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    Volume 1, Issue 1
    Research Article
    Sally Ann Wakeford*, Neal Hinvest, Howard Ring, and Mark Brosnan
    Introduction: There is a high prevalence of autism spectrum disorders (ASD) in epilepsy. ASDs are characterised by a deficit of social interaction, social communication, and restricted, repetitive behaviours. Previous research by Wakeford and colleagues reported higher autistic characteristics in adults with epilepsy who had no diagnosis of an ASD. A subsequent study found that while sameness behaviours were unimpaired, adults with epilepsy reported poor reciprocal social interaction, revealing difficulties in social interactions, a characteristic of autism. The Somatic Marker Hypothesis proposes that neural systems supporting decision-making overlap with components of a neural circuitry which guide social behaviour. Impaired decision-making abilities under ambiguity may indicate compromised somatic marker formation, crucial for social cognition. The present paper aims to investigate ambiguous decision making, and whether the Somatic Marker Hypothesis is a valid explanatory model for these cognitive features of epilepsy.
    Method: Our experiment investigated ambiguous decision-making ability measured by the IOWA Gambling Task in adults with epilepsy.
    Results: Adults with epilepsy demonstrated impaired decision-making abilities compared to adults without epilepsy, likely to result from compromised somatic marker formation.
    Conclusion: The somatic marker hypothesis contributes a neurobiological plausible account of the underlying impairment of decision-making in epilepsy. Given that intact somatic marker formation is important for social cognitive function, this model provides a mechanism for linking somatic function to decision-making and social behaviours in epilepsy, suggesting that disrupted neurobiological factors may be implicated in both.
    Domingo Garcia-Villamisar* and John Dattilo
    This study examined effects of the Interactive Emotional Enhancement Training (IEET) computer-based program on basic emotion recognition and social competence in a group of adults with autism spectrum disorders (ASD) (n = 42) with a mean age 32.98 +/- 6.19 years. A preliminary pre-test, post-test randomized control group experimental design was used to measure effects of a 36-week IEET program consisting of 410 activities. The IEET program uses instructional computer-based activities delivered during 144 1-hour sessions (5 hours/week). Results demonstrated that participants who received the intervention improved their emotion recognition skills, as well as their social competence. The current results suggest that the IEET program may represent an efficient and cost-effective strategy for teaching emotion recognition to adults with ASD.
    Perspective
    Kenneth C. Sassower*
    An international conference on autism entitled “Autism: Challenges and Solutions,” took place from April 28 through April 30, 2016 in downtown Moscow, and was described by conference organizers as being one of the most well-attended international conferences on autism in all of Europe. The international conference was attended by both healthcare professionals and interested family members alike.
    Short Communication
    Megumi Andoh, Ryuta Koyama* and Yuji Ikegaya
    Epilepsy is a common complication of autism spectrum disorders (ASDs). Clinical studies have estimated that the rate of epilepsy in ASD patients is approximately 30%. To examine the cellular and molecular links between ASD and epilepsy, proper animal models are necessary. Here, we investigated whether seizure severity is increased in the poly (I:C) model, a mouse model of maternal immune activation (MIA). MIA is a risk factor for ASD in offspring, and ASD-like features, including deficits in social interactions, have been observed in the mouse poly (I:C) model. The poly (I:C) mice were administered kainic acid (KA) at postnatal day 15 (P15) and P30 to induce limbic seizures. We found that there was no difference in seizure severity between poly (I:C) and control mice at P15 and 30. Further, immunohistochemical analysis at P15 revealed that the density of excitatory and inhibitory synapses was largely unchanged in the hippocampus of poly (I:C) mice, except for an increase in inhibitory synapses in CA1. Thus, our results indicate that KA-induced seizure severity is not increased in poly (I:C) mice and that the structural synapse E/I balance in the hippocampus is not largely impaired.
    Review Article
    Ning Cheng* and Jong M. Rho
    Autism spectrum disorder (hereafter referred to as “ASD”) has broad and heterogeneous clinical manifestations and has been associated with a plethora of possible etiological factors. As such, it has been a challenge to investigate underlying neurobiological mechanisms and to develop effective treatments. Recent studies have increasingly implicated mitochondrial dysfunction as a cause of ASD. Mitochondria are integrally involved in many cellular functions and hence susceptible to many pathophysiological insults. This could explain in part how a wide range of genetic and environmental factors can lead to the consistent behavioural phenotype observed in autistic individuals. Derangements in mitochondrial structure and function – while not unique to diseases such as ASD – nevertheless provide a scientific rationale for experimental therapeutics. Meanwhile, the ketogenic diet (KD), used for nearly a century to treat medically intractable epilepsy, has been shown to enhance mitochondrial function through a multiplicity of mechanisms. This review provides the clinical and basic laboratory evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD, as well as emerging co-morbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying novel mechanistic targets are also discussed.
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