The genetics myth: Clip from Zeitgeist 3: Moving forward. (13.57 minute video) Several prominent neuroscientists discuss epigenetic effects of the environment that are being brought to bear as we learn more about genetically predisposed behaviors, mental disorders, and physical disorders.
Exemplified, albeit without mention, in this next link is the latest information on the likely epigenetic effects of glucose in Alzheimer’s disease and in ALS. Researchers uncover toxic interaction in neurons that leads to dementia and ALS December 10, 2012 in Medical research
Excerpt: By improving the scientific community’s understanding of the biological processes leading to frontotemporal dementia, the researchers have also paved the way for the development of new therapies to prevent or combat the disease, says Leonard Petrucelli, Ph.D., chair of the Department of Neuroscience at Mayo Clinic in Florida, who led the research.
My comment: TDP-43 facilitates the production of a subset of precursor microRNAs (miRNAs). It’s involvement in miRNA biogenesis is indispensable for neuronal outgrowth. Glucose is indispensable for neuronal survival. If TDP-43 alters the glucose-dependent miRNA / messenger RNA balance that helps to ensure intracellular homeostasis in gonadotropin releasing hormone neurosecretory neurons of mammalian brain tissue, the results reported today on TDP-43 and Alzheimer’s support a broad-based approach to the study of glucose and post-transcriptional regulation of miRNA expression in both the nucleus and the cytoplasm.
The involvement of progranulin in hypothalamic glucose-sensing and the involvement of TDP-43 in dysregulation of progranulin, which protects against cell death associated with disease, suggests to me that what ALS and dementia have in common with other neurodegenerative diseases is that they are all linked to the microRNA / messenger RNA balance. This links epigenetic effects of nutrient chemicals and pheromones to intracellular signaling and to non-random stochastic gene expression via intermolecular changes in DNA that enable de novo gene creation of olfactory receptor genes. Altered creation and expression of olfactory receptor genes could thereby explain, at least in part, deficits in olfactory acuity and specificity associated with neurodegenerative diseases at the cellular level of the 4.5 million DNA switches in the human genome.
I mention this only to note that random mutations are not likely to be driving disease processes — like Alzheimer’s, and that proper nutrition and pheromone therapy offers hope to an aging population.