MEG Resting State Functional Connectivity and Network Topology in Dyslexia Related Genotype
Poster Sep 12, 2017
D. Brkić1, J.B. Talcott1 , A. Hillebrand2 , S. Paracchini3& C. Witton1
1Aston Brain Centre, School of Life & Health Sciences, Aston University, Birmingham, UK 2Department of Clinical Neurophysiology and MEG Center, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands 3 University of St Andrews, St Andrews, UK
One dyslexia candidate gene-PCSK6- has recently been proposed to provide a molecular link between brain asymmetry, handedness and reading impairment.
Studying resting state neuro-functional interactions and their network distribution may tell us more about differences in typical and a typical brain development.
Combining neuroimaging techniques and genetic information may provide a powerful means to investigate the biological basis of reading delay.
Here, we used a MEG source-space method and Minimum Spanning Tree sub-graph to investigate resting state functional connectivity and topology in children with diagnoses of dyslexia with and without PCSK6 genetic risk.
1.Shore et al. (2016) Human Molecular genetics
2.Hillebrand et al. (2012) Neuroimage, 59 (4)
3.ASEBA questionnaires (www.aseba.org)
4.Stam et al. (2014), Int. Journal of Psychophysiology
5.Nichols & Holmes (2001), Human Brain Mapping
6.Zhou et al. (2015) Frontiers, volume 9
This poster was presented at American Association of Clinical Chemistry
Spinal muscular atrophy (SMA) is an inheritable cause of infant mortality that is characterized by the loss of lower motor neurons and skeletal muscle atrophy. The degeneration of motor neurons is caused by insufficient levels of survival motor neuron (SMN) protein, which is encoded by two nearly identical genes SMN1 and SMN2. Most cases of SMA harbour homozygous deletions of the SMN1 gene and retain at least one copy of SMN2.READ MORE