Post-traumatic stress disorder is a debilitating psychiatric disorder with a lifetime preva- lence of ~8 percent, which develops in ~15 percent of individuals exposed to trauma.
There may be a role for non- coding RNAs (ncRNAs), including microRNAs (miRNAs), in ameliorating the impact of severe stress or trauma syndromes [51,52]. PTSD has a close association with the uncinate fasciculus syndrome and so may present with over- lap syndromes with frontotemporal syndromes [53]. Prazosin and meditation are both notable breakthrough therapies in the treatment of PTSD that will be further discussed in Chapter 10. Neurotoxicological syndromes such as heavy metal poisoning, lead in par- ticular, as well as solvents, may present with the primary syndromes of working memory impairment, disinhibition, and cognitive flexibility syndrome disorders.
The COMT genotype regulates dopamine availability and influences where a person is situated on the D1 inverted U curve. DAG kinase inhibits PKC signaling, which if altered genetically may lead to bipolar disorder [54]. Translocation genes, DISC1 regu- lated phosphodiesterase, which causes catabolism of the c- AMP signaling system, leads to neuropsychiatric disorders such as schizophrenia [55].
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Neuropharmacological therapies such as those forming the mainstay of psychiatry are limited in that they largely target the ascending neurotransmitter modulatory systems.
These conform to only part of the brain’s networks and are intrinsically limited and non- specific, with limited benefits for those affected. More robust and enduring therapies involve the manipulation of the brain’s inherent capacity for neuroplasticity. Such brain training is even more appealing because of the concept of generalization and transfer. A brain- training program may enhance a particular skill, but the effects may be more wide- spread within the brain circuitry. Preliminary data point to a possible “transfer effect” to a more general cognitive performance improvement that may translate to other cognitive functions. The molecular substrate of these plastic changes in the motor and sensory net- works, for example, is in the form of rapid dendritic spine formation and slower spine elimination during sleep.
Physical exercise and dietary factors have already been shown to improve general cognitive processing capacities. Meditation may facilitate specific prefrontal region brain building that is important in focusing and social abilities. More specific interven- tions include mirror feedback therapy, transcranial magnetic stimulation, and trans cranial direct current stimulation. The latter modalities enable advantageous stimulation or inhibition of different parts of the brain networks that are altered by injury or disease.
Working with the brain’s own neuroplasticity has been relatively less emphasized in the current era, with a more predominant focus on pharmacological pill- centric approaches.
A gene- centric approach had also been initially promising in lieu of the recently com- pleted Human Genome Project. Lastly, memory- centric diagnoses may have obscured other important symptoms and dementias other than Alzheimer’s disease. A triadic focus is advocated, with an intensification of disease mechanism elucidation (connect- omics), an emphasis on neuroplastic mechanisms for most conditions, and pill therapy for some. However, most important are the primary and secondary prevention opportun- ities through brain fitness rules adherence. This has never been more urgent with the advent of the tsunamis of Alzheimer’s disease and vascular dementias imminent. From the reviews earlier, the fundamental architecture of the brain is one of a massive evo- lutionary surge in white matter growth, brain networks, and connectivity that are sup- ported by clinical observations such as diaschisis. The daily formation and dismantling of neuronal assemblies is a normal part of the brain’s activity. Electrophysiological stud- ies have long recorded the orchestrated neuronal networks and their specific patterns in