Article List
List all articles in the database by earliest discovery_date
GET /articles/?format=api&page=2457
{ "count": 24879, "next": "http://api.gregory-ms.com/articles/?format=api&page=2458", "previous": "http://api.gregory-ms.com/articles/?format=api&page=2456", "results": [ { "article_id": 307, "title": "Serum markers of multiple sclerosis - a new approach", "summary": "Optic neuritis (ON) typically manifests with the classical triad of subacute unilateral vision loss, periocular pain and impaired colour vision. It is the first symptom of multiple sclerosis (MS) in about 20% of patients, and approximately half of those experiencing ON will develop MS. However, other inflammatory diseases like neuromyelitis optica spectrum disease (NMOSD), systemic lupus erythematosus (SLE), sarcoidosis, Behchet's disease or infectious diseases like toxoplasmosis can also manifest with ON [[1]]. Thus, it is of crucial importance to improve the diagnosis of early MS. A number of paraclinical measurements can assist in providing a correct diagnosis, most notably magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) examination [[1]]. Specific biomarkers for the differential diagnosis NMOSD have been developed, and most patients are tested for the specific antibodies AQP4-IgG and MOG-IgG on serum cell-based essays. However, no specific serological MS-biomarkers exist. In the present paper recently published in EBioMedicine, Sadam and colleagues [[2]] take a new approach to the question of how to increase diagnostic accuracy in ON patients. By using mimotope variation analysis (MVA), a next generation phage display method, they detected two viral antibody epitopes as possible new biomarkers of MS-risk after ON. The epitopes were gB CMV and VCA p18 EBV. Their approach is interesting for several reasons: First, the biomarkers detected seem to improve the diagnostic accuracy for diagnosing MS in early ON. Second, they could point to pathogenic mechanisms for MS-development. Third, serum biomarkers are available from blood and are much easier to acquire than MRI and lumbar puncture. Interestingly, although the authors have used a hypothesis-free approach, their findings point to two common viral pathogens, that have been linked to MS risk in epidemiological studies. While higher titres against Epstein-Barr virus (EBV) epitopes have been consistently found to increase the risk of developing MS [[3]], Cytomegalovirus (CMV) seropositivity has been negatively associated with MS risk [[4]]. The results of the current paper are in line with these previous findings. Sadam and colleagues [[2]] identified a clear negative association between epitopes against gB CMV and the risk of developing MS after ON. A negative association between previous infections with CMV and the risk of MS has been reported in one large Swedish population-based incident case-control study and in one small multi-ethnic US paediatric MS case-control study [[5]]. A more recent study found, however, inconsistency across ethnic groups [[6]], indicating that there might not be a causal association between CMV and MS. More consistent epidemiological results have been found for the second potential biomarker, VCA p18 EBV [[3],[6]], and some authors have suggested that MS could be considered a rare complication of EBV infection[[7]]. In one large study of early MS, it was found that 100% of the 901 patients were EBV positive, while controls did not reach 100% seropositvity in any of the investigated age cohorts [[8]]. Based on these findings, the authors suggested that negative EBV serology should alert clinicians to consider diagnoses other than MS. Most studies have examined the serum levels of EBNA-1, as a marker of previous EBV infection. In the present paper, the epitope VCA p18 EBV was found to be associated with risk of MS [[2]]. Interestingly, this could be consistent with the results from the Finish Maternity Cohort [[7]]. In this study, offspring of mothers with high VCA IgG during pregnancy had an increased risk of developing MS. The mechanism for how this could affect MS risk is however, still not determined. A number of precautions have to be taken before these biomarkers can be used in a clinical setting. First, the results should be replicated in larger independent cohorts. Preferentially, prospective cohort studies could examine the benefit of incorporating these biomarkers in a risk-evaluation scheme. Second, the biomarkers must be evaluated in different ethnic populations to determine if the findings are consistent across ethnic and regional groups. Based on previous trials, especially CMV antibody responses seem to be determined by ethnicity and possibly not causally linked to the risk of MS. Third, the sensitivity and specificity was only at 75%. We know that about half of all ON patients will go on to develop MS, and the diagnostic accuracy is still far from perfect. These potential biomarkers will probably need to be supplemented with other markers to improve their diagnostic accuracy. In summary, the present study adds to the growing number of findings, indicating that the immunological response to the herpes viruses CMV and EBV are linked to the risk of developing MS. This could reflect unique pathogenic mechanisms for how MS develops and could possibly improve future treatment and diagnosis of the disease.", "link": "https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(21)00022-0/fulltext", "published_date": "2021-01-28T00:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "EBioMedicine", "authors": [ { "author_id": 163680, "given_name": "Øivind", "family_name": "Torkildsen", "ORCID": "http://orcid.org/0000-0001-5294-2866", "country": "NO" } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "Serum markers", "multiple sclerosis", "a new approach" ], "doi": "10.1016/j.ebiom.2021.103229", "access": "open", "takeaways": "", "categories": [] }, { "article_id": 315, "title": "High-dose biotin in multiple sclerosis: the end of the road", "summary": "Since the first pilot study of high-dose biotin in patients with chronic progressive multiple sclerosis 1 and the subsequent phase 2 randomised, double-blind, placebo-controlled trial (MS-SPI), 2 biotin has been discussed as a potentially unique approach to treat progressive multiple sclerosis by targeting remyelination. Biotin, as a cofactor for four essential carboxylases, might support myelin repair by enhancing fatty acid synthesis and protect against hypoxia-driven axonal degeneration by augmenting energy production in neurons. 1 , 3", "link": "https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30353-7/fulltext", "published_date": "2020-10-22T23:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Neurology", "authors": [ { "author_id": 221282, "given_name": "Jeremias", "family_name": "Motte", "ORCID": "http://orcid.org/0000-0002-6624-8565", "country": null }, { "author_id": 147050, "given_name": "Ralf", "family_name": "Gold", "ORCID": "http://orcid.org/0000-0002-7223-3052", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "multiple sclerosis", "the road" ], "doi": "10.1016/S1474-4422(20)30353-7", "access": "restricted", "takeaways": " Biotin has been discussed as a potentially unique approach to treat progressive multiple sclerosis by targeting remyelination . Biotin might support myelin repair by enhancing fatty acid synthesis", "categories": [] }, { "article_id": 321, "title": "Paediatric multiple sclerosis and antibody-associated demyelination: clinical, imaging, and biological considerations for diagnosis and care", "summary": "<h2>Summary</h2><p>The field of acquired CNS neuroimmune demyelination in children is transforming. Progress in assay development, refinement of diagnostic criteria, increased biological insights provided by advanced neuroimaging techniques, and high-level evidence for the therapeutic efficacy of biological agents are redefining diagnosis and care. Three distinct neuroimmune conditions—multiple sclerosis, myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and aquaporin-4 antibody-associated neuromyelitis optica spectrum disorder (AQP4-NMOSD)—can now be distinguished, with evidence from humans and animal models supporting distinct pathobiological disease mechanisms. The development of highly effective therapies for adult-onset multiple sclerosis and AQP4-NMOSD that suppress relapse rate by more than 90% has motivated advocacy for trials in children. However, doing clinical trials is challenging because of the rarity of these conditions in the paediatric age group, necessitating new approaches to trial design, including age-based trajectory modelling based on phase 3 studies in adults. Despite these limitations, the future for children and adolescents living with multiple sclerosis, MOGAD, or AQP4-NMOSD is far brighter than in years past, and will be brighter still if successful therapies to promote remyelination, enhance neuroprotection, and remediate cognitive deficits can be further accelerated.</p>", "link": "https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30432-4/fulltext", "published_date": "2021-02-01T00:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Neurology", "authors": [ { "author_id": 159108, "given_name": "Giulia", "family_name": "Fadda", "ORCID": "http://orcid.org/0000-0001-9658-815X", "country": null }, { "author_id": 241673, "given_name": "Thais", "family_name": "Armangue", "ORCID": null, "country": null }, { "author_id": 210191, "given_name": "Yael", "family_name": "Hacohen", "ORCID": "http://orcid.org/0000-0001-8490-9657", "country": null }, { "author_id": 143340, "given_name": "Tanuja", "family_name": "Chitnis", "ORCID": "http://orcid.org/0000-0002-9897-4422", "country": null }, { "author_id": 241675, "given_name": "Brenda", "family_name": "Banwell", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "Paediatric multiple sclerosis", "antibody-associated demyelination", "clinical, imaging, and biological considerations", "diagnosis", "care" ], "doi": "10.1016/S1474-4422(20)30432-4", "access": "open", "takeaways": " The field of acquired CNS neuroimmune demyelination in children is transforming . The development of highly effective therapies for adult-onset multiple sclerosis and AQP4-NMOSD that suppress relapse rate by more than 90% has motivated advocacy for trials in children .", "categories": [] }, { "article_id": 322, "title": "Tolerance-inducing medicines in autoimmunity: rheumatology and beyond", "summary": "<h2>Summary</h2><p>Autoimmunity is currently managed with generalised immunosuppression, which is associated with serious side-effects such as infection and cancer. An ideal treatment strategy would be to induce immune tolerance—ie, to reprogramme the immune system to stop recognising the host itself as a threat. Drug-free remission should follow such an intervention, representing a change in the approach to the treatment of autoimmune disease. Tolerance induction is achievable in animal models of autoimmunity but translation to the clinic has been slow. Nonetheless, progress has been made—eg, restoration of therapeutic responsiveness and drug-free remission have been achieved with stem cell transplantation in refractory autoimmunity, and significant delays in onset of type 1 diabetes in individuals at high risk have been achieved following a brief treatment with anti-CD3 monoclonal antibody. In the future, antigen-specific interventions should provide highly targeted, personalised approaches, avoiding generalised immunosuppression entirely. Such trials have already started, using both direct autoantigenic peptide administration, cellular therapies, and other modalities. In this Series paper, we discuss the history of immune tolerance induction with a focus on rheumatological disease while also highlighting essential data from other specialties. We propose key unanswered questions, which will be covered in other papers in this Series.</p>", "link": "https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(20)30100-4/fulltext", "published_date": "2020-08-31T23:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Rheumatology", "authors": [ { "author_id": 241698, "given_name": "James A", "family_name": "Stanway", "ORCID": null, "country": null }, { "author_id": 241700, "given_name": "John D", "family_name": "Isaacs", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "Tolerance-inducing medicines", "autoimmunity", "rheumatology" ], "doi": "10.1016/S2665-9913(20)30100-4", "access": "restricted", "takeaways": " Autoimmunity is currently managed with generalised immunosuppression, which is associated with serious side-effects such as infection and cancer . The ideal treatment strategy would be to induce immune tolerance, reprogramme the immune system to stop recognising the host itself as a threat . Tolerance induction is achievable in animal models but translation to the clinic has been slow .", "categories": [] }, { "article_id": 318, "title": "Cognition in multiple sclerosis: Charcot was right", "summary": "Charcot's early descriptions of patients with multiple sclerosis noted “enfeeblement of memory” and “concepts formed slowly,” along with the classic triad of nystagmus, intention tremor, and ataxic dysarthria. 1 Charcot was trained in psychiatry and neurology, but for decades neither discipline took note of his psychological observations. Psychiatrists in the 1920s used interviews to probe mental status in people with multiple sclerosis, but estimates of the frequency of cognitive impairment were unreliable, ranging from two to 72%. 2", "link": "https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30306-9/fulltext", "published_date": "2020-09-30T23:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Neurology", "authors": [ { "author_id": 242082, "given_name": "Ralph H B", "family_name": "Benedict", "ORCID": null, "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "multiple sclerosis", "Charcot" ], "doi": "10.1016/S1474-4422(20)30306-9", "access": "restricted", "takeaways": " Charcot's early descriptions of patients with multiple sclerosis noted “enfeeblement of memory” and “concepts formed slowly” along with the classic triad", "categories": [] }, { "article_id": 312, "title": "Are drugs for multiple sclerosis fatigue just placebos?", "summary": "About 80% of multiple sclerosis patients have fatigue, which is commonly their most troublesome problem. 1 , 2 Fatigue is often disabling, affecting employment and other activities. Unfortunately, multiple sclerosis fatigue is difficult to treat, frustrating our patients and ourselves. Treatments include exercise, energy conservation, and cognitive behavioural counselling. As physicians, we are inclined to prescribe medications for our patients with multiple sclerosis who have fatigue, and our patients often report that a medication that we have prescribed has improved their fatigue. However, there is conflicting evidence about whether drugs commonly prescribed for multiple sclerosis fatigue are effective. 3 , 4 Are these medications truly effective or are they having a placebo effect?", "link": "https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30415-4/fulltext", "published_date": "2020-11-23T00:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Neurology", "authors": [ { "author_id": 154538, "given_name": "Dennis", "family_name": "Bourdette", "ORCID": "http://orcid.org/0000-0002-1312-8615", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "drugs", "multiple sclerosis fatigue", "just placebos" ], "doi": "10.1016/S1474-4422(20)30415-4", "access": "restricted", "takeaways": " 80% of multiple sclerosis patients have fatigue, which is commonly their most troublesome problem . Fatigue is often disabling, affecting employment and other activities . Treatments include exercise, energy conservation, and cognitive behavioural counselling .", "categories": [] }, { "article_id": 317, "title": "Cognitive impairment in multiple sclerosis: clinical management, MRI, and therapeutic avenues", "summary": "<h2>Summary</h2><p>Multiple sclerosis is a chronic, demyelinating disease of the CNS. Cognitive impairment is a sometimes neglected, yet common, sign and symptom with a profound effect on instrumental activities of daily living. The prevalence of cognitive impairment in multiple sclerosis varies across the lifespan and might be difficult to distinguish from other causes in older age. MRI studies show that widespread changes to brain networks contribute to cognitive dysfunction, and grey matter atrophy is an early sign of potential future cognitive decline. Neuropsychological research suggests that cognitive processing speed and episodic memory are the most frequently affected cognitive domains. Narrowing evaluation to these core areas permits brief, routine assessment in the clinical setting. Owing to its brevity, reliability, and sensitivity, the Symbol Digit Modalities Test, or its computer-based analogues, can be used to monitor episodes of acute disease activity. The Symbol Digit Modalities Test can also be used in clinical trials, and data increasingly show that cognitive processing speed and memory are amenable to cognitive training interventions.</p>", "link": "https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30277-5/fulltext", "published_date": "2020-09-30T23:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Neurology", "authors": [ { "author_id": 242082, "given_name": "Ralph H B", "family_name": "Benedict", "ORCID": null, "country": null }, { "author_id": 147708, "given_name": "Maria Pia", "family_name": "Amato", "ORCID": "http://orcid.org/0000-0003-3325-3760", "country": "IT" }, { "author_id": 167316, "given_name": "John", "family_name": "DeLuca", "ORCID": "http://orcid.org/0000-0003-3745-4156", "country": "US" }, { "author_id": 193679, "given_name": "Jeroen J G", "family_name": "Geurts", "ORCID": "http://orcid.org/0000-0003-1896-3748", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "Cognitive impairment", "multiple sclerosis", "clinical management", "MRI", "therapeutic avenues" ], "doi": "10.1016/S1474-4422(20)30277-5", "access": "restricted", "takeaways": " Multiple sclerosis is a chronic, demyelinating disease of the CNS . Neuropsychological research suggests that cognitive processing speed and episodic memory are the most frequently affected cognitive domains . Narrowing evaluation to these core areas permits brief, routine assessment in the clinical setting .", "categories": [] }, { "article_id": 313, "title": "Long-term ocrelizumab in progressive multiple sclerosis", "summary": " The pathophysiology of progressive multiple sclerosis includes acute inflammatory lesion activity, chronic inflammation, and neurodegeneration. 1 The exact relationship between these components remains unclear. Despite success in the development of disease-modifying therapies for relapsing-remitting multiple sclerosis, treatment of progressive multiple sclerosis has proven more difficult. Primary progressive multiple sclerosis is characterised by gradual disability accumulation from disease onset, sometimes with superimposed relapses, or MRI lesion activity, or both. 1 Currently, the anti-CD20 monoclonal antibody ocrelizumab is the only disease-modifying therapy approved to treat primary progressive multiple sclerosis. The evidence for ocrelizumab is based on the results of the ORATORIO phase 3 trial: 2 treatment with intravenous 600 mg of ocrelizumab every 6 months reduced 3-month-confirmed worsening of the Expanded Disability Status Scale (EDSS) score compared with placebo. These primary results were supported by benefit on 6-month-confirmed worsening of EDSS score and on the Timed 25-Foot Walk (T25FW; another measure of neurological disability), MRI lesion activity, and whole brain volume loss.", "link": "https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30399-9/fulltext", "published_date": "2020-10-29T00:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "The Lancet Neurology", "authors": [ { "author_id": 170212, "given_name": "Deja R", "family_name": "Rose", "ORCID": "http://orcid.org/0000-0003-0423-0551", "country": null }, { "author_id": 151378, "given_name": "Jeffrey A.", "family_name": "Cohen", "ORCID": "http://orcid.org/0000-0001-9245-9772", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "Long-term ocrelizumab", "progressive multiple sclerosis" ], "doi": "10.1016/S1474-4422(20)30399-9", "access": "restricted", "takeaways": " The anti-CD20 monoclonal antibody ocrelizumab is the only disease-modifying therapy approved to treat primary progressive multiple sclerosis . The evidence for the evidence is based on the results of the ORATORIO phase 3 trial: 2 treatment with intravenous 600 mg of oorelizmab every 6 months reduced 3-month-confirmed worsening of the", "categories": [ { "category_id": 8, "category_description": "", "category_name": "Ocrelizumab", "category_slug": "ocrelizumab", "category_terms": [ "ocrelizumab", "ocrevus" ], "article_count": 234 } ] }, { "article_id": 324, "title": "CXCL13/CXCR5 signalling is pivotal to preserve motor neurons in amyotrophic lateral sclerosis", "summary": "<h2>Abstract</h2><h3>Background</h3><p>CXCL13 is a B and T lymphocyte chemokine that mediates neuroinflammation through its receptor CXCR5. This chemokine is highly expressed by motoneurons (MNs) in Amyotrophic Lateral Sclerosis (ALS) SOD1G93A (mSOD1) mice during the disease, particularly in fast-progressing mice. Accordingly, in this study, we investigated the role of this chemokine in ALS.</p><h3>Methods</h3><p>We used i<i>n vitro</i> and <i>in vivo</i> experimental paradigms derived from ALS mice and patients to investigate the expression level and distribution of CXCL13/CXCR5 axis and its role in MN death and disease progression. Moreover, we compared the levels of CXCL13 in the CSF and serum of ALS patients and controls.</p><h3>Findings</h3><p>CXCL13 and CXCR5 are overexpressed in the spinal MNs and peripheral axons in mSOD1 mice. CXCL13 inhibition in the CNS of ALS mice resulted in the exacerbation of motor impairment (<i>n</i> = 4/group;Mean_Diff.=27.81) and decrease survival (<i>n</i> = 14_Treated:19.2 ± 1.05wks, <i>n</i> = 17_Controls:20.2 ± 0.6wks; 95% CI: 0.4687–1.929). This was corroborated by evidence from primary spinal cultures where the inhibition or activation of CXCL13 exacerbated or prevented the MN loss. Besides, we found that CXCL13/CXCR5 axis is overexpressed in the spinal cord MNs of ALS patients, and CXCL13 levels in the CSF discriminate ALS (<i>n</i> = 30) from Multiple Sclerosis (<i>n</i> = 16) patients with a sensitivity of 97.56%.</p><h3>Interpretation</h3><p>We hypothesise that MNs activate CXCL13 signalling to attenuate CNS inflammation and prevent the neuromuscular denervation. The low levels of CXCL13 in the CSF of ALS patients might reflect the MN dysfunction, suggesting this chemokine as a potential clinical adjunct to discriminate ALS from other neurological diseases.</p><h3>Funding</h3><p>Vaccinex, Inc.; Regione Lombardia (TRANS-ALS)</p>", "link": "https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(20)30473-4/fulltext", "published_date": "2020-11-05T00:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "eBioMedicine", "authors": [ { "author_id": 296303, "given_name": "Maria Chiara", "family_name": "Trolese", "ORCID": null, "country": null }, { "author_id": 296304, "given_name": "Alessandro", "family_name": "Mariani", "ORCID": null, "country": null }, { "author_id": 296305, "given_name": "Mineko", "family_name": "Terao", "ORCID": null, "country": null }, { "author_id": 296306, "given_name": "Massimiliano", "family_name": "de Paola", "ORCID": null, "country": null }, { "author_id": 296307, "given_name": "Paola", "family_name": "Fabbrizio", "ORCID": null, "country": null }, { "author_id": 296308, "given_name": "Francesca", "family_name": "Sironi", "ORCID": null, "country": null }, { "author_id": 296309, "given_name": "Mami", "family_name": "Kurosaki", "ORCID": null, "country": null }, { "author_id": 279271, "given_name": "Silvia", "family_name": "Bonanno", "ORCID": null, "country": null }, { "author_id": 296310, "given_name": "Stefania", "family_name": "Marcuzzo", "ORCID": null, "country": null }, { "author_id": 296311, "given_name": "Pia", "family_name": "Bernasconi", "ORCID": null, "country": null }, { "author_id": 148561, "given_name": "Francesca", "family_name": "Trojsi", "ORCID": "http://orcid.org/0000-0002-3790-8018", "country": "IT" }, { "author_id": 285586, "given_name": "Eleonora", "family_name": "Aronica", "ORCID": null, "country": null }, { "author_id": 231097, "given_name": "Caterina", "family_name": "Bendotti", "ORCID": "http://orcid.org/0000-0003-1055-1271", "country": null }, { "author_id": 201495, "given_name": "Giovanni", "family_name": "Nardo", "ORCID": "http://orcid.org/0000-0002-1803-1484", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "CXCL13/CXCR5 signalling", "motor neurons", "amyotrophic lateral sclerosis" ], "doi": "10.1016/j.ebiom.2020.103097", "access": "open", "takeaways": " CXCL13 is a B and T lymphocyte chemokine that mediates neuroinflammation through its receptor CXCR5 . It is highly expressed by motoneurons (MNs) in Amyotrophic Lateral Sclerosis (ALS) SOD1G93A (mSOD1) mice during the disease .", "categories": [] }, { "article_id": 306, "title": "Urolithin A ameliorates experimental autoimmune encephalomyelitis by targeting aryl hydrocarbon receptor", "summary": "<h2>Abstract</h2><h3>Background</h3><p>Urolithin A (URA) is an intestinal microbiota metabolic product from ellagitannin-containing foods with multiple biological activities. However, its role in autoimmune diseases is largely unknown. Here, for first time, we demonstrate the therapeutic effect of URA in an experimental autoimmune encephalomyelitis (EAE) animal model.</p><h3>Methods</h3><p>Therapeutic effect was evaluated via an active and passive EAE animal model <i>in vivo</i>. The function of URA on bone marrow-derived dendritic cells (BM-DCs), T cells, and microglia were tested <i>in vitro</i>.</p><h3>Findings</h3><p>Oral URA (25 mg/kg/d) suppressed disease progression at prevention, induction, and effector phases of preclinical EAE. Histological evaluation showed that significantly fewer inflammatory cells, decreased demyelination, lower numbers of M1-type microglia and activated DCs, as well as reduced infiltrating Th1/Th17 cells were present in the central nervous system (CNS) of the URA-treated group. URA treatment at 25 μM inhibited the activation of BM-DCs <i>in vitro</i>, restrained Th17 cell differentiation in T cell polarization conditions, and in a DC-CD4<sup>+</sup> T cell co-culture system. Moreover, we confirmed URA inhibited pathogenicity of Th17 cells in adoptive EAE. Mechanism of URA action was directly targeting Aryl Hydrocarbon Receptor (AhR) and modulating the signaling pathways.</p><h3>Interpretation</h3><p>Collectively, our study offers new evidence that URA, as a human microbial metabolite, is valuable to use as a prospective therapeutic candidate for autoimmune diseases.</p>", "link": "https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(21)00020-7/fulltext", "published_date": "2021-01-31T00:00:00Z", "sources": [ "The Lancet" ], "teams": [ { "id": 1, "name": "Team Gregory" } ], "subjects": [ { "subject_name": "Multiple Sclerosis", "description": null } ], "publisher": "Elsevier BV", "container_title": "EBioMedicine", "authors": [ { "author_id": 189876, "given_name": "Pei-Xin", "family_name": "Shen", "ORCID": "http://orcid.org/0000-0002-5022-3654", "country": null }, { "author_id": 147207, "given_name": "Xing", "family_name": "Li", "ORCID": "http://orcid.org/0000-0002-0742-1364", "country": null }, { "author_id": 264264, "given_name": "Si-Ying", "family_name": "Deng", "ORCID": null, "country": null }, { "author_id": 256097, "given_name": "Li", "family_name": "Zhao", "ORCID": null, "country": null }, { "author_id": 289338, "given_name": "Yan-Yan", "family_name": "Zhang", "ORCID": null, "country": null }, { "author_id": 289339, "given_name": "Xin", "family_name": "Deng", "ORCID": null, "country": null }, { "author_id": 289340, "given_name": "Bing", "family_name": "Han", "ORCID": null, "country": null }, { "author_id": 289341, "given_name": "Jie", "family_name": "Yu", "ORCID": null, "country": null }, { "author_id": 269411, "given_name": "Yin", "family_name": "Li", "ORCID": null, "country": null }, { "author_id": 289342, "given_name": "Zhe-Zhi", "family_name": "Wang", "ORCID": null, "country": null }, { "author_id": 147204, "given_name": "Yuan", "family_name": "Zhang", "ORCID": "http://orcid.org/0000-0002-2463-4599", "country": null } ], "relevant": null, "ml_prediction_gnb": false, "ml_prediction_lr": false, "ml_prediction_lsvc": false, "discovery_date": "2021-03-06T11:22:21Z", "noun_phrases": [ "Urolithin A", "experimental autoimmune encephalomyelitis", "aryl hydrocarbon receptor" ], "doi": "10.1016/j.ebiom.2021.103227", "access": "open", "takeaways": " Urolithin A (URA) is an intestinal microbiota metabolic product from ellagitannin-containing foods with multiple biological activities . URA (25 mg/kg/d) suppressed disease progression at prevention, induction, and effector phases of preclinical EAE . Mechanism of URA action was directly targeting Aryl Hydrocarbon Receptor (AhR) and modulating signaling pathways .", "categories": [] } ] }