Autism is generally considered to be incurable, however there is now a broad array of autism therapies with various goals, e.g. improving health and well-being, emotional problems, difficulties with communication and learning, and sensory problems for people withautism. The efficacy of each approach varies greatly from person to person. The method that has been best documented to show positive results is Applied Behavior Analysis (ABA), which systematically breaks down and teaches tasks. Progress toward development of other treatment approaches such as medical, behavioral and remedies for the more debilitating effects of autism has historically been slow-moving due to widespread disagreements over the nature and causes of autistic spectrum disorders and by a lack of funding for serious research into the many treatment approaches that are used around the world.
The causes and etiology of autism are areas of debate and controversy; there is currently no consensus, and researchers are studying a wide range of possible genetic and environmental causes. Since autistic individuals are all somewhat different from one another, there are likely multiple "causes" that interact with each other in subtle and complex ways, and thus give slightly differing outcomes in each individual. Two environmental theories include the impactof vaccines on the immune system (of which a statistically significant link has never been found despite many attempts; see the vaccine theory sub-heading in the Causes of autism page for a more extensive treatment) and a more recent theory relating autism to high levels of television viewing while young.
There is also a large genetic component to autism. Originally hinting toward this was the observation that there is about a 60% concordance rate for autism in monozygotic (identical) twins, while dizygotic (non-identical) twins and other siblings only exhibit about 4% concordance rates. A theory featuring mirror neurons states that autism may involve a dysfunction of specialized neurons in the brain that should activate when observing other people. In typically-developing people, these mirror neurons are thought to perhaps play a major part in social learning and general comprehension of the actions of others.
Researchers from France showed that the gene called SHANK3, also known as ProSAP2, regulates the structural organization of dendritic spines and is a binding partner of neuroligins; genes encoding neuroligins are mutated in autism and Asperger syndrome. A mutation of a single copy of the gene on chromosome 22q13 can result in language or social communication disorders. Though not present in all individuals with autism, the mutations hold potential to illustrate some of the genetic components of spectrum disorders.
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