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      Extracellular matrix and synapse formation

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          Abstract

          The extracellular matrix (ECM) is a complex molecular network distributed throughout the extracellular space of different tissues as well as the neuronal system. Previous studies have identified various ECM components that play important roles in neuronal maturation and signal transduction. ECM components are reported to be involved in neurogenesis, neuronal migration, and axonal growth by interacting or binding to specific receptors. In addition, the ECM is found to regulate synapse formation, the stability of the synaptic structure, and synaptic plasticity. Here, we mainly reviewed the effects of various ECM components on synapse formation and briefly described the related diseases caused by the abnormality of several ECM components.

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          Most cited references187

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          National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease: a practical approach.

          Thomas J Montine, Creighton H Phelps, Thomas G Beach … (2012)
          We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
          Article 0 comments Cited 1053 times – based on 0 reviews     Review now
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            Thrombospondins are astrocyte-secreted proteins that promote CNS synaptogenesis.

            Karen Christopherson, Erik Ullian, Caleb Stokes … (2005)
            The establishment of neural circuitry requires vast numbers of synapses to be generated during a specific window of brain development, but it is not known why the developing mammalian brain has a much greater capacity to generate new synapses than the adult brain. Here we report that immature but not mature astrocytes express thrombospondins (TSPs)-1 and -2 and that these TSPs promote CNS synaptogenesis in vitro and in vivo. TSPs induce ultrastructurally normal synapses that are presynaptically active but postsynaptically silent and work in concert with other, as yet unidentified, astrocyte-derived signals to produce functional synapses. These studies identify TSPs as CNS synaptogenic proteins, provide evidence that astrocytes are important contributors to synaptogenesis within the developing CNS, and suggest that TSP-1 and -2 act as a permissive switch that times CNS synaptogenesis by enabling neuronal molecules to assemble into synapses within a specific window of CNS development.
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              Neuroinflammation in Alzheimer's disease: Current evidence and future directions.

              Valeria Calsolaro, Paul Edison (2016)
              Several attempts have been made to treat Alzheimer's disease (AD) using anti-amyloid strategies with disappointing results. It is clear that the "amyloid cascade hypothesis" alone cannot fully explain the neuronal damage in AD, as evidenced both by autopsy and imaging studies. Neuroinflammation plays a significant role in neurodegenerative diseases, whereas the debate is ongoing about its precise role, whether it is protective or harmful. In this review, we focus on the potential mechanism of glial activation and how local and systemic factors influence disease progression. We focus on neuroinflammation in AD, especially in the earliest stages, a vicious cycle of glial priming, release of pro-inflammatory factors, and neuronal damage. We review the evidence from imaging studies, regarding the temporal relationship between amyloid deposition and neuroinflammation, the influence of systemic inflammation on glial activation, both in acute and chronic stimulation and the relevance of inflammation as a diagnostic and therapeutic target.
              Article 0 comments Cited 468 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Lei Yang:
                ORCID: https://orcid.org/0000-0002-2882-5560
                Role: Writing—original draftRole: Writing—review & editing
                Mengping Wei: Role: Writing—original draftRole: Writing—review & editing
                Biyu Xing:
                ORCID: https://orcid.org/0000-0002-1390-1970
                Role: Writing—original draft
                Chen Zhang: Role: Funding acquisitionRole: Writing—original draftRole: Writing—review & editing
                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci Rep
                Journal ID (publisher-id): bsr
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date Collection: 31 January 2023
                Publication date (Electronic): 06 January 2023
                Volume: 43
                Issue: 1
                Electronic Location Identifier: BSR20212411
                Affiliations
                School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China
                Author notes
                Correspondence: Mengping Wei ( weimengping@ 123456ccmu.edu.cn ) and Chen Zhang ( czhang@ 123456ccmu.edu.cn )
                [*]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-2882-5560
                https://orcid.org/0000-0002-1390-1970
                Article
                Publisher ID: BSR20212411
                DOI: 10.1042/BSR20212411
                PMC ID: 9829651
                PubMed ID: 36503961
                SO-VID: 5575bdde-4d34-4452-88a7-b01ae69f9d4c
                Copyright © © 2023 The Author(s).
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                Date received : 05 May 2022
                Date revision received : 08 November 2022
                Date accepted : 24 November 2022
                Date: 12 December 2022
                Page count
                Pages: 15
                Categories
                Subject: Neuroscience
                Subject: Molecular Scaffolds & Matrices
                Subject: Cell Migration, Adhesion & Morphology
                Subject: Review Articles

                ScienceOpen disciplines: Life sciences
                Keywords: extracellular matrix,neuroscience,synapse formation,synaptic plasticity,synaptogenesis
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: extracellular matrix, neuroscience, synapse formation, synaptic plasticity, synaptogenesis

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