Synapse Dysfunctions in Multiple Sclerosis

Multiple sclerosis (MS) is a chronic neuroinflammatory disease of the central nervous system (CNS) affecting nearly three million humans worldwide. In MS, cells of an auto-reactive immune system invade the brain and cause neuroinflammation. Neuroinflammation triggers a complex, multi-faceted harmful...

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Main Authors: Karin Schwarz, Frank Schmitz
Format: Article
Language:English
Published: MDPI AG 2023-01-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/2/1639
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author Karin Schwarz
Frank Schmitz
author_facet Karin Schwarz
Frank Schmitz
author_sort Karin Schwarz
collection DOAJ
description Multiple sclerosis (MS) is a chronic neuroinflammatory disease of the central nervous system (CNS) affecting nearly three million humans worldwide. In MS, cells of an auto-reactive immune system invade the brain and cause neuroinflammation. Neuroinflammation triggers a complex, multi-faceted harmful process not only in the white matter but also in the grey matter of the brain. In the grey matter, neuroinflammation causes synapse dysfunctions. Synapse dysfunctions in MS occur early and independent from white matter demyelination and are likely correlates of cognitive and mental symptoms in MS. Disturbed synapse/glia interactions and elevated neuroinflammatory signals play a central role. Glutamatergic excitotoxic synapse damage emerges as a major mechanism. We review synapse/glia communication under normal conditions and summarize how this communication becomes malfunctional during neuroinflammation in MS. We discuss mechanisms of how disturbed glia/synapse communication can lead to synapse dysfunctions, signaling dysbalance, and neurodegeneration in MS.
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spelling doaj.art-d5bc94c8a17f4c688b16c98c2b4052862023-11-30T22:43:26ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-01-01242163910.3390/ijms24021639Synapse Dysfunctions in Multiple SclerosisKarin Schwarz0Frank Schmitz1Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, 66421 Homburg, GermanyDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, 66421 Homburg, GermanyMultiple sclerosis (MS) is a chronic neuroinflammatory disease of the central nervous system (CNS) affecting nearly three million humans worldwide. In MS, cells of an auto-reactive immune system invade the brain and cause neuroinflammation. Neuroinflammation triggers a complex, multi-faceted harmful process not only in the white matter but also in the grey matter of the brain. In the grey matter, neuroinflammation causes synapse dysfunctions. Synapse dysfunctions in MS occur early and independent from white matter demyelination and are likely correlates of cognitive and mental symptoms in MS. Disturbed synapse/glia interactions and elevated neuroinflammatory signals play a central role. Glutamatergic excitotoxic synapse damage emerges as a major mechanism. We review synapse/glia communication under normal conditions and summarize how this communication becomes malfunctional during neuroinflammation in MS. We discuss mechanisms of how disturbed glia/synapse communication can lead to synapse dysfunctions, signaling dysbalance, and neurodegeneration in MS.https://www.mdpi.com/1422-0067/24/2/1639multiple sclerosissynapseastrocytemicrogliaglutamateionotropic glutamate receptors
spellingShingle Karin Schwarz
Frank Schmitz
Synapse Dysfunctions in Multiple Sclerosis
International Journal of Molecular Sciences
multiple sclerosis
synapse
astrocyte
microglia
glutamate
ionotropic glutamate receptors
title Synapse Dysfunctions in Multiple Sclerosis
title_full Synapse Dysfunctions in Multiple Sclerosis
title_fullStr Synapse Dysfunctions in Multiple Sclerosis
title_full_unstemmed Synapse Dysfunctions in Multiple Sclerosis
title_short Synapse Dysfunctions in Multiple Sclerosis
title_sort synapse dysfunctions in multiple sclerosis
topic multiple sclerosis
synapse
astrocyte
microglia
glutamate
ionotropic glutamate receptors
url https://www.mdpi.com/1422-0067/24/2/1639
work_keys_str_mv AT karinschwarz synapsedysfunctionsinmultiplesclerosis
AT frankschmitz synapsedysfunctionsinmultiplesclerosis