Autism - Wikipedia
Autism is a brain development disorder characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old.[2] The autism spectrum disorders (ASD) also include related conditions with milder signs and symptoms.[3]
Autism affects many parts of the brain; how this occurs is not understood. Parents usually notice signs in the first two years of their child’s life. Although early behavioral or cognitive intervention can help children gain self-care, social, and communication skills, there is no known cure.[3] Few children with autism live independently after reaching adulthood, but some become successful,[8] and an autistic culture has developed, with some seeking a cure and others believing that autism is a condition rather than a disorder.[9]
Unlike many other brain disorders such as Parkinson’s, autism does not have a clear unifying mechanism at either the molecular, cellular, or systems level; it is not known whether autism is a few disorders caused by mutations converging on a few common molecular pathways, or is (like intellectual disability) a large set of disorders with diverse mechanisms.[10] Autism appears to result from developmental factors that affect many or all functional brain systems,[60] and to disturb the course of brain development more than the final product.[61] Neuroanatomical studies and the associations with teratogens strongly suggest that autism’s mechanism includes alteration of brain development soon after conception.[5] This localized anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.[62] Although many major structures of the human brain have been implicated, almost all postmortem studies have been of individuals who also had mental retardation, making it difficult to draw conclusions.[61] Brain weight and volume and head circumference tend to be greater in autistic children.[63] The cellular and molecular bases of pathological early overgrowth are not known, nor is it known whether the overgrown neural systems cause autism’s characteristic signs.
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