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IMPACT FACTOR 5.923 an Open Access Journal by MDPI The Molecular Brain and Its Health Guest Editor: Message from the Guest Editor Dr. Leo Veenman Consorzio per Valutazioni Biologiche e Farmacologiche, Via Nicolò Putignani, 178, 70122 Bari, Italy [email protected] Deadline for manuscript submissions: 31 December 2021 mdpi.com/si/79189 SpeciaIslsue IMPACT FACTOR 5.923 an Open Access Journal by MDPI Editor-in-Chief Message from the Editor-in-Chief Prof. Dr. Maurizio Battino The International Journal of Molecular Sciences (IJMS, 1. Department of ISSN 1422-0067) is an open access journal, which was Odontostomatologic and established in 2000. The journal aims to provide a forum Specialized Clinical Sciences, Sez-Biochimica, Faculty of for scholarly research on a range of topics, including Medicine, Università Politecnica biochemistry, molecular and cell biology, molecular delle Marche, Via Ranieri 65, biophysics, molecular medicine, and all aspects of 60100 Ancona, Italy molecular research in chemistry. IJMS publishes both 2. International Research Center for Food Nutrition and Safety, original research and review articles, and regularly Jiangsu University, Zhenjiang publishes special issues to highlight advances at the 212013, China cutting edge of research. We invite you to read recent articles published in IJMS and consider publishing your next paper with us. Author Benefits Open Access:— free for readers, with article processing charges (APC) paid by authors or their institutions. High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, MEDLINE, Embase, CAPlus / SciFinder, and many other databases. Journal Rank: JCR - Q1 (Biochemistry & Molecular Biology) / CiteScore - Q1 (Inorganic Chemistry) Contact Us International Journal of Molecular Tel: +41 61 683 77 34 mdpi.com/journal/ijms Sciences Fax: +41 61 302 89 18 [email protected] MDPI, St. Alban-Anlage 66 www.mdpi.com @IJMS_MDPI 4052 Basel, Switzerland.

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Shedding New Light on the Brain with Tissue Clearing Robin J
Vigouroux et al. Molecular Brain (2017) 10:33 DOI 10.1186/s13041-017-0314-y REVIEW Open Access Neuroscience in the third dimension: shedding new light on the brain with tissue clearing Robin J. Vigouroux, Morgane Belle and Alain Chédotal* Abstract: For centuries analyses of tissues have depended on sectioning methods. Recent developments of tissue clearing techniques have now opened a segway from studying tissues in 2 dimensions to 3 dimensions. This particular advantage echoes heavily in the field of neuroscience, where in the last several years there has been an active shift towards understanding the complex orchestration of neural circuits. In the past five years, many tissue- clearing protocols have spawned. This is due to varying strength of each clearing protocol to specific applications. However, two main protocols have shown their applicability to a vast number of applications and thus are exponentially being used by a growing number of laboratories. In this review, we focus specifically on two major tissue-clearing method families, derived from the 3DISCO and the CLARITY clearing protocols. Moreover, we provide a “hands-on” description of each tissue clearing protocol and the steps to look out for when deciding to choose a specific tissue clearing protocol. Lastly, we provide perspectives for the development of tissue clearing protocols into the research community in the fields of embryology and cancer. Keywords: 3DISCO, iDISCO, Clarity, Tissue-clearing, Neuroscience Introduction (3D) form rather than in two-dimensions. Researchers Over the past century, biological sciences have evolved quickly understood that to observe an organ in 3D they from a physiological to a cellular and then a molecular un- had to: i) minimize light artifacts (scattering and absorp- derstanding.
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Molecular Brain BioMed Central Research Open Access Autophagy activation and enhanced mitophagy characterize the Purkinje cells of pcd mice prior to neuronal death Lisa Chakrabarti1, Jeremiah Eng1, Nishi Ivanov2, Gwenn A Garden2,4 and Albert R La Spada*1,2,3,4,5 Address: 1Department of Laboratory Medicine, University of Washington, Seattle, WA, USA, 2Department of Neurology, University of Washington, Seattle, WA, USA, 3Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA, USA, 4Center for Neurogenetics & Neurotherapeutics, University of Washington, Seattle, WA, USA and 5Departments of Pediatrics and Cellular & Molecular Medicine, University of California, San Diego, USA Email: Lisa Chakrabarti - [email protected]; Jeremiah Eng - [email protected]; Nishi Ivanov - [email protected]; Gwenn A Garden - [email protected]; Albert R La Spada* - [email protected] * Corresponding author Published: 29 July 2009 Received: 30 May 2009 Accepted: 29 July 2009 Molecular Brain 2009, 2:24 doi:10.1186/1756-6606-2-24 This article is available from: http://www.molecularbrain.com/content/2/1/24 © 2009 Chakrabarti et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Purkinje cells are a class of specialized neurons in the cerebellum, and are among the most metabolically active of all neurons, as they receive immense synaptic stimulation, and provide the only efferent output from the cerebellum. Degeneration of Purkinje cells is a common feature of inherited ataxias in humans and mice.
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Identification of a Single Amino Acid in Glun1 That Is Critical for Glycine-Primed Internalization of NMDA Receptors
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Evidence That the Presynaptic Vesicle Protein Cspalpha Is a Key Player in Synaptic Degeneration and Protection in Alzheimer's
Tiwari et al. Molecular Brain (2015) 8:6 DOI 10.1186/s13041-015-0096-z RESEARCH Open Access Evidence that the presynaptic vesicle protein CSPalpha is a key player in synaptic degeneration and protection in Alzheimer’s disease Sachin S Tiwari1, Marie d’Orange1, Claire Troakes2, Badrun N Shurovi1, Olivia Engmann1, Wendy Noble3, Tibor Hortobágyi2,4 and Karl P Giese1,5* Abstract Background: In Alzheimer’s disease synapse loss precedes neuronal loss and correlates best with impaired memory formation. However, the mechanisms underlying synaptic degeneration in Alzheimer’s disease are not well known. Further, it is unclear why synapses in AD cerebellum are protected from degeneration. Our recent work on the cyclin-dependent kinase 5 activator p25 suggested that expression of the multifunctional presynaptic molecule cysteine string protein alpha (CSPalpha) may be affected in Alzheimer’sdisease. Results: Using western blots and immunohistochemistry, we found that CSPalpha expression is reduced in hippocampus and superior temporal gyrus in Alzheimer’s disease. Reduced CSPalpha expression occurred before synaptophysin levels drop, suggesting that it contributes to the initial stages of synaptic degeneration. Surprisingly, we also found that CSPalpha expression is upregulated in cerebellum in Alzheimer’sdisease.This CSPalpha upregulation reached the same level as in young, healthy cerebellum. We tested the idea whether CSPalpha upregulation might be neuroprotective, using htau mice, a model of tauopathy that expresses the entire wild-type human tau gene in the absence of mouse tau. In htau mice CSPalpha expression was found to be elevated at times when neuronal loss did not occur. Conclusion: Our findings provide evidence that the presynaptic vesicle protein CSPalpha is a key player in synaptic degeneration and protection in Alzheimer’s disease.
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Synaptoimmunology - Roles in Health and Disease Robert Nisticò1,2* , Eric Salter3, Celine Nicolas4, Marco Feligioni2, Dalila Mango2, Zuner A
Nisticò et al. Molecular Brain (2017) 10:26 DOI 10.1186/s13041-017-0308-9 REVIEW Open Access Synaptoimmunology - roles in health and disease Robert Nisticò1,2* , Eric Salter3, Celine Nicolas4, Marco Feligioni2, Dalila Mango2, Zuner A. Bortolotto4, Pierre Gressens5,6, Graham L. Collingridge3,4 and Stephane Peineau4,5,7* Abstract: Mounting evidence suggests that the nervous and immune systems are intricately linked. Many proteins first identified in the immune system have since been detected at synapses, playing different roles in normal and pathological situations. In addition, novel immunological functions are emerging for proteins typically expressed at synapses. Under normal conditions, release of inflammatory mediators generally represents an adaptive and regulated response of the brain to immune signals. On the other hand, when immune challenge becomes prolonged and/or uncontrolled, the consequent inflammatory response leads to maladaptive synaptic plasticity and brain disorders. In this review, we will first provide a summary of the cell signaling pathways in neurons and immune cells. We will then examine how immunological mechanisms might influence synaptic function, and in particular synaptic plasticity, in the healthy and pathological CNS. A better understanding of neuro-immune system interactions in brain circuitries relevant to neuropsychiatric and neurological disorders should provide specific biomarkers to measure the status of the neuroimmunological response and help design novel neuroimmune-targeted therapeutics. Keywords: Nervous system, Immune system, Synaptic plasticity, Neuroinflammation, Microglia Introduction numerous physiological functions including neurite out- Following a pathogenic insult to the brain, most central growth, neurogenesis, neuronal survival, synaptic pruning, nervous system (CNS) cells, as well as some peripheral synaptic transmission and synaptic plasticity [2].
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