Linking autism to an imbalanced catabolism of synaptic monoamines

Abstract

An interdisciplinary study of autism led to implicate a relatively poor catabolism of one of the monoamines released in the synapse, namely serotonin . This deficit would result from persistent epigenetic regulations of two enzymes (i.e.: MAOA- and COMT+) across neural differentiation, for counteracting an accidental excess of MAOA in the early gestation. Epigenetic traits would outlast this temporary excess and be inherited by generations of neurons, and possibly by next human generations. In addition, the late occurrence of autistic symptoms may be consistent with the rising of the MAOB enzyme that degrades another monoamine ( dopamine ), but only significantly around two years after birth. The consequent long-term imbalance of synaptic monoamines is assumed here to impact the architecture of sleep and learning [1], inducing a range of developmental problems. This theory is drawn on Guided Propagation Networks (GPNs), the computer simulations of which show the growth of aberrant structures when modulation parameters akin to monoamines do not satisfy inner learning constraints. Comparisons are made between a reference well-tuned network and others grown with shifted parameters, all using the same learning data. Unlike the reference network, impaired GPNs display features that have been observed in the autistic