Research shows that IGF-1 may be an important constituent in a number of neurological conditions, including autism. In fact, children with autism show lower brain levels of IGF-1 than age-matched controls, suggesting that low IGF-1 concentrations in the brain, particularly at an early age, may disrupt normal development and be important in the pathogenesis of autism.
Research in mouse models of autism indicate that IGF-II and analogues like IGF-1 DES reverse all deficits associated with the conditions. Mice administered IGF-II for just five days showed improved social interaction, better novel-object recognition, enhanced contextual fear conditioning, reduced repetitive/compulsive behavior, better grooming, and more. The mice even showed improve memory.
These findings should not come as any surprise as research suggests that autism is likely caused by disruptions in synapse development and is similar pathologically, to other neurodevelopmental conditions like fragile X syndrome, tuberous sclerosis, and Angelman syndrome. IGF-1 and its analogues, which have potent effects on synapses, are therefore ideal candidates for exploring various treatment strategies in these disorders.
