Sun, 27 Jul 2008 11:13:00 BST CiteULike: awooga autism http://www.citeulike.org/user/awooga/tag/autism CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/awooga/article/2761137 <i>Brain, Behavior, and Immunity, Vol. In Press, Corrected Proof</i> Brief Commentary: Autistic children: A neuroimmune perspective Robert Dantzer Keith Kelley doi:10.1016/j.bbi.2008.03.001 Brain, Behavior, and Immunity, Vol. In Press, Corrected Proof 2008-05-06T13:26:59-00:00 Brain, Behavior, and Immunity In Press, Corrected Proof autism immunology http://www.citeulike.org/user/awooga/article/409442 <i>Annu Rev Neurosci, Vol. 28 (2005), pp. 109-126.</i><br /><br />Although the neurobiological understanding of autism has been increasing exponentially, the diagnosis of autism spectrum conditions still rests entirely on behavioral criteria. Autism is therefore most productively approached using a combination of biological and psychological theory. The triad of behavioral abnormalities in social function, communication, and restricted and repetitive behaviors and interests can be explained psychologically by an impaired capacity for empathizing, or modeling the mental states governing the behavior of people, along with a superior capacity for systemizing, or inferring the rules governing the behavior of objects. This empathizing-systemizing theory explains other psychological models such as impairments of executive function or central coherence, and may have a neurobiological basis in abnormally low activity of brain regions subserving social cognition, along with abnormally high activity of regions subserving lower-level, perceptual processing--a pattern that may result from a skewed balance of local versus long-range functional connectivity. Autism: a window onto the development of the social and the analytic brain. S Baron-Cohen MK Belmonte doi:10.1146/annurev.neuro.27.070203.144137 Annu Rev Neurosci, Vol. 28 (2005), pp. 109-126. 2005-11-27T02:07:54-00:00 2005 Annu Rev Neurosci 0147-006X 28 109 126 autism review http://www.citeulike.org/user/awooga/article/892724 <i>Curr Opin Neurobiol, Vol. 15, No. 2. (April 2005), pp. 225-230.</i><br /><br />Although it has long been thought that frontal lobe abnormality must play an important part in generating the severe impairment in higher-order social, emotional and cognitive functions in autism, only recently have studies identified developmentally early frontal lobe defects. At the microscopic level, neuroinflammatory reactions involving glial activation, migration defects and excess cerebral neurogenesis and/or defective apoptosis might generate frontal neural pathology early in development. It is hypothesized that these abnormal processes cause malformation and thus malfunction of frontal minicolumn microcircuitry. It is suggested that connectivity within frontal lobe is excessive, disorganized and inadequately selective, whereas connectivity between frontal cortex and other systems is poorly synchronized, weakly responsive and information impoverished. Increased local but reduced long-distance cortical-cortical reciprocal activity and coupling would impair the fundamental frontal function of integrating information from widespread and diverse systems and providing complex context-rich feedback, guidance and control to lower-level systems. Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection. E Courchesne K Pierce doi:10.1016/j.conb.2005.03.001 Curr Opin Neurobiol, Vol. 15, No. 2. (April 2005), pp. 225-230. 2006-10-11T13:16:24-00:00 2005 Curr Opin Neurobiol 0959-4388 15 2 225 230 autism frontalcortex http://www.citeulike.org/user/awooga/article/891552 <i>Psychol Rev, Vol. 113, No. 3. (July 2006), pp. 483-525.</i><br /><br />What brain mechanisms underlie autism, and how do they give rise to autistic behavioral symptoms? This article describes a neural model, called the Imbalanced Spectrally Timed Adaptive Resonance Theory (iSTART) model, that proposes how cognitive, emotional, timing, and motor processes that involve brain regions such as the prefrontal and temporal cortex, amygdala, hippocampus, and cerebellum may interact to create and perpetuate autistic symptoms. These model processes were originally developed to explain data concerning how the brain controls normal behaviors. The iSTART model shows how autistic behavioral symptoms may arise from prescribed breakdowns in these brain processes, notably a combination of underaroused emotional depression in the amygdala and related affective brain regions, learning of hyperspecific recognition categories in the temporal and prefrontal cortices, and breakdowns of adaptively timed attentional and motor circuits in the hippocampal system and cerebellum. The model clarifies how malfunctions in a subset of these mechanisms can, through a systemwide vicious circle of environmentally mediated feedback, cause and maintain problems with them all. Neural dynamics of autistic behaviors: cognitive, emotional, and timing substrates. S Grossberg D Seidman doi:10.1037/0033-295X.113.3.483 Psychol Rev, Vol. 113, No. 3. (July 2006), pp. 483-525. 2006-10-10T17:34:39-00:00 2006 Psychol Rev 0033-295X 113 3 483 525 autism