Down syndrome (DS) is one of the more commonly occurring genetic disorders, where mental retardation is combined with nutritional diseases. It is caused by having a third copy of chromosome 21, and there exist 3 forms; Simple Trisomy 21, Translocation Trisomy and Mosaic Trisomy. Symptoms include intellectual disability/mental retardation, early onset of Alzheimer’s disease and the appearance of various phenotypic features such as narrow slanted eyes, flat nose and short stature. In addition, there are other health problems throughout the body, consisting in part of cardiac defects and thyroid function abnormalities along with nutritional disorders (ie. overweight, obesity, hypercholesterolemia and deficiencies of vitamins and minerals). Those suffering DS have widespread body frame abnormalities and impaired brain development and function; the latter leading to impaired intellectual development. Many studies indicate excessive or deficient nutrient uptakes associated with making inappropriate foodstuff choices, food intolerance, (eg. celiac disease) or malabsorption. DS persons with overweight or obesity are linked with a slow metabolic rate, abnormal blood leptin concentrations and exhibit low levels of physical activity. Vitamin B group deficiencies and abnormal blood homocysteine levels decrease the rate of intellectual development in DS cases. Zinc deficiencies result in short stature, thyroid function disorders and an increased appetite caused by excessive supplementation. Scientific advances in the research and diagnosis of DS, as well as preventing any associated conditions, have significantly increased life expectancies of those with this genetic disorder. Early dietary interventions by parents or guardians of DS children afford an opportunity for decreasing the risk or delaying some of the DS associated conditions from appearing, thus beneficially impacting on their quality of life.
In this mini-review we were interested in describing the main genetic, biological and mechanistic aspects of the aggressive behaviour in human patients and animal models. It seems that violent behaviour and impulsive traits present a multifactorial substrate, which is determined by genetic and non-genetic factors. Thus, aggressivity is regulated by brain regions such as the amygdala, which controls neural circuits for triggering defensive, aggressive or avoidant behaviour. Moreover, other brain structures such as the anterior cingulate cortex and prefrontal cortex regionscould modulate circuits involved in aggression. Regarding the genetic aspects, we could mention the mutations in the monoamine oxidase or the polymorphisms of the genes involved in the metabolism of serotonin, such as tryptophan hydroxylase. Also, besides the low levels of serotonin metabolites, which seem to be associated with impulsive and aggressive traits, there are good evidences that deficiencies in glutamate transmission, as well as testosterone, vasopressin, hypochloesterolemia or oxytocin modifications could be related to the aggressive behaviour. Regarding oxytocin we present here in the last chapter the controversial results from the current literature regarding the various effects exhibited by oxytocin administration on the aggressive behavior, considering the increased interest in understanding the role of oxytocin on the main neuropsychiatric disorders.