01 NRDC Dyslexia 1-88 update - Texthelp

Developmental dyslexia in adults: a research review 31
From this perspective, atypical brain functioning may not be ‘pathological’ but rather an
adaptive response to atypical experience (Locke, 1997), representing variation within the
normal evolutionary range (Levelt, 2001). The discovery of a neural signature for this atypical
functioning—differential activation in the three brain areas identified above—does not
establish that dyslexic brains are inherently and categorically different from other brains.
Dyslexic brains differ by definition from non-dyslexic brains.
It has not been established that the observed differences are either inherent or categorical.
Is there a gene for dyslexia?
Introduction
We have seen that a careful interpretation of the brain imaging research does not— or not yet,
at any rate—validate the belief that ‘dyslexic’ and ‘non-dyslexic’ brains are inherently and
categorically different, as many people believe them to be. In the face of unwarranted
accusations of stupidity or laziness, the dyslexic person’s need for self-vindication cannot be
met by findings from imaging studies. Can this need be met by research in genetics?
Modes of inheritance and their implications
From time to time the media report that ‘Scientists identify dyslexia gene’ (BBC), or that
‘Dyslexia found in genetic jungle’ (Reuters), but such reports are potentially misleading: there
is no ‘gene for dyslexia’ in the same way that there is a gene for, say, cystic fibrosis. Although
single-gene inheritance once seemed a possible mode of transmission (Smith et al., 1990)
and has been reported to occur in some families (Fagerheim et al., 1999; Nopola-Hemmi et
al., 2001), it now appears unlikely that dyslexia could fit a single-gene, single-disease model
in which a simple genetic mutation results in failure to synthesise an essential protein
(Pennington, 1999).
In one single-gene model—namely, autosomal dominant transmission—where only one
parent has to transmit the gene for it to be expressed, the explanation would be consistent
with the observed prevalence rate, but inconsistent with the observation that some readingdisabled
individuals have no affected relatives (Plomin et al., 2001). In a second single-gene
model—namely, X-linked recessive transmission—either parent can transmit the abnormal
gene, but it will be expressed only if the son or daughter lacks a normal copy of it from the
other parent, so that a dyslexic son would need to have a dyslexic mother whereas, for a
dyslexic daughter, both parents would need to be dyslexic. This explanation is consistent with
a higher reported prevalence among males, but inconsistent with the observation that reading
disability passes as often from father to son as it does from mother to son (Plomin et al.,
2001).
A single-gene model of heritability does not fit the observations about dyslexia, not least
because of the problems it creates by assuming that dyslexics differ categorically from nondyslexics.
A better fit is offered by a multiple-gene model, which assumes that poorer readers
differ dimensionally from better readers both in their genetic constitution and also in the
environmental risk factors to which they are exposed (Pennington, 1999). According to this
model, which currently dominates research into the genetics of reading difficulty (e.g. Cardon
et al., 1994; Fisher et al., 2002; Fisher et al., 1999; Grigorenko et al., 2001; Wijsman et al.,
2000), a quantitative behavioural trait could be the effect of a number of genes—perhaps
dozens, perhaps hundreds—the variation in each of which adds a small difference to a wide
range of outcomes in the population (Plomin et al., 2001).