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STRATEGIC-BRAIN
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For years, scientists and medical doctors have relied on genetics, embryology, anthropology, dermatoglyphics, and anatomy to gain insight into the functioning of the brain.
The development of the human brain commences shortly after conception and persists until early adulthood. During the third week of gestation, the embryonic brain initiates its development, wherein neural progenitor cells undergo division and differentiation into neurons and glia, the fundamental cell types that constitute the nervous system. By the conclusion of the ninth week of gestation, the cerebral organ presents itself as a diminutive and unblemished entity.
Throughout the pregnancy, the cerebral structure undergoes modifications as it expands and develops the distinctive convolutions that demarcate specific cerebral regions. The alterations in cerebral anatomy are indicative of significant transformations at the cellular level. Neurons within the various cerebral regions commence the production of chemical signaling molecules that facilitate intercellular communication. The fiber pathways that will serve as the cerebral information superhighway are in the process of formation. The cells that will comprise the neocortex, the cerebral region responsible for coordinating visual and auditory perception, spatial reasoning, conscious thought, and language, initiate communication.
Whilst the foundation of a functional brain is established during the prenatal period, brain function undergoes further development postnatally, primarily influenced by sensory stimuli. The initial years of life witness a significant increase in the number of neural connections, commonly known as the synaptic "big bang."
Following the age of two years, there is a reduction in the quantity of neural connections. This phenomenon, referred to as synaptic pruning, involves the brain reorganizing its connectome to operate more effectively by eliminating inefficient connections and optimizing performance. A significant corpus of animal and epidemiological research indicates that prenatal exposure to detrimental environmental stimuli, such as maternal stress or toxic agents, has the potential to modify the developmental course of the fetal brain.
Nevertheless, the field of prenatal neurodevelopment remained a Black box until recently. According to Robert Wright, an environmental epidemiologist, and pediatrician at the Icahn School of Medicine at Mount Sinai in New York, “We don’t know a lot about what happens in fetal life, because we haven’t had the tools to measure brain development in fetal life,”. That is, our understanding of fetal development is limited due to the lack of tools available to measure brain development during this stage.
Furthermore, “It may even differ from [postnatal] development, as the sensory inputs are largely biochemical and passed from mother to child, unlike the direct experience of sound, light, temperature, and movement that a child experiences.” The maturation of the brain is contingent upon both environmental and endogenous stimuli, which aid in the determination of which neural connections ought to be pruned and which ought to be retained.
According to Wright, “When a neuron fires after a proper signal, its synaptic connections are solidified,” Wright explains. “If a neuron’s synaptic connection is rarely fired, it regresses and is removed.” That is, the solidification of synaptic connections occurs when a neuron is appropriately stimulated, whereas infrequent stimulation results in the regression and subsequent removal of synaptic connections. Toxic exposures have the potential to impede the brain's capacity to differentiate significant connections from insignificant ones, thereby modifying the development of the connectome. Lead, for instance, can trigger neurons to spontaneously fire without a proper signal, as stated by Wright. This inappropriate induction of neuronal activity can disrupt the typical course of synaptic formation and pruning, which is fundamental to the formation of the connectome. Ultimately, such interference can result in the establishment of maladaptive brain signaling networks.
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