Advanced Neurology https://journals.accscience.com/index.php/AN en-US <p><strong><em>Copyright</em></strong></p> <p>The authors shall retain the copyright of their work but allow the Publisher to publish, copy, distribute, and convey the work.</p> <p>&nbsp;</p> <p><strong><em>License</em></strong></p> <p><em>Advanced Neurology</em> publishes accepted manuscripts under&nbsp;<a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noopener"><strong>Creative Commons Attribution 4.0 International License (CC BY 4.0)</strong></a>. Authors who submit their papers for publication by&nbsp;<em>Advanced Neurology</em> agree to have the CC BY 4.0 license applied to their work, and that anyone is allowed to reuse the article or part of it free of charge for any purpose, including commercial use, as long as the author and original source is properly cited, anyone may copy, redistribute, reuse and transform the content.</p> <p>For more information, refer to the journal’s&nbsp;<strong>Copyright and License</strong>&nbsp;section on the <strong>About the Journal </strong>section.</p> editor.an@accscience.com (Adv Neuro Editor) editor.an@accscience.com (Adv Neuro Editor) Mon, 24 Jul 2023 10:19:32 +0800 OJS 3.1.2.0 http://blogs.law.harvard.edu/tech/rss 60 Transient receptor potential melastatin 7 signaling in U251 cell migration and invasion involves calcineurin https://journals.accscience.com/index.php/AN/article/view/334 <p>Transient receptor potential melastatin 7 (TRPM7) is a divalent cation channel that has crucial functions in glioblastoma (GBM), which remains the most prevalent and lethal primary brain tumor in adults. Altering TRPM7 activity has previously been reported to affect GBM cell function (i.e., migration, invasion, and proliferation), thus elucidating the TRPM7-mediated signaling pathway in GBM could reveal novel therapeutic targets. Calcineurin, a Ca2+-dependent phosphatase, also influences GBM cell survival and migration. However, the role or the relationship between TRPM7 and calcineurin in GBM signaling has not previously been investigated. In this study, we provide evidence that there is a possible interaction between TRPM7 and calcineurin in the GBM cell line U251. Moreover, we employed pharmacological approaches to show that TRPM7 regulates calcineurin function, thereby suggesting that calcineurin is a potential downstream target of TRPM7 signaling in U251 cell migration and invasion.</p> Haifan Gong, Raymond Wong, Julia Bandura, James T. Rutka, Zhong-Ping Feng, Hong-Shuo Sun Copyright (c) 2023 Author(s) https://creativecommons.org/licenses/by/4.0 https://journals.accscience.com/index.php/AN/article/view/334 Mon, 24 Jul 2023 10:19:14 +0800 Woven Endobridge embolization: Indications and innovation https://journals.accscience.com/index.php/AN/article/view/293 <p>The treatment of intracranial aneurysms has seen incredible advancements over the last few decades. Long-term occlusion of wide-neck bifurcation aneurysms remains technically challenging. The Woven Endobridge (WEB) embolization device is innovative in its construction and uses. The design of the device has evolved over the last decade. Pre-clinical and clinical trials are ongoing and continue to inform the development of intrasaccular flow-diverting devices. The WEB device is currently approved by the U.S. Food and Drug Administration (FDA) for treating wide-neck aneurysms. The safety and efficacy of the WEB device have yielded promising clinical results that may have additional indications. This review aims to discuss the development of the WEB device and the current state of the WEB device in the treatment of wide-neck aneurysms. We also summarize ongoing clinical studies and potential innovative uses.</p> Brandon Lucke-Wold, Ashley M. Carter, Bethsabe Romero , Harrison Dai , Simran Phuyal , Danxun Li Copyright (c) 2023 Author(s) https://creativecommons.org/licenses/by/4.0 https://journals.accscience.com/index.php/AN/article/view/293 Tue, 13 Jun 2023 00:00:00 +0800 The gut microbiota and associated metabolites in multiple sclerosis https://journals.accscience.com/index.php/AN/article/view/413 <p>Multiple sclerosis (MS) is a severe central nervous system autoimmune inflammatory disease featured by the presence of infiltrated immune cells, demyelination, and degeneration. Recent research has shown that gut microbiota, including some commensal bacteria, is capable of interacting with the host immune system and remarkably influencing the development and outcome of experimental autoimmune encephalomyelitis, a classic animal model of MS. In addition, gut dysbiosis, presented with a significantly altered composition of commensal bacteria, is linked to the immune response and inflammation, such as Th17 activation and B cell function. Moreover, it has been observed that microbiota impacts the immune system by regulating the metabolites in the gut. In this review, we summarize the new research on the relationship and mechanism between the gut microbiota and MS, as well as the implications for developing new strategies in MS by modulating the gut microbiota and metabolites.</p> Yunshu Wang, Zihao Li , Yun Xu, Cun-Jin Zhang Copyright (c) 2023 Author(s) https://creativecommons.org/licenses/by/4.0 https://journals.accscience.com/index.php/AN/article/view/413 Wed, 26 Jul 2023 14:29:42 +0800