Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome / L. E. ETHRIDGE in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 38p. Titre : Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome Type de document : texte imprimé Auteurs : L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur Article en page(s) : 38p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : [This corrects the article DOI: 10.1186/s13229-017-0140-1.]. En ligne : http://dx.doi.org/10.1186/s13229-017-0150-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330 [article] Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome [texte imprimé] / L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur . - 38p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 38p. Index. décimale : PER Périodiques Résumé : [This corrects the article DOI: 10.1186/s13229-017-0140-1.]. En ligne : http://dx.doi.org/10.1186/s13229-017-0150-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330

Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome / L. E. ETHRIDGE in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 22p. Titre : Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome Type de document : texte imprimé Auteurs : L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur Article en page(s) : 22p. Langues : Anglais (eng) Mots-clés : Chirp  Eeg  Fragile X syndrome  Gamma  Sensory Index. décimale : PER Périodiques Résumé : BACKGROUND: Studies in the fmr1 KO mouse demonstrate hyper-excitability and increased high-frequency neuronal activity in sensory cortex. These abnormalities may contribute to prominent and distressing sensory hypersensitivities in patients with fragile X syndrome (FXS). The current study investigated functional properties of auditory cortex using a sensory entrainment task in FXS. METHODS: EEG recordings were obtained from 17 adolescents and adults with FXS and 17 age- and sex-matched healthy controls. Participants heard an auditory chirp stimulus generated using a 1000-Hz tone that was amplitude modulated by a sinusoid linearly increasing in frequency from 0-100 Hz over 2 s. RESULTS: Single trial time-frequency analyses revealed decreased gamma band phase-locking to the chirp stimulus in FXS, which was strongly coupled with broadband increases in gamma power. Abnormalities in gamma phase-locking and power were also associated with theta-gamma amplitude-amplitude coupling during the pre-stimulus period and with parent reports of heightened sensory sensitivities and social communication deficits. CONCLUSIONS: This represents the first demonstration of neural entrainment alterations in FXS patients and suggests that fast-spiking interneurons regulating synchronous high-frequency neural activity have reduced functionality. This reduced ability to synchronize high-frequency neural activity was related to the total power of background gamma band activity. These observations extend findings from fmr1 KO models of FXS, characterize a core pathophysiological aspect of FXS, and may provide a translational biomarker strategy for evaluating promising therapeutics. En ligne : http://dx.doi.org/10.1186/s13229-017-0140-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330 [article] Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome [texte imprimé] / L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur . - 22p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 22p. Mots-clés : Chirp  Eeg  Fragile X syndrome  Gamma  Sensory Index. décimale : PER Périodiques Résumé : BACKGROUND: Studies in the fmr1 KO mouse demonstrate hyper-excitability and increased high-frequency neuronal activity in sensory cortex. These abnormalities may contribute to prominent and distressing sensory hypersensitivities in patients with fragile X syndrome (FXS). The current study investigated functional properties of auditory cortex using a sensory entrainment task in FXS. METHODS: EEG recordings were obtained from 17 adolescents and adults with FXS and 17 age- and sex-matched healthy controls. Participants heard an auditory chirp stimulus generated using a 1000-Hz tone that was amplitude modulated by a sinusoid linearly increasing in frequency from 0-100 Hz over 2 s. RESULTS: Single trial time-frequency analyses revealed decreased gamma band phase-locking to the chirp stimulus in FXS, which was strongly coupled with broadband increases in gamma power. Abnormalities in gamma phase-locking and power were also associated with theta-gamma amplitude-amplitude coupling during the pre-stimulus period and with parent reports of heightened sensory sensitivities and social communication deficits. CONCLUSIONS: This represents the first demonstration of neural entrainment alterations in FXS patients and suggests that fast-spiking interneurons regulating synchronous high-frequency neural activity have reduced functionality. This reduced ability to synchronize high-frequency neural activity was related to the total power of background gamma band activity. These observations extend findings from fmr1 KO models of FXS, characterize a core pathophysiological aspect of FXS, and may provide a translational biomarker strategy for evaluating promising therapeutics. En ligne : http://dx.doi.org/10.1186/s13229-017-0140-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330

A resting EEG study of neocortical hyperexcitability and altered functional connectivity in fragile X syndrome / J. WANG in Journal of Neurodevelopmental Disorders, 9-1 (December 2017)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 9-1 (December 2017) . - p.11 Titre : A resting EEG study of neocortical hyperexcitability and altered functional connectivity in fragile X syndrome Type de document : texte imprimé Auteurs : J. WANG, Auteur ; L. E. ETHRIDGE, Auteur ; M. W. MOSCONI, Auteur ; S. P. WHITE, Auteur ; D. K. BINDER, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur Article en page(s) : p.11 Langues : Anglais (eng) Mots-clés : Cross-frequency coupling  Eeg  Fragile X syndrome  Gamma  Hyperexcitability  Top-down modulation Index. décimale : PER Périodiques Résumé : BACKGROUND: Cortical hyperexcitability due to abnormal fast-spiking inhibitory interneuron function has been documented in fmr1 KO mice, a mouse model of the fragile X syndrome which is the most common single gene cause of autism and intellectual disability. METHODS: We collected resting state dense-array electroencephalography data from 21 fragile X syndrome (FXS) patients and 21 age-matched healthy participants. RESULTS: FXS patients exhibited greater gamma frequency band power, which was correlated with social and sensory processing difficulties. Second, FXS patients showed increased spatial spreading of phase-synchronized high frequency neural activity in the gamma band. Third, we observed increased negative theta-to-gamma but decreased alpha-to-gamma band amplitude coupling, and the level of increased theta power was inversely related to the level of resting gamma power in FXS. CONCLUSIONS: Increased theta band power and coupling from frontal sources may represent a mechanism providing compensatory inhibition of high-frequency gamma band activity, potentially contributing to the widely varying level of neurophysiological and behavioral abnormalities and treatment response seen in full-mutation FXS patients. These findings extend preclinical observations and provide new mechanistic insights into brain alterations and their variability across FXS patients. Electrophysiological measures may provide useful translational biomarkers for advancing drug development and individualizing treatments for neurodevelopmental disorders with associated neuronal hyperexcitability. En ligne : http://dx.doi.org/10.1186/s11689-017-9191-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=350 [article] A resting EEG study of neocortical hyperexcitability and altered functional connectivity in fragile X syndrome [texte imprimé] / J. WANG, Auteur ; L. E. ETHRIDGE, Auteur ; M. W. MOSCONI, Auteur ; S. P. WHITE, Auteur ; D. K. BINDER, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur . - p.11. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 9-1 (December 2017) . - p.11 Mots-clés : Cross-frequency coupling  Eeg  Fragile X syndrome  Gamma  Hyperexcitability  Top-down modulation Index. décimale : PER Périodiques Résumé : BACKGROUND: Cortical hyperexcitability due to abnormal fast-spiking inhibitory interneuron function has been documented in fmr1 KO mice, a mouse model of the fragile X syndrome which is the most common single gene cause of autism and intellectual disability. METHODS: We collected resting state dense-array electroencephalography data from 21 fragile X syndrome (FXS) patients and 21 age-matched healthy participants. RESULTS: FXS patients exhibited greater gamma frequency band power, which was correlated with social and sensory processing difficulties. Second, FXS patients showed increased spatial spreading of phase-synchronized high frequency neural activity in the gamma band. Third, we observed increased negative theta-to-gamma but decreased alpha-to-gamma band amplitude coupling, and the level of increased theta power was inversely related to the level of resting gamma power in FXS. CONCLUSIONS: Increased theta band power and coupling from frontal sources may represent a mechanism providing compensatory inhibition of high-frequency gamma band activity, potentially contributing to the widely varying level of neurophysiological and behavioral abnormalities and treatment response seen in full-mutation FXS patients. These findings extend preclinical observations and provide new mechanistic insights into brain alterations and their variability across FXS patients. Electrophysiological measures may provide useful translational biomarkers for advancing drug development and individualizing treatments for neurodevelopmental disorders with associated neuronal hyperexcitability. En ligne : http://dx.doi.org/10.1186/s11689-017-9191-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=350

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