Brain-Derived Neurotrophic Factor: A Key Molecule for Memory in the Healthy and the Pathological Brain

Miranda, Magdalena; Morici, Juan Facundo; Zanoni, María Belén; Bekinschtein, Pedro

doi:10.3389/fncel.2019.00363

Cited by 956 publications

(688 citation statements)

References 433 publications

(474 reference statements)

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“…Oxidative stress-induced neuronal damage following ischemia/reperfusion (I/R) in the brain has been crucially implicated in the pathophysiology of many neurological disorders [14,15]. The neurotrophic support compromised in the aging brain also affects the survival of brain neurons [16]. In light of these phenomena, pharmacological agents that could help overcome these pathological consequences might hold therapeutic promise against the associated brain disorders.…”

Section: Discussionmentioning

confidence: 99%

Gelidium amansii Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

et al. 2020

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Oxidative stress is known to be critically implicated in the pathophysiology of several neurological disorders, including Alzheimer’s disease and ischemic stroke. The remarkable neurotrophic activity of Gelidium amansii, which has been reported consistently in a series of our previous studies, inspired us to investigate whether this popular agarophyte could protect against hypoxia/reoxygenation (H/R)-induced oxidative injury in hippocampal neurons. The primary culture of hippocampal neurons challenged with H/R suffered from a significant loss of cell survival, accompanied by apoptosis and necrosis, DNA damage, generation of reactive oxygen species (ROS), and dissipation of mitochondrial membrane potential (ΔΨm), which were successfully attenuated when the neuronal cultures were preconditioned with ethanolic extract of G. amansii (GAE). GAE also attenuated an H/R-mediated increase of BAX and caspase 3 expressions while promoting Bcl-2 expression. Moreover, the expression of N-methyl-d-acetate receptor subunit 2B (GluN2B), an extrasynaptic glutamate receptor, was significantly repressed, while synaptic GluN2A expression was preserved in GAE-treated neurons as compared to those without GAE intervention. Together, this study demonstrates that GAE attenuated H/R-induced oxidative injury in hippocampal neurons through, at least in part, a potential neuroprotective mechanism that involves inhibition of GluN2B-mediated excitotoxicity and suppression of ROS production, and suggests that this edible seaweed could be a potential source of bioactive metabolites with therapeutic significance against oxidative stress-related neurodegeneration, including ischemic stroke and neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

Gelidium amansii Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

et al. 2020

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“…Oxidative stress-induced neuronal damage following ischemia/reperfusion (I/R) in the brain has been crucially implicated in the pathophysiology of many neurological disorders [13,14]. The neurotrophic support compromised in the aging brain also affects the survival of brain neurons [15]. In light of these phenomena, pharmacological agents that could help overcome these pathological consequences might hold therapeutic promise against the associated brain disorders.…”

Section: Discussionmentioning

confidence: 99%

<i>Gelidium amansii</i> Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

Hannan¹,

Haque²,

Mohibbullah³

et al. 2020

Preprint

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Oxidative stress is known to be critically implicated in the pathophysiology of several neurological disorders, including Alzheimer’s disease and ischemic stroke. The remarkable neurotrophic activity of Gelidium amansii, has been reported consistently in a series of our previous studies, inspired us to investigate whether this popular agarophyte could protect against hypoxia/reoxygenation (H/R)-induced oxidative injury in hippocampal neurons. The primary culture of hippocampal neurons challenged with H/R suffered from a significant loss of cell survival, accompanied by apoptosis and necrosis, DNA damage, generation of reactive oxygen species (ROS), and dissipation of mitochondrial membrane potential (MMP) which were successfully attenuated when the neuronal cultures were preconditioned with GAE, an optimized ethanolic extract of G. amansii. Moreover, the expression of N-methyl-D-acetate receptor subunit 2B (GluN2B), an extrasynaptic glutamate receptor, was significantly repressed in GAE-treated neurons as compared to those without GAE intervention. Together, this study demonstrates that GAE attenuated H/R-induced oxidative injury in hippocampal neurons through, at least in part, a potential neuroprotective mechanism that involves inhibition of GluN2B-mediated excitotoxicity and suppression of ROS production, and suggest that this edible seaweed could be a potential source of bioactive metabolites having therapeutic significance against oxidative stress-related neurodegeneration, including ischemic stroke and neurodegenerative diseases.

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“…Changes in this marker have been also related to the pathophysiological mechanism of brain injury in various neurodegenerative diseases, including PD and AD (Covaceuszach et al, 2009;Kojima & Mizui, 2017). However, in these diseases, as well as in aging and psychiatric disorders, a decrease rather than an increase in circulating concentrations of this protein was observed (Miranda, Morici, Zanoni, & Bekinschtein, 2019).…”

Section: We Investigated Various Markers Of Neurodegeneration and Infmentioning

confidence: 99%

Elevated levels of BDNF and cathepsin‐das possible peripheral markers of neurodegeneration in plasma of patients with glutaric acidemia type I

Guerreiro

Jaques

Wajner

et al. 2020

Intl J of Devlp Neuroscience

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Glutaric acidemia type I (GA1) is caused by severe deficiency of glutaryl‐CoA dehydrogenase activity, resulting in an accumulation of glutaric acid and glutarylcarnitine (C5DC) in the organism. Patients affected by GA1 are asymptomatic in the neonate period but usually manifest chronically progressive neurodegeneration apart from severe encephalopathic crises associated with acute striatum necrosis. Neurological manifestations like dyskinesia, dystonia, hypotonia, muscle stiffness, and spasticity are present. Treatment is based on protein/lysine restriction and l‐carnitine supplementation. In this work, we evaluated markers of neurodegeneration and inflammation, namely BDNF (brain‐derived neurotrophic factor), NCAM (neuronal adhesion molecule), PDGF‐AA (platelet‐derived growth factor), and cathepsin‐d in plasma of six treated GA1 patients. We first found marked increases of plasma C5DC concentrations in GA1 patients, as well as increased levels of the markers BDNF and cathepsin‐d as compared to those of age‐matched healthy children. Furthermore, C5DC concentrations were highly correlated with the levels of cathepsin‐d. These results may demonstrate that brain tissue degeneration is present in GA1 patients and that there is a relationship between increased metabolites concentrations with this process. To the best of our knowledge, this is so far the first study showing altered peripheral parameters of neurodegeneration and inflammation in GA1 patients.

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Brain-Derived Neurotrophic Factor: A Key Molecule for Memory in the Healthy and the Pathological Brain

Cited by 956 publications

References 433 publications

Gelidium amansii Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

Gelidium amansii Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

<i>Gelidium amansii</i> Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

Elevated levels of BDNF and cathepsin‐das possible peripheral markers of neurodegeneration in plasma of patients with glutaric acidemia type I

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