@article{Hakim201716,
title = {Neuron-specific splicing},
author = {N H A Hakim and B Y Majlis and H Suzuki and T Tsukahara},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85014435502&doi=10.5582%2fbst.2016.01169&partnerID=40&md5=8a5044dbf3b905fc2553520a048bcd59},
doi = {10.5582/bst.2016.01169},
issn = {18817815},
year = {2017},
date = {2017-01-01},
journal = {BioScience Trends},
volume = {11},
number = {1},
pages = {16-22},
publisher = {International Advancement Center for Medicine and Health Research Co., Ltd.},
abstract = {During pre-mRNA splicing events, introns are removed from the pre-mRNA, and the remaining exons are connected together to form a single continuous molecule. Alternative splicing is a common mechanism for the regulation of gene expression in eukaryotes. More than 90% of human genes are known to undergo alternative splicing. The most common type of alternative splicing is exon skipping, which is also known as cassette exon. Other known alternative splicing events include alternative 5' splice sites, alternative 3' splice sites, intron retention, and mutually exclusive exons. Alternative splicing events are controlled by regulatory proteins responsible for both positive and negative regulation. In this review, we focus on neuronal splicing regulators and discuss several notable regulators in depth. In addition, we have also included an example of splicing regulation mediated by the RBFox protein family. Lastly, as previous studies have shown that a number of splicing factors are associated with neuronal diseases such as Alzheime's disease (AD) and Autism spectrum disorder (ASD), here we consider their importance in neuronal diseases wherein the underlying mechanisms have yet to be elucidated.},
note = {cited By 0},
keywords = {Alternative RNA Splicing, Alternative Splicing, Animals, Antibody Specificity, Biological, Biological Model, Diseases, Genetics, Human, Metabolism, Models, Nerve Cell, Neurons, Organ Specificity, RNA Splicing},
pubstate = {published},
tppubtype = {article}
}

@article{Gravier201649,
title = {Neural network modelling of the influence of channelopathies on reflex visual attention},
author = {A Gravier and C Quek and W Duch and A Wahab and J Gravier-Rymaszewska},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84955207541&doi=10.1007%2fs11571-015-9365-x&partnerID=40&md5=52f56b25f1d05a2d8eb0249e67e49f45},
doi = {10.1007/s11571-015-9365-x},
issn = {18714080},
year = {2016},
date = {2016-01-01},
journal = {Cognitive Neurodynamics},
volume = {10},
number = {1},
pages = {49-72},
publisher = {Springer Netherlands},
abstract = {This paper introduces a model of Emergent Visual Attention in presence of calcium channelopathy (EVAC). By modelling channelopathy, EVAC constitutes an effort towards identifying the possible causes of autism. The network structure embodies the dual pathways model of cortical processing of visual input, with reflex attention as an emergent property of neural interactions. EVAC extends existing work by introducing attention shift in a larger-scale network and applying a phenomenological model of channelopathy. In presence of a distractor, the channelopathic network’s rate of failure to shift attention is lower than the control network’s, but overall, the control network exhibits a lower classification error rate. The simulation results also show differences in task-relative reaction times between control and channelopathic networks. The attention shift timings inferred from the model are consistent with studies of attention shift in autistic children. © 2015, Springer Science+Business Media Dordrecht.},
note = {cited By 8},
keywords = {Article, Artificial Neural Network, Attention, Autism, Calcium Channelopathy, Cell Structure, Cognition, Connectome, Electric Activity, Learning, Mathematical Analysis, Mathematical Model, Nerve Cell, Simulation, Visual Reflex},
pubstate = {published},
tppubtype = {article}
}

@article{Assaf2013321,
title = {Mentalizing and motivation neural function during social interactions in autism spectrum disorders},
author = {M Assaf and C J Hyatt and C G Wong and M R Johnson and R T Schultz and T Hendler and G D Pearlson},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84885394367&doi=10.1016%2fj.nicl.2013.09.005&partnerID=40&md5=b63630c997b658167792266e40e855b6},
doi = {10.1016/j.nicl.2013.09.005},
issn = {22131582},
year = {2013},
date = {2013-01-01},
journal = {NeuroImage: Clinical},
volume = {3},
pages = {321-331},
abstract = {Autism Spectrum Disorders (ASDs) are characterized by core deficits in social functions. Two theories have been suggested to explain these deficits: mind-blindness theory posits impaired mentalizing processes (i.e. decreased ability for establishing a representation of others' state of mind), while social motivation theory proposes that diminished reward value for social information leads to reduced social attention, social interactions, and social learning. Mentalizing and motivation are integral to typical social interactions, and neuroimaging evidence points to independent brain networks that support these processes in healthy individuals. However, the simultaneous function of these networks has not been explored in individuals with ASDs. We used a social, interactive fMRI task, the Domino game, to explore mentalizing- and motivation-related brain activation during a well-defined interval where participants respond to rewards or punishments (i.e. motivation) and concurrently process information about their opponent's potential next actions (i.e. mentalizing). Thirteen individuals with high-functioning ASDs, ages 12-24, and 14 healthy controls played fMRI Domino games against a computer-opponent and separately, what they were led to believe was a human-opponent. Results showed that while individuals with ASDs understood the game rules and played similarly to controls, they showed diminished neural activity during the human-opponent runs only (i.e. in a social context) in bilateral middle temporal gyrus (MTG) during mentalizing and right Nucleus Accumbens (NAcc) during reward-related motivation (Pcluster < 0.05 FWE). Importantly, deficits were not observed in these areas when playing against a computer-opponent or in areas related to motor and visual processes. These results demonstrate that while MTG and NAcc, which are critical structures in the mentalizing and motivation networks, respectively, activate normally in a non-social context, they fail to respond in an otherwise identical social context in ASD compared to controls. We discuss implications to both the mind-blindness and social motivation theories of ASD and the importance of social context in research and treatment protocols. © 2013 The Authors.},
note = {cited By 28},
keywords = {Adolescent, Adult, Article, Autism, Brain Function, Children, Computer, Controlled Study, Female, Functional Magnetic Resonance Imaging, Games, Groups by Age, Human, Major Clinical Study, Male, Mental Capacity, Middle Temporal Gyrus, Motivation, Motor Performance, Nerve Cell, Nerve Function, Nucleus Accumbens, Priority Journal, Punishment, Reward, School Child, Social Cognition, Social Environment, Social Interactions, Task Performance, Theory of Mind, Vision},
pubstate = {published},
tppubtype = {article}
}