The surplus synapses - places where neurons connect and communicate - is due to a lack of "pruning" that normally occurs early in life.
In mice with autistic traits, scientists were able to restore synaptic pruning and reduce symptoms with a drug used to suppress the immune systems of transplant patients.
The drug, rapamycin, has side-effects that make it unsuitable as an autism treatment. But the discovery opens up possibilities for other therapies based on synaptic pruning.
Excessive synapses could be a fundamental causal factor behind autism, the scientists believe.
"This is an important finding that could lead to a novel and much-needed therapeutic strategy for autism," said Professor Jeffrey Lieberman, chairman of psychiatry at Columbia University Medical Centre in New York, where the research took place.
Autism, which affects about 500,000 people in the UK, covers a range of behavioural disorders that reduce the ability of sufferers to communicate with and relate to other people.
It is though to be triggered by a combination of genetic and environmental factors. During normal brain development, a burst of synapse formation occurs in infancy, especially in the cortex - a region closely linked to autistic behaviour. Pruning removes more than half of these cortical synapses by late adolescence.
The Columbia University scientists examined the brains of 26 autistic children and young people aged two to 20 who had died from a variety of causes. Brains from 22 non-autistic children were used as a comparison.
Synaptic density in samples of brain tissue was measured. By late childhood, spine density had dropped by about half in the "healthy" brains, but by only 16 per cent in the brains of autistic individuals.
Lead researcher Professor David Sulzer said: "While people usually think of learning as requiring formation of new synapses, the removal of inappropriate synapses may be just as important."