In 1866, John Langdon Down, a British doctor, first described the characteristics of people with Down syndrome.

In 1959, Dr. Jérôme Lejeune discovered the chromosomal abnormality linked to Down syndrome. Persons with Down syndrome exhibited an extra copy of chromosome 21.

Over the intervening years, Down syndrome cognitive research had been largely lacking because many in the medical field and those in the agencies that supported them with funding have considered the problem too complex. The thinking was that little could be done to alter the impact on cognition imparted by the extra chromosome 21 in Ds individuals. Supporting this argument was been the assumption that cognitive impairment is permanent, as it develops very early in development.

However, through the availability of mouse models, and because of our remarkably increased knowledge of the human genome, and, specifically, the genes coded on chromosome 21, recent research into Down syndrome and cognitive impairment has been rapid and significant. Research using mouse models points to learning and memory defects arising from over- expression of certain genes. This suggests that trisomy of such genes on human chromosome 21 may impact multiple learning pathways because of impaired neuronal and synaptic signal transport. (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19297404)

Such recent breakthroughs offer hope that further exploration will lead to efforts that translate into safe and effective, approved therapies to treat the cognitive impairment in individuals of all ages with Down syndrome.