Immunological Factors in Dyslexia

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As many parents know all too well, dyslexic children and their families tend be prone to allergies, such as skin rashes, eczema and asthma. These conditions are due to the body producing antibodies which attack your own skin or lungs for some reason. They are much more common in people with dyslexia.

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The development of magnocells is under the control of the immune gene complex on chromosome 6. We wondered therefore whether immune attack, directed against magnocellular nerve cells might be partly responsible for the brain differences in dyslexics that impede their reading.

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Since half a baby's genes are inherited from its father, a mother's baby is actually 'foreign' to her in her womb, and she automatically produces antibodies against it. These do not normally harm the baby because they do not get across the placenta into the baby's blood stream. But a small proportion may do so and cause damage. With Professor Angela Vincent at Oxford's Institute of Molecular Medicine we therefore sought to find out whether mothers with dyslexic children may produce antibodies that can attack nerve cells in the brain. So we injected blood serum (which contains the antibodies) from these mothers into the wombs of pregnant mice to see if the antibodies affected the development of the pups' brains.

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Of course mice cannot read; but we can test their coordination autopilot, the cerebellum, which is mildly affected in many dyslexics. When the mice offspring were a few months old we tested their cerebellar coordination and metabolism, and we found that indeed their coordination was impaired. We also showed that the mother's antibodies homed in on magnocells in the cerebellum to cause this incoordination. Thus maternal antibodies may sometimes play a role in the development of neurodevelopmental disorders. Perhaps the genes on the short arm of chromosome 6 that we have linked with dyslexia are involved. We are following up the tantalizing hypothesis that these genes specifically affect immunological control of the development and connections of magnocellular neurons both in the foetus and later.

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However mothers antibodies are not by any means the only factor and of course it does not mean that it is the mother's 'fault'. Probably dyslexics inherit some special genetic vulnerability making their magnocellular nerve cells prone to such antibody attack.

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