Dyslexia may be caused by a fault in a single gene, scientists have suggested.
One in 10 children is dyslexic
Researchers in Finland say their finding may explain why the condition seems to run in families.
Dyslexia affects about one in 10 people. It is the most common learning disorder in children. Many find it difficult to recognise and read words.
Writing in the Proceedings of the National Academy of Sciences, scientists said a flaw in a gene called DYXC1 may cause the condition.
Previous studies have suggested that people with dyslexia process information in a different area of the brain than the average person does, even though they are often of average or above-average intelligence.
Other studies have suggested they use the right side of the brain for reading instead of the left side, which is better set up for processing words.
Scientists have also suspected that the condition may also have a genetic component.
Researchers at the University of Helsinki carried out tests on 20 Finnish families, many of whom had several cases of dyslexia.
They found that the DYXC1 gene was disrupted in a number of these families.
The scientists were unable to say exactly what role this gene has but they do believe it could play a role in determining who is at risk of dyslexia.
They suggested it may be involved in helping cells cope with stress but they acknowledged that much more study is needed. They added that faults in other genes may also cause dyslexia.
But writing in the PNAS, they said: "We conclude that DYXC1 should be regarded as a candidate gene for developmental dyslexia."
They added: "There is overwhelming evidence that dyslexia is a genetically complex condition."
If their findings are backed up in other studies, it could allow doctors to test children for this particular genetic fault.
This, in turn, could enable these children to get the additional help they need to make sure they no longer fall behind in their studies.
In the longer term, it could enable scientists to start working on drugs to treat the condition.