2020
DOI: 10.1177/1177271920950319
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Fluid Biomarkers for Synaptic Dysfunction and Loss

Abstract: 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, t… Show more

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Cited by 89 publications
(112 citation statements)
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References 311 publications
(458 reference statements)
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“…GAP-43 is mainly expressed in the endoolfactory cortex, neocortex, and hippocampus, and is anchored on the cytoplasmic side of the presynaptic plasma membrane where it regulates synaptic plasticity and regenerative axonal growth and plays a critical role in neural development, axonal outgrowth, and stabilisation of synaptic function ( Holahan, 2017 ). GAP-43 was shown to promote neurite outgrowth during development and nervous system repair by inducing F-actin accumulation, stimulating morphogenic activity, and preventing growth cone retraction ( Zhang et al., 2018 ; Camporesi et al., 2020 ); changes in GAP-43 expression have been reported following nerve injury and in CNS diseases such as stroke, Alzheimer disease, epilepsy, and Parkinson disease ( Tönges et al., 2014 ; Nemes et al., 2017 ; Sandelius et al., 2018 ; Sandelius et al., 2019 ; Tible et al., 2020 ).…”
Section: Discussionmentioning
confidence: 99%
“…GAP-43 is mainly expressed in the endoolfactory cortex, neocortex, and hippocampus, and is anchored on the cytoplasmic side of the presynaptic plasma membrane where it regulates synaptic plasticity and regenerative axonal growth and plays a critical role in neural development, axonal outgrowth, and stabilisation of synaptic function ( Holahan, 2017 ). GAP-43 was shown to promote neurite outgrowth during development and nervous system repair by inducing F-actin accumulation, stimulating morphogenic activity, and preventing growth cone retraction ( Zhang et al., 2018 ; Camporesi et al., 2020 ); changes in GAP-43 expression have been reported following nerve injury and in CNS diseases such as stroke, Alzheimer disease, epilepsy, and Parkinson disease ( Tönges et al., 2014 ; Nemes et al., 2017 ; Sandelius et al., 2018 ; Sandelius et al., 2019 ; Tible et al., 2020 ).…”
Section: Discussionmentioning
confidence: 99%
“…GAP-43 is mainly expressed in the endoolfactory cortex, neocortex, and hippocampus, and is anchored on the cytoplasmic side of the presynaptic plasma membrane where it regulates synaptic plasticity and regenerative axonal growth and plays a critical role in neural development, axonal outgrowth, and stabilisation of synaptic function [26]. GAP-43 was shown to promote neurite outgrowth during development and nervous system repair by inducing F-actin accumulation, stimulating morphogenic activity, and preventing growth cone retraction [27,28]; changes in GAP-43 expression have been reported following nerve injury and in CNS diseases such as stroke, Alzheimer disease, epilepsy, and Parkinson disease [29][30][31][32][33].…”
Section: Discussionmentioning
confidence: 99%
“… 20 , 50 , 51 Among the most promising markers of synaptic injury in AD are the post-synaptic protein neurogranin (Ng), 52 , 53 and the pre-synaptic proteins synaptosome–associated protein-25 (SNAP-25) 54 , 55 and synaptotagmin-1 (Syt-1), 56 although several others have been examined. 57 The abundant expression and relative neuronal specificity of these markers allow them to reliably reflect neuronal and synaptic loss, as their CSF levels correlate with damage to neuronal and synaptic structures and the release of abundant neuronal or synaptic constituents into the extracellular compartment in the setting of neurodegeneration.…”
Section: Biomarkers Of Pathological Substrates Of Admentioning
confidence: 99%