List all articles in the database by earliest discovery_date

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    "count": 24924,
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        {
            "article_id": 436,
            "title": "Regulation of the expression of human endogenous retroviruses (HERVs): elements in fetal development and a possible role in the development of cancer and neurological diseases",
            "summary": "<div><p>APMIS. 2021 Mar 8. doi: 10.1111/apm.13130. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">Human endogenous retroviruses (HERVs) are remnants of ancient retroviral germline infections. Most HERV sequences are silenced in somatic cells, but interest is emerging on the involvement of HERV derived transcripts and proteins in human physiology and disease. A HERV-W encoded protein, syncytin-1, has been co-opted into fetal physiology, where it plays a role in trophoblast formation. Altered HERV transcription and expression of HERV derived proteins are associated with various cancer types and neurological diseases such as multiple sclerosis (MS). The implication of HERVs as potential mediators of both health and disease suggests important roles of regulatory mechanisms and alterations of these in physiological and pathological processes. The regulation of HERV sequences is mediated by a wide variety of mechanisms, and the focus of this review is on selected aspects of these, including epigenetic mechanisms such as CpG methylation and histone modifications of the HP1-H3K9me axis, viral transactivation events, and regulatory perspectives of transient stimuli in the microenvironment. Increasing knowledge of the regulation of HERV sequences will not only contribute to the understanding of complex pathogeneses, but may pinpoint potential targets for better diagnosis and treatment in complex diseases as MS.</p><p>PMID:<a href=\"https://pubmed.ncbi.nlm.nih.gov/33683784/?utm_source=Other&amp;utm_medium=rss&amp;utm_campaign=pubmed-2&amp;utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&amp;fc=20210216052009&amp;ff=20210308191644&amp;v=2.14.2\">33683784</a> | DOI:<a href=\"https://doi.org/10.1111/apm.13130\">10.1111/apm.13130</a></p></div>",
            "link": "https://pubmed.ncbi.nlm.nih.gov/33683784/#x3D;Other&utm_medium=rss&utm_campaign=pubmed-2&utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&fc&#x",
            "published_date": "2021-01-05T00:00:00Z",
            "sources": [
                "PubMed"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Wiley",
            "container_title": "APMIS",
            "authors": [
                {
                    "author_id": 305161,
                    "given_name": "Maiken Kruse",
                    "family_name": "Kristensen",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 305162,
                    "given_name": "Tove",
                    "family_name": "Christensen",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-09T00:16:46Z",
            "noun_phrases": [
                "Regulation",
                "the expression",
                "human endogenous retroviruses",
                "HERVs",
                "elements",
                "fetal development",
                "a possible role",
                "the development",
                "cancer",
                "neurological diseases"
            ],
            "doi": "10.1111/apm.13130",
            "access": "restricted",
            "takeaways": " HERV-W encoded protein, syncytin-1, has been co-opted into fetal physiology, where it plays a role in trophoblast formation . Altered HERV transcription and expression of HERV derived proteins are associated with various cancer types and neurological diseases such as multiple sclerosis .",
            "categories": []
        },
        {
            "article_id": 435,
            "title": "Cholesterol alters mitophagy by impairing optineurin recruitment and lysosomal clearance in Alzheimer’s disease",
            "summary": "Background: Emerging evidence indicates that impaired mitophagy-mediated clearance of defective mitochondria is a critical event in Alzheimer’s disease (AD) pathogenesis. Amyloid-beta (Aβ) metabolism and the microtubule-associated protein tau have been reported to regulate key components of the mitophagy machinery. However, the mechanisms that lead to mitophagy dysfunction in AD are not fully deciphered. We have previously shown that intraneuronal cholesterol accumulation can disrupt the autophagy flux, resulting in low Aβ clearance. In this study, we examine the impact of neuronal cholesterol changes on mitochondrial removal by autophagy.MethodsRegulation of PINK1-parkin-mediated mitophagy was investigated in conditions of acute (in vitro) and chronic (in vivo) high cholesterol loading using cholesterol-enriched SH-SY5Y cells, cultured primary neurons from transgenic mice overexpressing active SREBF2 (sterol regulatory element binding factor 2), and mice of increasing age that express the amyloid precursor protein with the familial Alzheimer Swedish mutation (Mo/HuAPP695swe) and mutant presenilin 1 (PS1-dE9) together with active SREBF2.ResultsIn cholesterol-enriched SH-SY5Y cells and cultured primary neurons, high intracellular cholesterol levels stimulated mitochondrial PINK1 accumulation and mitophagosomes formation triggered by Aβ while impairing lysosomal-mediated clearance. Antioxidant recovery of cholesterol-induced mitochondrial glutathione (GSH) depletion prevented mitophagosomes formation indicating mitochondrial ROS involvement. Interestingly, when brain cholesterol accumulated chronically in aged APP-PSEN1-SREBF2 mice the mitophagy flux was affected at the early steps of the pathway, with defective recruitment of the key autophagy receptor optineurin (OPTN). Sustained cholesterol-induced alterations in APP-PSEN1-SREBF2 mice promoted an age-dependent accumulation of OPTN into HDAC6-positive aggresomes, which disappeared after in vivo treatment with GSH ethyl ester (GSHee). The analyses in post-mortem brain tissues from individuals with AD confirmed these findings, showing OPTN in aggresome-like structures that correlated with high mitochondrial cholesterol levels in late AD stages.ConclusionsOur data demonstrate that accumulation of intracellular cholesterol reduces the clearance of defective mitochondria and suggest recovery of the cholesterol homeostasis and the mitochondrial scavenging of ROS as potential therapeutic targets for AD.",
            "link": "https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-021-00435-6",
            "published_date": "2021-03-08T00:00:00Z",
            "sources": [
                "BioMedCentral"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Springer Science and Business Media LLC",
            "container_title": "Molecular Neurodegeneration",
            "authors": [
                {
                    "author_id": 243275,
                    "given_name": "Vicente",
                    "family_name": "Roca-Agujetas",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243276,
                    "given_name": "Elisabet",
                    "family_name": "Barbero-Camps",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243277,
                    "given_name": "Cristina",
                    "family_name": "de Dios",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243278,
                    "given_name": "Petar",
                    "family_name": "Podlesniy",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243279,
                    "given_name": "Xenia",
                    "family_name": "Abadin",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243280,
                    "given_name": "Albert",
                    "family_name": "Morales",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243281,
                    "given_name": "Montserrat",
                    "family_name": "Marí",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243282,
                    "given_name": "Ramon",
                    "family_name": "Trullàs",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 232983,
                    "given_name": "Anna",
                    "family_name": "Colell",
                    "ORCID": "http://orcid.org/0000-0001-5236-1834",
                    "country": "ES"
                }
            ],
            "relevant": false,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T21:43:30Z",
            "noun_phrases": [
                "Cholesterol alters",
                "optineurin recruitment",
                "lysosomal clearance",
                "Alzheimer’s disease"
            ],
            "doi": "10.1186/s13024-021-00435-6",
            "access": "open",
            "takeaways": " Evidence indicates that impaired mitophagy-mediated clearance of defective mitochondria is a critical event in Alzheimer’s disease pathogenesis . Amyloid-beta (Aβ) metabolism and the microtubule-associated protein tau have been reported to regulate key components of the mitrophagy machinery . We have previously shown that intraneuronal cholesterol accumulation can disrupt the autophagy flux .",
            "categories": []
        },
        {
            "article_id": 433,
            "title": "Correction to: Development and evaluation of an interactive web-based decision-making programme on relapse management for people with multiple sclerosis (POWER@MS2)—study protocol for a randomised controlled trial",
            "summary": "An amendment to this paper has been published and can be accessed via the original article.",
            "link": "https://trialsjournal.biomedcentral.com/articles/10.1186/s13063-021-05152-5",
            "published_date": "2021-03-08T00:00:00Z",
            "sources": [
                "BioMedCentral"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Springer Science and Business Media LLC",
            "container_title": "Trials",
            "authors": [
                {
                    "author_id": 156488,
                    "given_name": "Anne Christin",
                    "family_name": "Rahn",
                    "ORCID": "http://orcid.org/0000-0002-9051-3621",
                    "country": null
                },
                {
                    "author_id": 229918,
                    "given_name": "Lisa",
                    "family_name": "Wenzel",
                    "ORCID": "http://orcid.org/0000-0002-4862-6008",
                    "country": null
                },
                {
                    "author_id": 243307,
                    "given_name": "Andrea",
                    "family_name": "Icks",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 148868,
                    "given_name": "Alexander",
                    "family_name": "Stahmann",
                    "ORCID": "http://orcid.org/0000-0001-5308-105X",
                    "country": "DE"
                },
                {
                    "author_id": 243308,
                    "given_name": "Jutta",
                    "family_name": "Scheiderbauer",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243310,
                    "given_name": "Kristina",
                    "family_name": "Grentzenberg",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243311,
                    "given_name": "Markus",
                    "family_name": "Vomhof",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243313,
                    "given_name": "Joseph",
                    "family_name": "Montalbo",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 164296,
                    "given_name": "Tim",
                    "family_name": "Friede",
                    "ORCID": "http://orcid.org/0000-0001-5347-7441",
                    "country": "DE"
                },
                {
                    "author_id": 162588,
                    "given_name": "Christoph",
                    "family_name": "Heesen",
                    "ORCID": "http://orcid.org/0000-0001-8131-9467",
                    "country": null
                },
                {
                    "author_id": 156494,
                    "given_name": "Sascha",
                    "family_name": "Köpke",
                    "ORCID": "http://orcid.org/0000-0003-4106-4919",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T21:43:30Z",
            "noun_phrases": [
                "Correction to: Development",
                "evaluation",
                "an interactive web-based decision-making programme",
                "relapse management",
                "people",
                "multiple sclerosis",
                "POWER@MS2)—study protocol",
                "a randomised controlled trial"
            ],
            "doi": "10.1186/s13063-021-05152-5",
            "access": "open",
            "takeaways": "",
            "categories": []
        },
        {
            "article_id": 434,
            "title": "Pexidartinib treatment in Alexander disease model mice reduces macrophage numbers and increases glial fibrillary acidic protein levels, yet has minimal impact on other disease phenotypes",
            "summary": "Background: Alexander disease (AxD) is a rare neurodegenerative disorder that is caused by dominant mutations in the gene encoding glial fibrillary acidic protein (GFAP), an intermediate filament that is primarily expressed by astrocytes. In AxD, mutant GFAP in combination with increased GFAP expression result in astrocyte dysfunction and the accumulation of Rosenthal fibers. A neuroinflammatory environment consisting primarily of macrophage lineage cells has been observed in AxD patients and mouse models.MethodsTo examine if macrophage lineage cells could serve as a therapeutic target in AxD, GFAP knock-in mutant AxD model mice were treated with a colony-stimulating factor 1 receptor (CSF1R) inhibitor, pexidartinib. The effects of pexidartinib treatment on disease phenotypes were assessed.ResultsIn AxD model mice, pexidartinib administration depleted macrophages in the CNS and caused elevation of GFAP transcript and protein levels with minimal impacts on other phenotypes including body weight, stress response activation, chemokine/cytokine expression, and T cell infiltration.ConclusionsTogether, these results highlight the complicated role that macrophages can play in neurological diseases and do not support the use of pexidartinib as a therapy for AxD.",
            "link": "https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-021-02118-x",
            "published_date": "2021-03-08T00:00:00Z",
            "sources": [
                "BioMedCentral"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Springer Science and Business Media LLC",
            "container_title": "Journal of Neuroinflammation",
            "authors": [
                {
                    "author_id": 243325,
                    "given_name": "Michelle M.",
                    "family_name": "Boyd",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243327,
                    "given_name": "Suzanne J.",
                    "family_name": "Litscher",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243329,
                    "given_name": "Laura L.",
                    "family_name": "Seitz",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243331,
                    "given_name": "Albee",
                    "family_name": "Messing",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243333,
                    "given_name": "Tracy L.",
                    "family_name": "Hagemann",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 183357,
                    "given_name": "Lara S.",
                    "family_name": "Collier",
                    "ORCID": "http://orcid.org/0000-0001-6746-1256",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T21:43:30Z",
            "noun_phrases": [
                "Pexidartinib treatment",
                "Alexander disease model mice",
                "macrophage numbers",
                "glial fibrillary acidic protein levels",
                "minimal impact",
                "other disease phenotypes"
            ],
            "doi": "10.1186/s12974-021-02118-x",
            "access": "open",
            "takeaways": " Alexander disease (AxD) is a rare neurodegenerative disorder that is caused by dominant mutations in the gene encoding glial fibrillary acidic protein (GFAP), an intermediate filament that is primarily expressed by astrocytes .",
            "categories": []
        },
        {
            "article_id": 431,
            "title": "Magnetic Resonance Imaging of Multiple Sclerosis at 7.0 Tesla",
            "summary": "<div><p>J Vis Exp. 2021 Feb 19;(168). doi: 10.3791/62142.</p><p><b>ABSTRACT</b></p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">The overall goal of this article is to demonstrate a state-of-the-art ultrahigh field (UHF) magnetic resonance (MR) protocol of the brain at 7.0 Tesla in multiple sclerosis (MS) patients. MS is a chronic inflammatory, demyelinating, neurodegenerative disease that is characterized by white and gray matter lesions. Detection of spatially and temporally disseminated T2-hyperintense lesions by the use of MRI at 1.5 T and 3 T represents a crucial diagnostic tool in clinical practice to establish accurate diagnosis of MS based on the current version of the 2017 McDonald criteria. However, the differentiation of MS lesions from brain white matter lesions of other origins can sometimes be challenging due to their resembling morphology at lower magnetic field strengths (typically 3 T). Ultrahigh field MR (UHF-MR) benefits from increased signal-to-noise ratio and enhanced spatial resolution, both key to superior imaging for more accurate and definitive diagnoses of subtle lesions. Hence, MRI at 7.0 T has shown encouraging results to overcome the challenges of MS differential diagnosis by providing MS-specific neuroimaging markers (e.g., central vein sign, hypointense rim structures and differentiation of MS grey matter lesions). These markers and others can be identified by other MR contrasts other than T1 and T2 (T2*, phase, diffusion) and substantially improve the differentiation of MS lesions from those occurring in other neuroinflammatory conditions such as neuromyelitis optica and Susac syndrome. In this article, we describe our current technical approach to study cerebral white and grey matter lesions in MS patients at 7.0 T using different MR acquisition methods. The up-to-date protocol includes the preparation of the MR setup including the radio-frequency coils customized for UHF-MR, standardized screening, safety and interview procedures with MS patients, patient positioning in the MR scanner and acquisition of dedicated brain scans tailored for examining MS.</p><p>PMID:<a href=\"https://pubmed.ncbi.nlm.nih.gov/33682856/?utm_source=Other&amp;utm_medium=rss&amp;utm_campaign=pubmed-2&amp;utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&amp;fc=20210216052009&amp;ff=20210308135644&amp;v=2.14.2\">33682856</a> | DOI:<a href=\"https://doi.org/10.3791/62142\">10.3791/62142</a></p></div>",
            "link": "https://pubmed.ncbi.nlm.nih.gov/33682856/#x3D;Other&utm_medium=rss&utm_campaign=pubmed-2&utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&fc&#x",
            "published_date": "2021-02-19T00:00:00Z",
            "sources": [
                "PubMed"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "MyJove Corporation",
            "container_title": "Journal of Visualized Experiments",
            "authors": [
                {
                    "author_id": 213612,
                    "given_name": "Sonia",
                    "family_name": "Waiczies",
                    "ORCID": "http://orcid.org/0000-0002-9916-9572",
                    "country": "DE"
                },
                {
                    "author_id": 243292,
                    "given_name": "Antje",
                    "family_name": "Els",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 324714,
                    "given_name": "Joseph",
                    "family_name": "Kuchling",
                    "ORCID": "http://orcid.org/0000-0002-7981-2073",
                    "country": null
                },
                {
                    "author_id": 243296,
                    "given_name": "Karin",
                    "family_name": "Markenroth Bloch",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243298,
                    "given_name": "Anna",
                    "family_name": "Pankowska",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243299,
                    "given_name": "Helmar",
                    "family_name": "Waiczies",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243300,
                    "given_name": "Carl",
                    "family_name": "Herrmann",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 143294,
                    "given_name": "Claudia",
                    "family_name": "Chien",
                    "ORCID": "http://orcid.org/0000-0001-8280-9513",
                    "country": null
                },
                {
                    "author_id": 202091,
                    "given_name": "Carsten",
                    "family_name": "Finke",
                    "ORCID": "http://orcid.org/0000-0002-7665-1171",
                    "country": null
                },
                {
                    "author_id": 237109,
                    "given_name": "Friedemann",
                    "family_name": "Paul",
                    "ORCID": "https://orcid.org/0000-0002-6378-0070",
                    "country": "DE"
                },
                {
                    "author_id": 243301,
                    "given_name": "Thoralf",
                    "family_name": "Niendorf",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T18:56:46Z",
            "noun_phrases": [
                "Magnetic Resonance Imaging",
                "Multiple Sclerosis",
                "7.0 Tesla"
            ],
            "doi": "10.3791/62142",
            "access": "restricted",
            "takeaways": " MS is a chronic inflammatory, demyelinating, neurodegenerative disease that is characterized by white and gray matter lesions . Ultrahigh field MR (UHF-MR) benefits from increased signal-to-noise ratio and enhanced spatial resolution .",
            "categories": []
        },
        {
            "article_id": 430,
            "title": "The cerebellum and its network: Disrupted static and dynamic functional connectivity patterns and cognitive impairment in multiple sclerosis",
            "summary": "<div><p>Mult Scler. 2021 Mar 8:1352458521999274. doi: 10.1177/1352458521999274. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">BACKGROUND: The impact of cerebellar damage and (dys)function on cognition remains understudied in multiple sclerosis.</p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">OBJECTIVE: To assess the cognitive relevance of cerebellar structural damage and functional connectivity (FC) in relapsing-remitting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS).</p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">METHODS: This study included 149 patients with early RRMS, 81 late RRMS, 48 SPMS and 82 controls. Cerebellar cortical imaging included fractional anisotropy, grey matter volume and resting-state functional magnetic resonance imaging (MRI). Cerebellar FC was assessed with literature-based resting-state networks, using static connectivity (that is, conventional correlations), and dynamic connectivity (that is, fluctuations in FC strength). Measures were compared between groups and related to disability and cognition.</p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">RESULTS: Cognitive impairment (CI) and cerebellar damage were worst in SPMS. Only SPMS showed cerebellar connectivity changes, compared to early RRMS and controls. Lower static FC was seen in fronto-parietal and default-mode networks. Higher dynamic FC was seen in dorsal and ventral attention, default-mode and deep grey matter networks. Cerebellar atrophy and higher dynamic FC together explained 32% of disability and 24% of cognitive variance. Higher dynamic FC was related to working and verbal memory and to information processing speed.</p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">CONCLUSION: Cerebellar damage and cerebellar connectivity changes were most prominent in SPMS and related to worse CI.</p><p>PMID:<a href=\"https://pubmed.ncbi.nlm.nih.gov/33683158/?utm_source=Other&amp;utm_medium=rss&amp;utm_campaign=pubmed-2&amp;utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&amp;fc=20210216052009&amp;ff=20210308135644&amp;v=2.14.2\">33683158</a> | DOI:<a href=\"https://doi.org/10.1177/1352458521999274\">10.1177/1352458521999274</a></p></div>",
            "link": "https://pubmed.ncbi.nlm.nih.gov/33683158/#x3D;Other&utm_medium=rss&utm_campaign=pubmed-2&utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&fc&#x",
            "published_date": "2021-01-11T00:00:00Z",
            "sources": [
                "PubMed"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 151932,
                    "given_name": "Menno M",
                    "family_name": "Schoonheim",
                    "ORCID": "http://orcid.org/0000-0002-2504-6959",
                    "country": "NL"
                },
                {
                    "author_id": 243283,
                    "given_name": "Linda",
                    "family_name": "Douw",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243284,
                    "given_name": "Tommy AA",
                    "family_name": "Broeders",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243285,
                    "given_name": "Anand JC",
                    "family_name": "Eijlers",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243286,
                    "given_name": "Kim A",
                    "family_name": "Meijer",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 243288,
                    "given_name": "Jeroen JG",
                    "family_name": "Geurts",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T18:56:46Z",
            "noun_phrases": [
                "The cerebellum",
                "its network",
                "Disrupted static and dynamic functional connectivity patterns",
                "cognitive impairment",
                "multiple sclerosis"
            ],
            "doi": "10.1177/1352458521999274",
            "access": "open",
            "takeaways": " The impact of cerebellar damage and (dys)function on cognition remains understudied in multiple sclerosis . Cerebellar atrophy and higher dynamic FC explained 32% of disability and 24% of cognitive variance .",
            "categories": []
        },
        {
            "article_id": 432,
            "title": "Synergic use of botulinum toxin injection and radial extracorporeal shockwave therapy in Multiple Sclerosis spasticity",
            "summary": "<div><p>Acta Biomed. 2021 Jan 28;92(1):e2021076. doi: 10.23750/abm.v92i1.11101.</p><p><b>ABSTRACT</b></p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">BACKGROUND AND AIM: In Multiple Sclerosis (MS) spasticity worsen patient's quality of life. Botulinum NeuroToxin TypeA (BoNT-A) is extensively used in focal spasticity, frequently combined with physical therapies. Radial extracorporeal shock waves (rESW) were already used in association with BoNT-A. Considering that loss of efficacy and adverse events are determinants of BoNT-A treatment interruption, this study aimed to evaluate the possibility to prolong BoNT-A's effect by using rESW in MS focal spasticity.</p><p xmlns:mml=\"http://www.w3.org/1998/Math/MathML\" xmlns:p1=\"http://pubmed.gov/pub-one\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">METHODS: Sixteen MS patients with spasticity of triceps surae muscles were first subjected to BoNT-A therapy and, four months later, to 4 sections of rESWT. Patients were evaluated before, 30, 90 days after the end of the treatments, by using Modified Ashworth Scale (MAS), Modified Tardieu Scale (MTS) and kinematic analysis of passive and active ankle ROM. Results: BoNT-A determined a significant reduction of spasticity evaluated by MAS with a reduction of positive effects after 4months (p&lt;0.05); MTS highlighted the efficacy only 90 days after injection (p&lt;0.05). rESWT decreased MAS values at the end and 30 days later the treatment (p&lt;0.01); MTS values showed instead a prolonged effect (p&lt;0.01). BoNT-A determined a gain of passive and active ankle ROM, persisting along with treatment and peaking the maximum value after rESWT (p&lt;0.05). Conclusions: rESWT can prolong BoNT-A effect inducing significant reduction of spasticity and improvement in passive and active ankle ROM in MS patients. The use of rESWT following BoNT-A injection is useful to avoid some limitations and to prolong the therapeutic effects of BoNT-A therapy.</p><p>PMID:<a href=\"https://pubmed.ncbi.nlm.nih.gov/33682833/?utm_source=Other&amp;utm_medium=rss&amp;utm_campaign=pubmed-2&amp;utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&amp;fc=20210216052009&amp;ff=20210308135644&amp;v=2.14.2\">33682833</a> | DOI:<a href=\"https://doi.org/10.23750/abm.v92i1.11101\">10.23750/abm.v92i1.11101</a></p></div>",
            "link": "https://pubmed.ncbi.nlm.nih.gov/33682833/#x3D;Other&utm_medium=rss&utm_campaign=pubmed-2&utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&fc&#x",
            "published_date": "2021-01-28T00:00:00Z",
            "sources": [
                "PubMed"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": null,
            "container_title": null,
            "authors": [],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T18:56:46Z",
            "noun_phrases": [
                "Synergic use",
                "botulinum toxin injection",
                "radial extracorporeal shockwave therapy",
                "Multiple Sclerosis spasticity"
            ],
            "doi": "10.23750/abm.v92i1.11101",
            "access": "restricted",
            "takeaways": " Botulinum NeuroToxin TypeA (BoNT-A) is extensively used in focal spasticity, frequently combined with physical therapies . Radial extracorporeal shock waves (rESW) were already used .",
            "categories": [
                {
                    "category_id": 18,
                    "category_description": "Search terms: telerehabilitation, physical therapy, virtual reality, gamification, neurostimulation, cognitive training, spasticity, motor control.\n\nSuggested by Alejandro Carrabs",
                    "category_name": "Physical therapy and Telerehabilitation",
                    "category_slug": "physical-therapy-and-telerehabilitation",
                    "category_terms": [
                        "telerehabilitation",
                        "physical therapy",
                        "virtual reality",
                        "gamification",
                        "neurostimulation",
                        "cognitive training",
                        "spasticity",
                        "motor control"
                    ],
                    "article_count": 181
                }
            ]
        },
        {
            "article_id": 428,
            "title": "An old weapon with a new function: PIWI-interacting RNAs in neurodegenerative diseases",
            "summary": "AbstractPIWI-interacting RNAs (piRNAs) are small non-coding transcripts that are highly conserved across species and regulate gene expression through pre- and post-transcriptional processes. piRNAs were originally discovered in germline cells and protect against transposable element expression to promote and maintain genome stability. In the recent decade, emerging roles of piRNAs have been revealed, including the roles in sterility, tumorigenesis, metabolic homeostasis, neurodevelopment, and neurodegenerative diseases. In this review, we summarize piRNA biogenesis in C. elegans, Drosophila, and mice, and further elaborate upon how piRNAs mitigate the harmful effects of transposons. Lastly, the most recent findings on piRNA participation in neurological diseases are highlighted. We speculate on the mechanisms of piRNA action in the development and progression of neurodegenerative diseases. Understanding the roles of piRNAs in neurological diseases may facilitate their applications in diagnostic and therapeutic practice.",
            "link": "https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/s40035-021-00233-6",
            "published_date": "2021-03-08T00:00:00Z",
            "sources": [
                "BioMedCentral"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Springer Science and Business Media LLC",
            "container_title": "Translational Neurodegeneration",
            "authors": [
                {
                    "author_id": 269011,
                    "given_name": "Xiaobing",
                    "family_name": "Huang",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 170909,
                    "given_name": "Garry",
                    "family_name": "Wong",
                    "ORCID": "http://orcid.org/0000-0003-4566-9958",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T18:43:30Z",
            "noun_phrases": [
                "An old weapon",
                "a new function",
                "PIWI-interacting RNAs",
                "neurodegenerative diseases"
            ],
            "doi": "10.1186/s40035-021-00233-6",
            "access": "open",
            "takeaways": " PIWI-interacting RNAs (piRNAs) are small non-coding transcripts that are highly conserved across species . They regulate gene expression through pre- and post-transcriptional processes . Understanding the roles of piRNAs in neurological diseases may facilitate their applications in diagnostic and therapeutic practice .",
            "categories": []
        },
        {
            "article_id": 429,
            "title": "A pilot study of the impact of an exercise intervention on brain structure, cognition, and psychosocial symptoms in individuals with relapsing-remitting multiple sclerosis",
            "summary": "Background: Despite pharmacological treatment, many individuals with multiple sclerosis (MS) continue to experience symptoms and medication side effects. Exercise holds promise for MS, but changes in brain structure following exercise have not been thoroughly investigated, and important cognitive and psychosocial variables are rarely primary outcomes. The aim of this pilot study was to investigate whether a 12-week exercise intervention would improve white matter integrity in the brain, or cognition, symptoms of fatigue, and depressed mood for individuals with relapsing-remitting MS (RRMS).MethodThirteen participants completed 12 weeks of speeded walking. Baseline and post-intervention testing included 3T diffusion tensor imaging (DTI) to assess white matter and neuropsychological testing to assess cognition, fatigue, and mood. Image pre-processing and analyses were performed in functional magnetic resonance imaging of the Brain Software Library.ResultsPost-intervention, there were no significant changes in white matter compared to baseline. Post-intervention, individuals with RRMS performed significantly better on the Symbol Digit Modalities Test (SDMT), reported fewer perceived memory problems, and endorsed less fatigue. Performance was not significantly different on Trails or Digit Span, and there were no significant changes in reports of mood.ConclusionAlthough 12 weeks of speeded walking did not improve white matter integrity, exercise may hold promise for managing some symptoms of RRMS in the context of this study population.",
            "link": "https://pilotfeasibilitystudies.biomedcentral.com/articles/10.1186/s40814-021-00806-2",
            "published_date": "2021-03-08T00:00:00Z",
            "sources": [
                "BioMedCentral"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Springer Science and Business Media LLC",
            "container_title": "Pilot and Feasibility Studies",
            "authors": [
                {
                    "author_id": 240820,
                    "given_name": "Chantel D.",
                    "family_name": "Mayo",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 304578,
                    "given_name": "Laureen",
                    "family_name": "Harrison",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 304579,
                    "given_name": "Kristen",
                    "family_name": "Attwell-Pope",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 304580,
                    "given_name": "Lynneth",
                    "family_name": "Stuart-Hill",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 219696,
                    "given_name": "Jodie R.",
                    "family_name": "Gawryluk",
                    "ORCID": "http://orcid.org/0000-0003-4924-7517",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T18:43:30Z",
            "noun_phrases": [
                "A pilot study",
                "the impact",
                "an exercise intervention",
                "brain structure",
                "cognition",
                "psychosocial symptoms",
                "individuals",
                "relapsing-remitting multiple sclerosis"
            ],
            "doi": "10.1186/s40814-021-00806-2",
            "access": "open",
            "takeaways": " The aim of this pilot study was to investigate whether a 12-week exercise intervention would improve white matter integrity in the brain, cognition, symptoms of fatigue, and depressed mood for individuals with relapsing-remitting MS (RRMS)",
            "categories": []
        },
        {
            "article_id": 427,
            "title": "Thyroid hormone: sex-dependent role in nervous system regulation and disease",
            "summary": "AbstractThyroid hormone (TH) regulates many functions including metabolism, cell differentiation, and nervous system development. Alteration of thyroid hormone level in the body can lead to nervous system-related problems linked to cognition, visual attention, visual processing, motor skills, language, and memory skills. TH has also been associated with neuropsychiatric disorders including schizophrenia, bipolar disorder, anxiety, and depression. Males and females display sex-specific differences in neuronal signaling. Steroid hormones including testosterone and estrogen are considered to be the prime regulators for programing the neuronal signaling in a male- and female-specific manner. However, other than steroid hormones, TH could also be one of the key signaling molecules to regulate different brain signaling in a male- and female-specific manner. Thyroid-related diseases and neurological diseases show sex-specific incidence; however, the molecular mechanisms behind this are not clear. Hence, it will be very beneficial to understand how TH acts in male and female brains and what are the critical genes and signaling networks. In this review, we have highlighted the role of TH in nervous system regulation and disease outcome and given special emphasis on its sex-specific role in male and female brains. A network model is also presented that provides critical information on TH-regulated genes, signaling, and disease.",
            "link": "https://bsd.biomedcentral.com/articles/10.1186/s13293-021-00367-2",
            "published_date": "2021-03-08T00:00:00Z",
            "sources": [
                "BioMedCentral"
            ],
            "teams": [
                {
                    "id": 1,
                    "name": "Team Gregory"
                }
            ],
            "subjects": [
                {
                    "subject_name": "Multiple Sclerosis",
                    "description": null
                }
            ],
            "publisher": "Springer Science and Business Media LLC",
            "container_title": "Biology of Sex Differences",
            "authors": [
                {
                    "author_id": 237604,
                    "given_name": "Shounak",
                    "family_name": "Baksi",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 151244,
                    "given_name": "Ajay",
                    "family_name": "Pradhan",
                    "ORCID": "http://orcid.org/0000-0003-2305-8574",
                    "country": "SE"
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2021-03-08T18:43:30Z",
            "noun_phrases": [
                "Thyroid hormone",
                "sex-dependent role",
                "nervous system regulation",
                "disease"
            ],
            "doi": "10.1186/s13293-021-00367-2",
            "access": "open",
            "takeaways": " Alteration of thyroid hormone level in the body can lead to nervous system-related problems linked to cognition, visual attention, visual processing, motor skills, language, and memory skills . TH has also been associated with neuropsychiatric disorders including schizophrenia, bipolar disorder, anxiety, and depression .",
            "categories": []
        }
    ]
}