Study shows gene defect’s role in autism-like behavior
August 10, 2012 in Autism spectrum disorders
Excerpt: “The research showed that, when defective, pten’s protein interacts with the protein of a second gene known as p53 to dampen energy production in neurons. This severe stress leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus — brain regions critical for social behavior and cognition.”
My comment:
It will be interesting to see how much longer it is before researchers link p53 to the diet-responsive hypothalamic gonadotropin releasing hormone (GnRH) neurogenic niche. The epigenetic effects of nutrient chemicals, endocrine disruptors, and pheromones on GnRH are more clearly viewed in the context of the genetically predisposed development of ASDs during the first two years of postnatal life in humans. That’s when the epigenetic effects of olfactory/pheromonal input have their most important developmental effects on GnRH and other hormones that affect behavior.
If I were a molecular biologist I would attempt to look at cause and effect as has been done in this article: Using perceptual signatures to define and dissociate condition-specific neural etiology: autism and fragile X syndrome as model conditions. I think, however, at this point, that the level of specialization required may be prohibitive in the context of modeling the development of atypical social behaviors.
My model suggests olfactory/pheromonal cause, but the current focus on oxytocin and social bonding makes it clear that few people are interested in the role that pheromones play in the development of human behavior. For example, I haven’t heard any of the oxytocin researchers mention how its release is centrally controlled.
Yet, here we have mice that might otherwise help us sniff out more information about cause and effect relationships that link sensory input directly to behavior and to disorders of behavioral development. See, for example: Napoli E, Ross-Inta C, Wong S, Hung C, Fujisawa Y, et al. (2012) Mitochondrial Dysfunction in Pten Haplo-Insufficient Mice with Social Deficits and Repetitive Behavior: Interplay between Pten and p53. PLoS ONE 7(8): e42504.
and
Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338
