2019
DOI: 10.1080/17512433.2019.1612744
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Play in advance against neurodegeneration: exploring enteric glial cells in gut-brain axis during neurodegenerative diseases

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Cited by 25 publications
(26 citation statements)
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“…In this way, the suggestion that PD could onset in the gut emerges from the identification of activated EGCs, local inflammation, impaired IEB, aggregation of α-synuclein in neurons, and GI disorders in a window prior to the appearance of classic motor deficits. Recently, Seguella et al suggest that EGCs could be the "missing link" that connects the ENS to the CNS [139]. The authors called attention to enteric glial cell-mediated inflammatory response, which could reach the CNS by the gut-brain axis and lead to neuronal cell death and disruption of synaptic interactions [139,140].…”
Section: Parkinson's Diseasementioning
confidence: 99%
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“…In this way, the suggestion that PD could onset in the gut emerges from the identification of activated EGCs, local inflammation, impaired IEB, aggregation of α-synuclein in neurons, and GI disorders in a window prior to the appearance of classic motor deficits. Recently, Seguella et al suggest that EGCs could be the "missing link" that connects the ENS to the CNS [139]. The authors called attention to enteric glial cell-mediated inflammatory response, which could reach the CNS by the gut-brain axis and lead to neuronal cell death and disruption of synaptic interactions [139,140].…”
Section: Parkinson's Diseasementioning
confidence: 99%
“…Recently, Seguella et al suggest that EGCs could be the "missing link" that connects the ENS to the CNS [139]. The authors called attention to enteric glial cell-mediated inflammatory response, which could reach the CNS by the gut-brain axis and lead to neuronal cell death and disruption of synaptic interactions [139,140]. Thus, EGCs would function as an "entrance door" to noxious stimuli from the intestinal lumen that could damage the CNS.…”
Section: Parkinson's Diseasementioning
confidence: 99%
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“…The neuroglial junctions, calcium signals and neurotransmitter receptors on EGCs, allows for communication with the ENS (Sharkey, 2015;Ochoa-Cortes et al, 2016). Dysfunction of each of these has been implicated as a possible source for gut mobility issues and possibly even neurodegeneration (Coelho-Aguiar et al, 2015;Ochoa-Cortes et al, 2016;Sequella, Capuana, Sarnelli, & Esposito, 2019). Furthermore, EGCs have been proposed to serve as a reservoir for prions and aberrant alpha-synuclein; with several studies showing that these molecules are readily able to travel from the gut to the brain and vice versa (Albanese et al, 2008;Sharkey, 2015).…”
Section: Decreased Cell Mobilization With Glial Activationmentioning
confidence: 99%