The genetic basis of cognition

The molecular characterization of single-gene disorders or chromosomal abno rmalities that result in a cognitive abnormality (predominantly mental reta rdation) and of the genetic variants responsible for variation in intellect ual abilities (such as IQ, language impairment and dyslexia) is expected to provide new insights into the biology of human cognitive processes. To dat e this hope has not been realized. Success in finding mutations that give r ise to mental retardation has not been matched by advances in our understan ding of how genes influence cognition. In contrast, the use of engineered m utations in mice to study models of learning and memory has cast new light on the molecular basis of memory, A comparison of studies of human and mous e mutations indicates the limitations of current genetic approaches to the understanding of human cognition, It is essential to interpret a mutation's effect within a well-characterized neural system; mutations can be used to define gene function only when the mutation has an effect on a system whos e constituents form a serial causal chain, such as the molecular components of a signal transduction pathway. Typically, however, genetic mutations wi th a cognitive and behavioural phenotype are characterized by specific effe cts on different systems whose inter-relationships are unknown. Genetic app roaches are currently limited to exploring neuronal function; it is not yet clear whether they will throw light on how neuronal connections give rise to cognitive processes. We need a much greater integration of different lev els of understanding of cognition in order to exploit the genetic discoveri es. In short, a rapprochement between molecular and systems neuroscience is required.