The aim of this investigation is to compare EEG power-density spectra between dyslexic and normal children. The children have been selected on the basis of specific reading and writing tasks; those with severe organic diseases and mental disorders were excluded. Groups aged 8, 9 and 10 years have been compared. In the 8-year-old group the power in the alpha band is higher in normals, in the 9-year-old group there was a higher power of the mu rhythm in normals and in the 10-year-old group the power in the temporal theta band is lower in normals. A possible relation between these findings and psychomotor development is discussed.
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http://dx.doi.org/10.1007/BF00314642 | DOI Listing |
Ann Dyslexia
July 2023
Department of General Psychology, University of Padova, Via Venezia, 8, 35133, Padua, Italy.
Dyslexia is one of the most studied learning disorders. Despite this, its biological basis and main causes are still not fully understood. Electroencephalography (EEG) could be a powerful tool in identifying the underlying mechanisms, but knowledge of the EEG correlates of developmental dyslexia (DD) remains elusive.
View Article and Find Full Text PDFBrain Sci
January 2021
Deptment Physiology, Anatomy & Genetics, University of Oxford, Oxford OX1 3PT, UK.
(1) Background-the magnocellular hypothesis proposes that impaired development of the visual timing systems in the brain that are mediated by magnocellular (M-) neurons is a major cause of dyslexia. Their function can now be assessed quite easily by analysing averaged visually evoked event-related potentials (VERPs) in the electroencephalogram (EEG). Such analysis might provide a useful, objective biomarker for diagnosing developmental dyslexia.
View Article and Find Full Text PDFHum Mutat
January 2020
Department of translational medicine and Neurogenetics, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Calcium (Ca ) acts as a ubiquitous second messenger, and normal cell and tissue physiology strictly depends on the precise regulation of Ca entry, storage, and release. Store-operated Ca entry (SOCE) is a major mechanism controlling extracellular Ca entry, and mainly relies on the accurate interplay between the Ca sensor STIM1 and the Ca channel ORAI1. Mutations in STIM1 or ORAI1 result in abnormal Ca homeostasis and are associated with severe human disorders.
View Article and Find Full Text PDFHum Mol Genet
May 2019
Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Inserm, CNRS, Université de Strasbourg, Illkirch, France.
Strict regulation of Ca2+ homeostasis is essential for normal cellular physiology. Store-operated Ca2+ entry (SOCE) is a major mechanism controlling basal Ca2+ levels and intracellular Ca2+ store refilling, and abnormal SOCE severely impacts on human health. Overactive SOCE results in excessive extracellular Ca2+ entry due to dominant STIM1 or ORAI1 mutations and has been associated with tubular aggregate myopathy (TAM) and Stormorken syndrome (STRMK).
View Article and Find Full Text PDFMed Sci (Paris)
November 2018
Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France - Centre National de la Recherche Scientifique (CNRS), UMR7104, Illkirch, France - Institut National de la Santé et de la Recherche Médicale (INSERM), U1258, Illkirch, France - Université de Strasbourg, Illkirch, France.
Calcium (Ca) is an essential regulator for a large number of cellular functions in various tissues and organs, and small disturbances of Ca homeostasis can severely compromise normal physiology. Intracellular Ca balance is mainly controlled by the reticular Ca sensor STIM1 and the plasma membrane Ca channel ORAI1 through a mechanism known as store-operated Ca entry (SOCE). Gain-of-function mutations in STIM1 or ORAI1 cause excessive extracellular Ca influx, resulting in tubular aggregate myopathy (TAM) and Stormorken syndrome (STRMK).
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