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• 1 2016-11-04T06:47:22-07:00 The Neuroscience of Autism Spectrum Disorder 9 plain 2016-12-12T05:36:26-08:00 The brain mechanisms that underly ASD is a major emerging field of research. While there are many factors that have been proposed to increase risk of having ASD, there is no one cause that is apparent or has been discovered by research. For this reason, ASD continues to largely be an enigma in the Neuroscience world. Because the differences between the brains of individuals with ASD and typically developing individuals are vast, it is possible that the varied social behaviors and mindsets of individuals with ASD are the result of many altered brain mechanisms or biochemical pathways, and less likely to be pinpointed to just one source. Below, various papers in published in the last few years about potential genetic and neural markers for ASD have been outlined:
  
  1) Manuel F. Casanova, David G. Amaral, John L. R. Rubenstein, Sally J. Rogers (2015): Genetic Markers - Research shows that there are several developmental and genetic mechanisms are implicated in the cause of Autism. Currently, genes that have been associated with ASD cause defects in molecular pathways that link synaptic and nonsynaptic signals with changes in protein synthesis that can modulate neural response properties (FRMR1, MET, NGLN3/4, PTEN, SHANK3, TSC1/2), defects in transcriptional regulation of neural genes (DLX2/5, EN2, and MeCP2), defects in neural excitatory state (CACNA1C, CACNA1H, SLC6A4, SCN1A, and SCN2A), defects in signals within specific neural circuits important for social behavior (AVPR1a; OXTR)
  
  2) Matthew K. Belmonte,  Greg Allen, Andrea Beckel-Mitchener, Lisa M. Boulanger, Ruth A. Carper,and Sara J. Webb (2004): Abnormal Brain Connectivity Hypothesis- It has been seen that many individuals with ASD have anatomic abnormality in the cerebellum, suggesting it may play a role in Autism. The reduced size of cerebellar subregions in individuals with ASD release the deep cerebellar nuclei from inhibition, producing abnormally strong physical connectivity and potentially abnormally weak computational connectivity along the cerebello-thalamocortical circuit. This abnormal connectivity hypothesis potentially serves as a framework for the genetic and neuropathological mechanism of ASD. 
  
  3) Diana L. Vargas, MD, Caterina Nascimbene, MD, Chitra Krishnan, MHS, Andrew W. Zimmerman, MD, and Carlos A. Pardo, MD (2005): Neuroglial Activation and Immune-Mediated Mechanisms in Pathogenesis of Autism - There are distinct active neuroinflammatory responses in the cerebral cortex, white matter, and cerebellum of ASD individuals. This suggests that innate immune responses and neuroglial activity may play a role in the pathogenesis of autism. Once again the cerebellum is seen to be significant in ASD, as this study provides evidence that is the center of an active and chronic neuroinflammatory process. 
  
  4) Simon Baron-Cohen (2002): Extreme Male Brain Theory of Autism - The ASD brain is an extreme of the characteristics associated with the male brain. Evidence shows that individuals with ASD have subpar theory of mind understanding, score low on the empathy quotient, have difficulty deciphering complex face expression, make little eye contact, develop language slowly and have a hard time judging what is socially insensitive or hurtful (Faux Pas test). 
  
  5) Emily Simonoff (2012): Importance of Gene-Environment Interplay - Along with genetic and neural mechanisms that are heavily studied in ASD, environmental factors must also be considered when understanding the growing prevalence of ASD.