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Fluid Biomarkers for Synaptic Dysfunction and Loss

Synapses are the site for brain communication where information is transmitted between neurons and stored for memory formation. Synaptic degeneration is a global and early pathogenic event in neurodegenerative disorders with reduced levels of pre- and postsynaptic proteins being recognized as a core...

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Autores principales: Camporesi, Elena, Nilsson, Johanna, Brinkmalm, Ann, Becker, Bruno, Ashton, Nicholas J, Blennow, Kaj, Zetterberg, Henrik
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444114/
https://www.ncbi.nlm.nih.gov/pubmed/32913390
http://dx.doi.org/10.1177/1177271920950319
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author Camporesi, Elena
Nilsson, Johanna
Brinkmalm, Ann
Becker, Bruno
Ashton, Nicholas J
Blennow, Kaj
Zetterberg, Henrik
author_facet Camporesi, Elena
Nilsson, Johanna
Brinkmalm, Ann
Becker, Bruno
Ashton, Nicholas J
Blennow, Kaj
Zetterberg, Henrik
author_sort Camporesi, Elena
collection PubMed
description Synapses are the site for brain communication where information is transmitted between neurons and stored for memory formation. Synaptic degeneration is a global and early pathogenic event in neurodegenerative disorders with reduced levels of pre- and postsynaptic proteins being recognized as a core feature of Alzheimer’s disease (AD) pathophysiology. Together with AD, other neurodegenerative and neurodevelopmental disorders show altered synaptic homeostasis as an important pathogenic event, and due to that, they are commonly referred to as synaptopathies. The exact mechanisms of synapse dysfunction in the different diseases are not well understood and their study would help understanding the pathogenic role of synaptic degeneration, as well as differences and commonalities among them and highlight candidate synaptic biomarkers for specific disorders. The assessment of synaptic proteins in cerebrospinal fluid (CSF), which can reflect synaptic dysfunction in patients with cognitive disorders, is a keen area of interest. Substantial research efforts are now directed toward the investigation of CSF synaptic pathology to improve the diagnosis of neurodegenerative disorders at an early stage as well as to monitor clinical progression. In this review, we will first summarize the pathological events that lead to synapse loss and then discuss the available data on established (eg, neurogranin, SNAP-25, synaptotagmin-1, GAP-43, and α-syn) and emerging (eg, synaptic vesicle glycoprotein 2A and neuronal pentraxins) CSF biomarkers for synapse dysfunction, while highlighting possible utilities, disease specificity, and technical challenges for their detection.
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spelling pubmed-74441142020-09-09 Fluid Biomarkers for Synaptic Dysfunction and Loss Camporesi, Elena Nilsson, Johanna Brinkmalm, Ann Becker, Bruno Ashton, Nicholas J Blennow, Kaj Zetterberg, Henrik Biomark Insights Novel Biomarkers of Neurodegenerative Disorders: Updates and Challenges Synapses are the site for brain communication where information is transmitted between neurons and stored for memory formation. Synaptic degeneration is a global and early pathogenic event in neurodegenerative disorders with reduced levels of pre- and postsynaptic proteins being recognized as a core feature of Alzheimer’s disease (AD) pathophysiology. Together with AD, other neurodegenerative and neurodevelopmental disorders show altered synaptic homeostasis as an important pathogenic event, and due to that, they are commonly referred to as synaptopathies. The exact mechanisms of synapse dysfunction in the different diseases are not well understood and their study would help understanding the pathogenic role of synaptic degeneration, as well as differences and commonalities among them and highlight candidate synaptic biomarkers for specific disorders. The assessment of synaptic proteins in cerebrospinal fluid (CSF), which can reflect synaptic dysfunction in patients with cognitive disorders, is a keen area of interest. Substantial research efforts are now directed toward the investigation of CSF synaptic pathology to improve the diagnosis of neurodegenerative disorders at an early stage as well as to monitor clinical progression. In this review, we will first summarize the pathological events that lead to synapse loss and then discuss the available data on established (eg, neurogranin, SNAP-25, synaptotagmin-1, GAP-43, and α-syn) and emerging (eg, synaptic vesicle glycoprotein 2A and neuronal pentraxins) CSF biomarkers for synapse dysfunction, while highlighting possible utilities, disease specificity, and technical challenges for their detection. SAGE Publications 2020-08-21 /pmc/articles/PMC7444114/ /pubmed/32913390 http://dx.doi.org/10.1177/1177271920950319 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Novel Biomarkers of Neurodegenerative Disorders: Updates and Challenges
Camporesi, Elena
Nilsson, Johanna
Brinkmalm, Ann
Becker, Bruno
Ashton, Nicholas J
Blennow, Kaj
Zetterberg, Henrik
Fluid Biomarkers for Synaptic Dysfunction and Loss
title Fluid Biomarkers for Synaptic Dysfunction and Loss
title_full Fluid Biomarkers for Synaptic Dysfunction and Loss
title_fullStr Fluid Biomarkers for Synaptic Dysfunction and Loss
title_full_unstemmed Fluid Biomarkers for Synaptic Dysfunction and Loss
title_short Fluid Biomarkers for Synaptic Dysfunction and Loss
title_sort fluid biomarkers for synaptic dysfunction and loss
topic Novel Biomarkers of Neurodegenerative Disorders: Updates and Challenges
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444114/
https://www.ncbi.nlm.nih.gov/pubmed/32913390
http://dx.doi.org/10.1177/1177271920950319
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