Selective Upregulation of Brain-Derived Neurotrophic Factor (BDNF) Transcripts and BDNF Direct Induction of Activity Independent <i>N</i>-Methyl-D-Aspartate Currents in Temporal Lobe Epilepsy Patients with Hippocampal Sclerosis

Wang, FJ; Li, CM; Hou, XH; Wang, R; Zhang, LM

doi:10.1177/147323001103900422

Cited by 16 publications

(11 citation statements)

References 46 publications

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“…In surgically-resected hippocampi from patients with epilepsy, increased levels of BDNF mRNA and protein have been noted, indicating that epileptic activity may up-regulate protein levels via BDNF gene expression [52, 53]. In patients with chronic epilepsy, however, decreased BDNF secretion has been associated with a decompensated hippocampus [54].…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent genotype effects of BDNF Val66Met polymorphism on default mode network in early stage Alzheimer's disease

et al. 2016

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In humans, brain-derived neurotrophic factor (BDNF) has been shown to play a pivotal role in neurocognition, and its gene contains a functional polymorphism (Val66Met) that may explain individual differences in brain volume and memory-related activity.In this study, we enrolled 186 Alzheimer's disease (AD) patients who underwent 3D T1 magnetic resonance imaging, and explored the gray matter (GM) structural covariance networks (SCN). The patients were divided into three groups according to their genotype: Met/Met (n = 45), Val/Met (n = 86) and Val/Val (n = 55). Seed-based analysis was performed focusing on four SCN networks. Neurobehavioral scores served as the major outcome factor.Only peak cluster volumes of default mode medial temporal lobe network showed significant genotype interactions, of which the interconnected peak clusters showed dose-dependent genotype effects. There were also significant correlations between the cognitive test scores and interconnected-cluster volumes, especially in the orbitofrontal cortex.These findings support the hypothesis that BDNF rs6265 polymorphisms modulate entorhinal cortex-interconnected clusters and the valine allele was associated with stronger structural covariance patterns that determined the cognitive outcomes.

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Section: Discussionmentioning

confidence: 99%

Dose-dependent genotype effects of BDNF Val66Met polymorphism on default mode network in early stage Alzheimer's disease

et al. 2016

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“…The observations here cannot represent the ictal pathogenesis in TLE. In surgically-resected hippocampus, increase levels of BDNF mRNA and protein was found, indicating epileptic activity may up-regulate the protein level via BDNF gene expression [32,45]. Finally, there were other factors that can interfere with the serum levels of BDNF that included the oxidative stress, blood brain barrier damage and deregulated neuroinflammation [25,46,47] all coexisted in TLE.…”

Section: Relationships With Aeds and Possible Limitationsmentioning

confidence: 97%

“…The positive correlations between cognitive performance and BDNF levels in our study validated the protective role of BDNF in TLE. In literature reviews, hippocampus network activity stimulates transcription of the Bdnf gene and translation of Bdnf mRNA, while exogenous BDNF injected into the murine hippocampus was reported to increase proliferation [30][31][32]. There was a significant compensatory increase in BDNF mRNA in TLE patients with hippocampus sclerosis, compared with those without [32].…”

Section: Serum Bdnf Levels Are Predictive Of Cognitive Dysfunction Anmentioning

confidence: 98%

“…In literature reviews, hippocampus network activity stimulates transcription of the Bdnf gene and translation of Bdnf mRNA, while exogenous BDNF injected into the murine hippocampus was reported to increase proliferation [30][31][32]. There was a significant compensatory increase in BDNF mRNA in TLE patients with hippocampus sclerosis, compared with those without [32]. As serum BDNF levels were related to short-and long-delay verbal memory, visual memory, speech and language ability and executive functions in this study, we suggested the measure of BDNF level may extend the prognostic repertoire in relating cognitive severities in TLE patients.…”

Section: Serum Bdnf Levels Are Predictive Of Cognitive Dysfunction Anmentioning

confidence: 99%

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Serum Brain-derived neurotrophic factor level and Depressive severity in patients with Chronic Temporal lobe Epilepsy: A Case-control study

Chen¹,

Chen²,

Chuang³

et al. 2017

Neuropsychiatry

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Most cases of temporal lobe epilepsy (TLE) had epileptic foci originating from the hippocampal networks. As Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin growth factor and mainly expressed in the hippocampus, it is not known the circulating level of BDNF may correlate with cognitive performance and depression severities in patients with chronic TLE. Forty-eight patients with TLE and 48 age-and gender-matched controls were enrolled for standardized cognitive tests, geriatric depression scale (GDS) and serum BDNF measurement. The study results showed significantly lower BDNF levels in the TLE patients compared with the controls, and the significance was found in the age ranges of 30 to 65 yearold. There was no gender effect of BDNF whether in the patients or in controls. In the patients, the BDNF levels were related to the antiepileptic drug (AED) numbers (σ=-0.287, p =0.048), GDS scores (σ=-0.306, p=0.044) and all cognitive test scores (p<0.05). None of the test scores showed significance in the controls. Using regression model, independent role of BDNF level on predicting verbal memory score and visual memory was found in the patients. Our study suggested that serum BDNF levels were of diagnostic repertoire in reflecting poor cognitive functions, higher depressive severity and greater numbers of AEDs in TLE patients.

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“…In fact, epileptogenesis has been shown to be promoted by an increase in BDNF and BDNF‐mediated activation of the TrkB in the hippocampus in mice after intrahippocampal injections of kainic acid (Heinrich et al., 2011). Studies in patients with drug‐resistant TLE with hippocampal sclerosis have found an increase in BDNF mRNA expression in the hippocampus compared with those without hippocampal sclerosis (Wang et al., 2011). BDNF has been reported to regulate synaptic transmission by a variety of mechanisms including increasing NMDA currents in human patients with TLE and hippocampal sclerosis and animal hippocampal slices and attenuating inhibition on GABAergic postsynaptic cells by down‐regulating chloride transport (Wang et al., 2011).…”

Section: Neuropeptide Modulators Of Synaptic Neurotransmissionmentioning

confidence: 99%

Regulators of synaptic transmission: Roles in the pathogenesis and treatment of epilepsy

2012

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SUMMARYSynaptic transmission is the communication between a presynaptic and a postsynaptic neuron, and the subsequent processing of the signal. These processes are complex and highly regulated, reflecting their importance in normal brain functioning and homeostasis. Sustaining synaptic transmission depends on the continuing cycle of synaptic vesicle formation, release, and endocytosis, which requires proteins such as dynamin, syndapin, synapsin, and synaptic vesicle protein 2A. Synaptic transmission is regulated by diverse mechanisms, including presynaptic modulators of synaptic vesicle formation and release, postsynaptic receptors and signaling, and modulators of neurotransmission.Neurotransmitters released presynaptically can bind to their postsynaptic receptors, the inhibitory c-aminobutyric acid (GABA)ergic receptors or the excitatory glutamate receptors. Once released, glutamate activates a variety of postsynaptic receptors including a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl-D-aspartate (NMDA), kainate, and metabotropic receptors. The activation of the receptors triggers downstream signaling cascades generating a vast array of effects, which can be modulated by a numerous auxiliary regulatory subunits. Moreover, different neuropeptides such as neuropeptide Y, brain-derived neurotrophic factor (BDNF), somatostatin, ghrelin, and galanin, act as regulators of diverse synaptic functions and along with the classic neurotransmitters. Abnormalities in the regulation of synaptic transmission play a critical role in the pathogenesis of numerous brain diseases, including epilepsy. This review focuses on the different mechanisms involved in the regulation of synaptic transmission, which may play a role in the pathogenesis of epilepsy: the presynaptic modulators of synaptic vesicle formation and release, postsynaptic receptors, and modulators of neurotransmission, including the mechanism by which drugs can modulate the frequency and severity of epileptic seizures.

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Selective Upregulation of Brain-Derived Neurotrophic Factor (BDNF) Transcripts and BDNF Direct Induction of Activity Independent N-Methyl-D-Aspartate Currents in Temporal Lobe Epilepsy Patients with Hippocampal Sclerosis

Cited by 16 publications

References 46 publications

Dose-dependent genotype effects of BDNF Val66Met polymorphism on default mode network in early stage Alzheimer's disease

Dose-dependent genotype effects of BDNF Val66Met polymorphism on default mode network in early stage Alzheimer's disease

Serum Brain-derived neurotrophic factor level and Depressive severity in patients with Chronic Temporal lobe Epilepsy: A Case-control study

Regulators of synaptic transmission: Roles in the pathogenesis and treatment of epilepsy

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