It is universally accepted that developmental dyslexia is often found in members of the same family, which indicates a genetic component.
As the human’s complete genetic information (the genome) is now known researchers can compare very precise positions on chromosomes, assess where the DNA (deoxyribonucleic acid) code is different, and then show how the protein is synthesized from the code. An aberrant protein may cause, amongst many other outcomes, an undesirable structural modification, a metabolic defect because an enzyme malfunctions, an impairment in the immune system, or the capacity of the cell to emit signals to or receive signals from other cells.
The example below is from the work of John Stein’s group at the University of Oxford. The figure shows six chromosomes (but it is thought that many more are implicated in dyslexia). The fourth one from the left (chromosome 6) has a site where the genes for cell-cell recognition and immune control are mutated, and the last (chromosome 18) has a site where the gene for a melanocortin receptor may be mutated. Melanocortin is a hormone which has wide-ranging physiological effects, including response to daylight. Chromosome 6 is also where the KIAA 0319gene is situated and this is dealt with in the next department, ‘Molecular biology’.
Finally, there is no such thing as ‘a gene for dyslexia’. There are multiple genes each of which may contribute in a very inter-related way to a disposition to dyslexia in any of its various forms.
The brain is modified by the environment as it develops and its ‘plasticity’ means that new connections may be laid down late into life, with compensatory mechanisms that can substitute for many lost or weaker functions.