": "Christodoulou", "ORCID": null, "country": null }, { "author_id": 348394, "given_name": "Iswanto", "family_name": "Sucandy", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-18T05:25:35.444898Z", "noun_phrases": null, "doi": "10.1245/s10434-024-15258-0", "access": "restricted", "takeaways": null, "categories": [] }, { "article_id": 283094, "title": "Reverse causation between multiple sclerosis and psoriasis: a genetic correlation and Mendelian randomization study", "summary": "<jats:title>Abstract</jats:title><jats:p>Observational studies have found a potential bidirectional positive association between multiple sclerosis and psoriasis, but these studies are susceptible to confounding factors. We examined the directionality of causation using Mendelian randomization and estimated the genetic correlation using the linkage disequilibrium score. We performed Mendelian randomization analysis using large-scale genome-wide association studies datasets from the International Multiple Sclerosis Genetics Consortium (IMSGC, 115,803 individuals of European ancestry) and FinnGen (252,323 individuals of European ancestry). We selected several Mendelian randomization methods including causal analysis using summary effect (CAUSE), inverse variance-weighted (IVW), and pleiotropy-robust methods. According to CAUSE and IVW the genetic liability to MS reduces the risk of psoriasis (CAUSE odds ratio [OR] 0.93, <jats:italic>p</jats:italic> = 0.045; IVW OR 0.93, <jats:italic>p</jats:italic> = 2.51 × 10<jats:sup>–20</jats:sup>), and vice versa (CAUSE OR 0.72, <jats:italic>p</jats:italic> = 0.001; IVW OR 0.71, <jats:italic>p</jats:italic> = 4.80 × 10<jats:sup>–26</jats:sup>). Pleiotropy-robust methods show the same results, with all <jats:italic>p</jats:italic>-values < 0.05. The linkage disequilibrium score showed no genetic correlation between psoriasis and MS (rg = − 0.071, <jats:italic>p</jats:italic> = 0.2852). In summary, there is genetic evidence that MS reduces the risk of psoriasis, and vice versa.</jats:p>", "link": "https://pubmed.ncbi.nlm.nih.gov/38632254/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": "Springer Science and Business Media LLC", "container_title": "Scientific Reports", "authors": [ { "author_id": 237136, "given_name": "Hao", "family_name": "Zhou", "ORCID": null, "country": null }, { "author_id": 348386, "given_name": "Yajie", "family_name": "Qi", "ORCID": null, "country": null }, { "author_id": 348387, "given_name": "Yingxin", "family_name": "Xu", "ORCID": null, "country": null }, { "author_id": 348388, "given_name": "Xiaoyi", "family_name": "Qi", "ORCID": null, "country": null }, { "author_id": 348389, "given_name": "Hui", "family_name": "Qi", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-18T05:25:34.317862Z", "noun_phrases": null, "doi": "10.1038/s41598-024-58182-9", "access": "open", "takeaways": null, "categories": [] }, { "article_id": 283093, "title": "Increased IL-22 in cerebrospinal fluid of neuro-behçet’s disease patients", "summary": "Remitting-Relapsing Multiple Sclerosis (RRMS) and Neuro-Behçet Disease (NBD) are two chronic neuro-inflammatory disorders leading to brain damage and disability in young adults. Herein, we investigated in these patients the cytokine response by beads-based multiplex assays during the early stages of these disorders. Cytokine investigations were carried out on treatment-naive patients suffering from RRMS and NBD recruited at the first episode of clinical relapse. Our findings demonstrate that...", "link": "https://pubmed.ncbi.nlm.nih.gov/38631183/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": "Elsevier BV", "container_title": "Cytokine", "authors": [ { "author_id": 244423, "given_name": "Meriam", "family_name": "Belghith", "ORCID": null, "country": null }, { "author_id": 173726, "given_name": "Olfa", "family_name": "Maghrebi", "ORCID": "http://orcid.org/0000-0002-8824-6659", "country": null }, { "author_id": 348379, "given_name": "Rafika", "family_name": "Ben Laamari", "ORCID": null, "country": null }, { "author_id": 244415, "given_name": "Mariem", "family_name": "Hanachi", "ORCID": null, "country": null }, { "author_id": 348380, "given_name": "Sana", "family_name": "Hrir", "ORCID": null, "country": null }, { "author_id": 173731, "given_name": "Zakaria", "family_name": "Saied", "ORCID": "http://orcid.org/0000-0002-4115-8758", "country": "TN" }, { "author_id": 244419, "given_name": "Samir", "family_name": "Belal", "ORCID": null, "country": null }, { "author_id": 348381, "given_name": "Adel", "family_name": "Driss", "ORCID": null, "country": null }, { "author_id": 244420, "given_name": "Samia", "family_name": "Ben Sassi", "ORCID": null, "country": null }, { "author_id": 348382, "given_name": "Thouraya", "family_name": "Boussoffara", "ORCID": null, "country": null }, { "author_id": 244421, "given_name": "Mohamed-Ridha", "family_name": "Barbouche", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-18T05:25:31.674605Z", "noun_phrases": null, "doi": "10.1016/j.cyto.2024.156617", "access": "open", "takeaways": null, "categories": [] }, { "article_id": 283091, "title": "Immune checkpoint inhibitors in Cancer patients with rheumatologic preexisting autoimmune diseases: a systematic review and meta-analysis", "summary": null, "link": "https://bmccancer.biomedcentral.com/articles/10.1186/s12885-024-12256-z", "published_date": "2024-04-16T23:00:00Z", "source": "BioMedCentral", "publisher": null, "container_title": null, "authors": [], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-18T00:26:48.364387Z", "noun_phrases": null, "doi": "10.1186/s12885-024-12256-z", "access": null, "takeaways": null, "categories": [] }, { "article_id": 283089, "title": "Genetics of immune response to Epstein-Barr virus: prospects for multiple sclerosis pathogenesis", "summary": "<jats:title>Abstract</jats:title>\n<jats:p>Epstein-Barr virus (EBV) infection has been advocated as a prerequisite for developing multiple sclerosis (MS) and possibly the propagation of the disease. However, the precise mechanisms for such influences are still unclear. A large-scale study investigating the host genetics of EBV serology and related clinical manifestations, such as infectious mononucleosis (IM), may help us better understand the role of EBV in MS pathogenesis. This study evaluates the host genetic factors that influence serological response against EBV and history of IM and cross-evaluates them with MS risk and genetic susceptibility in the Swedish population.</jats:p>\n<jats:p>Plasma IgG antibody levels against EBV nuclear antigen-1 (EBNA-1, truncated=aa[325-641], peptide=aa[385-420]) and viral capsid antigen p18 (VCAp18) were measured using bead-based multiplex serology for 8744 MS cases and 7229 population-matched controls. The MS risk association for high/low EBV antibody levels and history of IM was compared to relevant clinical measures along with sex, age at sampling, and associated HLA allele variants. Genome-wide and HLA allele association analyses were also performed to identify genetic risk factors for EBV antibody response and IM history.</jats:p>\n<jats:p>Higher antibody levels against VCAp18 (OR=1.74, 95% CI=1.60-1.88) and EBNA-1, particularly the peptide (OR=3.13, 95% CI=2.93-3.35), were associated with an increased risk for MS. The risk increased with higher anti-EBNA-1 IgG levels up to twelve times the reference risk. We also identified several independent HLA haplotypes associated with EBV serology overlapping with known MS risk alleles (e.g., DRB1*15:01). Although there were several candidates, no variants outside the HLA region reached genome-wide significance. Cumulative HLA risk for anti-EBNA-1 IgG levels, particularly the peptide fragment, was strongly associated with MS. In contrast, the genetic risk for high anti-VCAp18 IgG levels was not as strongly associated with MS risk. IM history was not associated with class II HLA genes but negatively associated with A*02:01, which is protective against MS.</jats:p>\n<jats:p>Our findings emphasize that the risk association between anti-EBNA-1 IgG levels and MS may be partly due to overlapping HLA associations. Additionally, the increasing MS risk with increasing anti-EBNA-1 levels would be consistent with a pathogenic role of the EBNA-1 immune response, perhaps through molecular mimicry. Given that high anti-EBNA-1 antibodies may reflect a poorly controlled T-cell defense against the virus, our findings would be consistent with DRB1*15:01 being a poor class II antigen in the immune defense against EBV. Lastly, the difference in genetic control of IM supports the independent roles of EBNA-1 and IM in MS susceptibility.</jats:p>", "link": "https://pubmed.ncbi.nlm.nih.gov/38630618/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": null, "container_title": null, "authors": [ { "author_id": 218791, "given_name": "Katarina", "family_name": "Tengvall", "ORCID": "http://orcid.org/0000-0003-0424-3571", "country": null }, { "author_id": 348369, "given_name": "Izaura", "family_name": "Bomfim Lima", "ORCID": null, "country": null }, { "author_id": 152921, "given_name": "Anna Karin", "family_name": "Hedström", "ORCID": "http://orcid.org/0000-0002-6612-4749", "country": null }, { "author_id": 333907, "given_name": "Julia", "family_name": "Butt", "ORCID": "http://orcid.org/0000-0001-7738-8611", "country": null }, { "author_id": 209290, "given_name": "Nicole", "family_name": "Brenner", "ORCID": "http://orcid.org/0000-0002-7690-4925", "country": null }, { "author_id": 348370, "given_name": "Alexandra", "family_name": "Gyllenberg", "ORCID": null, "country": null }, { "author_id": 170369, "given_name": "Pernilla", "family_name": "Stridh", "ORCID": "http://orcid.org/0000-0003-4855-0039", "country": null }, { "author_id": 218796, "given_name": "Mohsen", "family_name": "Khademi", "ORCID": "http://orcid.org/0000-0003-0801-1444", "country": null }, { "author_id": 169285, "given_name": "Ingemar", "family_name": "Ernberg", "ORCID": "http://orcid.org/0000-0001-6518-1648", "country": null }, { "author_id": 218794, "given_name": "Faiez", "family_name": "Al Nimer", "ORCID": "http://orcid.org/0000-0003-0937-5995", "country": null }, { "author_id": 142972, "given_name": "Ali", "family_name": "Manouchehrinia", "ORCID": "http://orcid.org/0000-0003-4857-5762", "country": "SE" }, { "author_id": 152920, "given_name": "Jan", "family_name": "Hillert", "ORCID": "http://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": 150782, "given_name": "Oluf", "family_name": "Andersen", "ORCID": "http://orcid.org/0000-0002-9089-0451", "country": null }, { "author_id": 206107, "given_name": "Peter", "family_name": "Sundström", "ORCID": "http://orcid.org/0000-0003-3552-1861", "country": null }, { "author_id": 209328, "given_name": "Tim", "family_name": "Waterboer", "ORCID": "http://orcid.org/0000-0002-0616-6963", "country": null }, { "author_id": 218798, "given_name": "Tomas", "family_name": "Olsson", "ORCID": "http://orcid.org/0000-0002-2938-1877", "country": "SE" }, { "author_id": 160914, "given_name": "Ingrid", "family_name": "Kockum", "ORCID": "http://orcid.org/0000-0002-0867-4726", "country": null }, { "author_id": 258953, "given_name": "Jesse", "family_name": "Huang", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-17T23:25:35.477161Z", "noun_phrases": null, "doi": "10.1093/brain/awae110", "access": "restricted", "takeaways": null, "categories": [] }, { "article_id": 283088, "title": "Insulin-like growth factor-1 (IGF-1) levels in multiple sclerosis patients: A systematic review and meta-analysis", "summary": "<jats:sec>\n<jats:title>Background and objective</jats:title>\n<jats:p>Multiple sclerosis (MS) is a chronic progressive autoimmune disorder of the central nervous system (CNS) that can cause inflammation, demyelination, and axon degeneration. Insulin-like growth factor-1 (IGF-1) is a single-chain polypeptide mainly synthesized in the liver and brain. IGF-1 causes neuronal and non-neuronal cell proliferation, survival, and differentiation. Therefore, it can be used in treating neuro-demyelinating diseases such as MS. The current systematic review and meta-analysis aims to compare the levels of IGF-1 in MS patients and healthy controls and also investigates IGF binding proteins (IGF-BP) and growth hormone (GH) levels between MS patients and healthy controls.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Methods</jats:title>\n<jats:p>In this study, we systematically searched electronic databases of PubMed, Scopus, Web of Science (WOS), and Google Scholar, up to December 2022. Studies that measured IGF-1, GH, IGFBP-1, IGFBP-2, or IGFBP-3 in MS patients and healthy controls in either blood or cerebral spinal fluid (CSF) were identified. We calculated Standardized mean differences (SMD) to compare levels of IGF-1, GH, IGFBP-1, IGFBP-2, or IGFBP-3 in MS patients and controls.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Results</jats:title>\n<jats:p>Finally, we included 11 eligible studies from 1998 to 2018. The sample size of included studies varied from 20 to 200 resulting in a total sample size of 1067 individuals, 531 MS patients, and 536 healthy controls. The mean age of the patient and control groups were 38.96 and 39.38, respectively. The average EDSS among patients was 4.56. We found that blood levels of IGF-1 (SMD = 0.20, 95% CI = -0.20 to 0.59, I2 = 82.4%, K = 8, n = 692), CSF level of IGF-1 (SMD = 0.25, 95% CI = -0.06 to 0.56, I2 = 0.0%, K = 3 n = 164) and blood levels of GH were not significantly higher in MS patients than controls (SMD = 0.08, 95% CI = -0.33 to 0.49, I2 = 77.0% K = 3, n = 421). Moreover, the blood levels of IGFBP-1 (SMD = 0.70, 95% CI = 0.01 to 1.40, I2 = 77%, K = 4, n = 255) were significantly higher in MS cases than in controls. However, the blood levels of IGFBP-2 (SMD = 0.43, 95% CI = -0.34 to 1.21, I2 = 64.2%, K = 3, n = 78) and blood levels of IGFBP-3 (SMD = 1.04, 95% CI = -0.09 to 2.17, I2 = 95.6%, K = 6, n = 443) were not significantly higher in patients than controls.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Conclusion</jats:title>\n<jats:p>Our meta-analysis revealed no significant difference in serum levels of IGF-1, GH, IGFBP-2, and IGFBP-3 between the MS group and healthy controls, except for IGFBP1. However, our systematic review showed that the studies were controversial for IGFBP-3 serum levels. Some studies found an increase in serum level of IGFBP-3 in MS patients compared to the healthy group, while others showed a decrease.</jats:p>\n</jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/38630771/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": null, "container_title": null, "authors": [ { "author_id": 348360, "given_name": "Shirin", "family_name": "Yaghoobpoor", "ORCID": "http://orcid.org/0000-0002-8904-6229", "country": null }, { "author_id": 306581, "given_name": "Mobina", "family_name": "Fathi", "ORCID": null, "country": null }, { "author_id": 306582, "given_name": "Kimia", "family_name": "Vakili", "ORCID": null, "country": null }, { "author_id": 306591, "given_name": "Fatemeh", "family_name": "Sayehmiri", "ORCID": null, "country": null }, { "author_id": 348361, "given_name": "Milad", "family_name": "Alipour", "ORCID": null, "country": null }, { "author_id": 348362, "given_name": "Zahra sadat", "family_name": "Miriran", "ORCID": null, "country": null }, { "author_id": 348363, "given_name": "Hani", "family_name": "Ghayyem", "ORCID": "http://orcid.org/0000-0002-6725-9960", "country": null }, { "author_id": 348364, "given_name": "Zohreh", "family_name": "Tutunchian", "ORCID": null, "country": null }, { "author_id": 348365, "given_name": "Ramtin", "family_name": "Hajibeygi", "ORCID": null, "country": null }, { "author_id": 348366, "given_name": "Zehra", "family_name": "Batool", "ORCID": null, "country": null }, { "author_id": 348367, "given_name": "Moein", "family_name": "Mirzadeh", "ORCID": null, "country": null }, { "author_id": 348368, "given_name": "Mohammad Hossein", "family_name": "Aghazadeh", "ORCID": null, "country": null }, { "author_id": 306590, "given_name": "Mohammadreza", "family_name": "Hajiesmaeili", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-17T23:25:34.633578Z", "noun_phrases": null, "doi": "10.1371/journal.pone.0297091", "access": "restricted", "takeaways": null, "categories": [] }, { "article_id": 283087, "title": "Glial Activity Load on PET Reveals Persistent “Smoldering” Inflammation in MS Despite Disease-Modifying Treatment", "summary": "<jats:sec>\n<jats:title>Purpose of the Report</jats:title>\n<jats:p>\n<jats:sup>18</jats:sup>F-PBR06-PET targeting 18-kDa translocator protein can detect abnormal microglial activation (MA) in multiple sclerosis (MS). The objectives of this study are to develop individualized mapping of MA using <jats:sup>18</jats:sup>F-PBR06, to determine the effect of disease-modifying treatment (DMT) efficacy on reducing MA, and to determine its clinical, radiological, and serological correlates in MS patients.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Patients and Methods</jats:title>\n<jats:p>Thirty <jats:sup>18</jats:sup>F-PBR06-PET scans were performed in 22 MS patients (mean age, 46 ± 13 years; 16 females) and 8 healthy controls (HCs). Logarithmically transformed “glial activity load on PET” scores (calculated as the sum of voxel-by-voxel <jats:italic toggle=\"yes\">z</jats:italic>-scores ≥4), “lnGALP,” were compared between MS and HC and between MS subjects on high-efficacy DMTs (H-DMT, n = 13) and those on no or lower-efficacy treatment, and correlated with clinical measures, serum biomarkers, and cortical thickness.</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Results</jats:title>\n<jats:p>Cortical gray matter (CoGM) and white matter (WM) lnGALP scores were higher in MS versus HC (+33% and +48%, <jats:italic toggle=\"yes\">P</jats:italic> < 0.001). In H-DMT group, CoGM and WM lnGALP scores were significantly lower than lower-efficacy treatment (<jats:italic toggle=\"yes\">P</jats:italic> < 0.01) but remained abnormally higher than in HC group (<jats:italic toggle=\"yes\">P</jats:italic> = 0.006). Within H-DMT patients, CoGM lnGALP scores correlated positively with physical disability, fatigue and serum glial fibrillary acid protein levels (<jats:italic toggle=\"yes\">r</jats:italic> = 0.65–0.79, all <jats:italic toggle=\"yes\">P</jats:italic>'s < 0.05), and inversely with cortical thickness (<jats:italic toggle=\"yes\">r</jats:italic> = −0.66, <jats:italic toggle=\"yes\">P</jats:italic> < 0.05).</jats:p>\n</jats:sec>\n<jats:sec>\n<jats:title>Conclusions</jats:title>\n<jats:p>High-efficacy DMTs decrease, but do not normalize, CoGM and WM MA in MS patients. Such “residual” MA in CoGM is associated with clinical disability, serum biomarkers, and cortical degeneration. Individualized mapping of translocator protein PET using <jats:sup>18</jats:sup>F-PBR06 is clinically feasible and can potentially serve as an imaging biomarker for evaluating “smoldering” inflammation in MS patients.</jats:p>\n</jats:sec>", "link": "https://pubmed.ncbi.nlm.nih.gov/38630948/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": null, "container_title": null, "authors": [ { "author_id": 261972, "given_name": "Tarun", "family_name": "Singhal", "ORCID": null, "country": null }, { "author_id": 200628, "given_name": "Steven", "family_name": "Cicero", "ORCID": "http://orcid.org/0000-0001-6425-5668", "country": null }, { "author_id": 200627, "given_name": "Eero", "family_name": "Rissanen", "ORCID": "http://orcid.org/0000-0001-5677-8856", "country": "FI" }, { "author_id": 286927, "given_name": "John", "family_name": "Ficke", "ORCID": null, "country": null }, { "author_id": 348355, "given_name": "Preksha", "family_name": "Kukreja", "ORCID": null, "country": null }, { "author_id": 348356, "given_name": "Steven", "family_name": "Vaquerano", "ORCID": null, "country": null }, { "author_id": 287314, "given_name": "Bonnie", "family_name": "Glanz", "ORCID": null, "country": null }, { "author_id": 289810, "given_name": "Shipra", "family_name": "Dubey", "ORCID": null, "country": null }, { "author_id": 348357, "given_name": "William", "family_name": "Sticka", "ORCID": null, "country": null }, { "author_id": 348358, "given_name": "Kyle", "family_name": "Seaver", "ORCID": null, "country": null }, { "author_id": 286928, "given_name": "Marie", "family_name": "Kijewski", "ORCID": null, "country": null }, { "author_id": 348359, "given_name": "Alexis M.", "family_name": "Callen", "ORCID": null, "country": null }, { "author_id": 285723, "given_name": "Renxin", "family_name": "Chu", "ORCID": null, "country": null }, { "author_id": 261967, "given_name": "Kelsey", "family_name": "Carter", "ORCID": null, "country": null }, { "author_id": 286932, "given_name": "David", "family_name": "Silbersweig", "ORCID": null, "country": null }, { "author_id": 143340, "given_name": "Tanuja", "family_name": "Chitnis", "ORCID": "http://orcid.org/0000-0002-9897-4422", "country": null }, { "author_id": 163065, "given_name": "Rohit", "family_name": "Bakshi", "ORCID": "http://orcid.org/0000-0001-8601-5534", "country": "US" }, { "author_id": 163920, "given_name": "Howard L.", "family_name": "Weiner", "ORCID": "http://orcid.org/0000-0003-0203-9681", "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-17T23:25:33.780518Z", "noun_phrases": null, "doi": "10.1097/RLU.0000000000005201", "access": "restricted", "takeaways": null, "categories": [] }, { "article_id": 283086, "title": "Leukocyte telomere length in multiple sclerosis: relationship between disability severity and pregnancy history", "summary": "CONCLUSIONS: The correlation between LTL and disability independent of chronological age and other factors points to a link between neurological reserve in MS and biological aging, and a potential research target for pathophysiological and therapeutic mechanisms. Although LTL did not significantly differ by pregnancy history, longitudinal analyses could help identify interactions with prospectively captured pregnancy effects.", "link": "https://pubmed.ncbi.nlm.nih.gov/38631073/?fc=20210216052009&ff=20240418022536&v=2.18.0.post9+e462414", "published_date": "2024-04-17T10:00:00Z", "source": "PubMed", "publisher": "Elsevier BV", "container_title": "Multiple Sclerosis and Related Disorders", "authors": [ { "author_id": 200544, "given_name": "Michael", "family_name": "Zhong", "ORCID": "http://orcid.org/0000-0002-0769-8320", "country": null }, { "author_id": 348354, "given_name": "Sabrina", "family_name": "Salberg", "ORCID": null, "country": null }, { "author_id": 276451, "given_name": "Sandeep", "family_name": "Sampangi", "ORCID": null, "country": null }, { "author_id": 160166, "given_name": "Anneke", "family_name": "van der Walt", "ORCID": "http://orcid.org/0000-0002-4278-7003", "country": null }, { "author_id": 171213, "given_name": "Helmut", "family_name": "Butzkueven", "ORCID": "http://orcid.org/0000-0003-3940-8727", "country": "AU" }, { "author_id": 254027, "given_name": "Richelle", "family_name": "Mychasiuk", "ORCID": null, "country": null }, { "author_id": 177176, "given_name": "Vilija", "family_name": "Jokubaitis", "ORCID": "http://orcid.org/0000-0002-3942-4340", "country": null } ], "relevant": null, "ml_prediction_gnb": null, "ml_prediction_lr": null, "ml_prediction_lsvc": null, "discovery_date": "2024-04-17T23:25:32.546846Z", "noun_phrases": null, "doi": "10.1016/j.msard.2024.105607", "access": "open", "takeaways": null, "categories": [] } ] }