1. Cornew L, Roberts TP, Blaskey L, Edgar JC. {{Resting-State Oscillatory Activity in Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2011 Dec 30.
Neural oscillatory anomalies in autism spectrum disorders (ASD) suggest an excitatory/inhibitory imbalance; however, the nature and clinical relevance of these anomalies are unclear. Whole-cortex magnetoencephalography data were collected while 50 children (27 with ASD, 23 controls) underwent an eyes-closed resting-state exam. A Fast Fourier Transform was applied and oscillatory activity examined from 1 to 120 Hz at 15 regional sources. Associations between oscillatory anomalies and symptom severity were probed. Children with ASD exhibited regionally specific elevations in delta (1-4 Hz), theta (4-8 Hz), alpha (8-12 Hz), and high frequency (20-120 Hz) power, supporting an imbalance of neural excitation/inhibition as a neurobiological feature of ASD. Increased temporal and parietal alpha power was associated with greater symptom severity and thus is of particular interest.
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2. Hampson DR, Gholizadeh S, Pacey LK. {{Pathways to Drug Development for Autism Spectrum Disorders}}. {Clin Pharmacol Ther}. 2011 Dec 28.
Autism spectrum disorders (ASDs) are neurodevelopmental disorders whose prevalence has risen over the past two decades. Current drug treatments for ASDs and the related disorders-fragile X syndrome (FXS) and Rett syndrome-target specific symptoms but do not address the basic underlying etiologies. However, based partly on an improved understanding of the neurochemical underpinnings of FXS, pharmacotherapy for this syndrome has progressed to the point of clinical trials of several novel drug treatments. By contrast, our overall understanding of the neuropathophysiology of ASDs is still rudimentary. There is hope in the field that knowledge and experience gained in the study of fragile X and Rett syndromes may be applicable to the larger autism patient population. In this review, we discuss how recent advances in our understanding of the biochemistry and neuropathology of these disorders could lead to new more effective treatments for ASDs.
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3. Heulens I, Braat S, Kooy RF. {{Metabonomics adds a new dimension to fragile x syndrome}}. {Genome Med}. 2011 Dec 28;3(12):80.
ABSTRACT: Fragile x syndrome is the most common cause of inherited intellectual disability, but the underlying pathophysiology is complex and effective treatments are lacking. In a recent study of fragile x mental retardation 1 (Fmr1) knockout mice, the metabolic profile of the fragile x brain was determined using proton high-resolution magic angle spinning nuclear magnetic resonance spectroscopy. This analysis revealed deficiencies in four metabolic categories: neurotransmission, osmoregulation, energy metabolism and oxidative stress response. Abnormalities in the metabolic phenotype were linked to the fragile x mental retardation protein using an integrated metabolome and interactome mapping approach, allowing a global picture of the disorder to emerge.
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4. Hong S, Ke X, Tang T, Hang Y, Chu K, Huang H, et al. {{Detecting abnormalities of corpus callosum connectivity in autism using magnetic resonance imaging and diffusion tensor tractography}}. {Psychiatry Res}. 2011 Dec 30;194(3):333-9.
The corpus callosum (CC) has emerged as one of the primary targets of autism research. To detect aberrant CC interhemispheric connectivity in autism, we performed T1-weighted magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI)-based tractography in 18 children with high functioning autism (HFA) and 16 well-matched typically developing (TD) children. We compared global and regional T1 measures (CC volume, and CC density), and the DTI measures [fractional anisotropy (FA), apparent diffusion coefficient (ADC), average fiber length (AFL), and fiber number (FN)] of transcallosal fibers, between the two groups. We also evaluated the relationships between scores on the Childhood Autism Rating Scale (CARS) and CC T1 or DTI measurements. Significantly less white matter density in the anterior third of the CC, and higher ADC and lower FN values of the anterior third transcallosal fiber tracts were found in HFA patients compared to TD children. These results suggested that the anterior third CC density and transcallosal fiber connectivity were affected in HFA children.
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5. Wang L, Li J, Jia M, Yue W, Ruan Y, Lu T, et al. {{No association of polymorphisms in the CDK5, NDEL1, and LIS1 with autism in Chinese Han population}}. {Psychiatry Res}. 2011 Dec 30;190(2-3):369-71.
Autism is a pervasive neurodevelopmental disorder. CDK5 (cyclin-dependent kinase 5) and its interacting molecules are involved in neurodevelopment. We performed a family-based association analysis between CDK5, NDEL1, and LIS1 polymorphisms and autism in a Chinese Han population. Our study did not detect a significant association. It indicated that common genetic variations in these genes might not play a role in the genetic predisposition to autism.
