Impact of thousand-and-one amino acid 2 kinase mediated neurodifferentiation in cerebral cortex and impairment of mirror neuron pathways on autism spectrum disorders

Abstract

An understanding of how neurons develop their morphology and their distinct physiology is the key to the elucidation of the mechanisms underlying sophisticated cognitive functions in normal and disease conditions. Evidence suggests that neurodevelopmental disorders with delayed onset, such as autism spectrum disorders (ASDs) might be a consequence of aberrant dendritic arborization. This review is dedicated toward the discussion of a new pathway that specifically affects the formation of basal dendrites and axonal projections in cortical pyramidal neurons. With reference to this pathway, the function of thousand-and-one amino acid 2 kinase, in relation to dendrite morphogenesis has been elaborated. Mirror neuron system dysfunction may underlie a self-other matching impairment which has been suggested to account for autism. The hypotheses of deficit an impaired mirror neuron function in autism have now been well supported by studies employing a range of methodologies. However, underlying mechanisms require further exploration to explain how mirror neurons may be involved in attention and metalizing processes. It seems possible that different sub-populations of mirror neurons, distinct in particular anatomical regions of the brain, contribute differentially to social cognitive functions. Mirror neuron networks dysfunction in ASD-affected individuals leading to dampened imitation learning, misguided development of “egocentrism” and even failure to comprehend the intention behind a motor act. While it seems clear that autism is associated with impaired development of embodied aspects of cognition, the ways that mirror neurons contribute to these brain-behavior links are likely to be complex and demands further research.