This book reviews experimental contributions from many sources to search for a model of structure and molecular function of the blood-astrocytes-neuronal-system. The initial premise involved the dynamics of the hydrated shells of ions and proteins. An oxy-Hb of lower pka compared to deoxy-Hb allows for a higher dissociation of protons. This functioning for the mutual inclusion of O2 and Mg2+ is surrounded by a hydration shell of about 60 molecules. 2,3 DPG-dependent deoxygenation involves the tetramer chains of hydrophobic attractions. Their favourable thermodynamics allows for the dissociation of O2 and Mg2+ by breaking the H-bonds between the protein and the water shell. The turnover between hydrated versus hydrophobic forms of proteins involved in enzyme kinetics requires energy expenditures during the turnover of [ES], changing the enzyme hydration states into its [EP] form. A divalent metal (Mg++) when chelated by a protein loses its hydration sphere. It then releases its hydration (which is incomplete) and shows an intrinsic stronger charge. This is the denominated Mg2+ nascent, which functions by capturing water from Na+ and K+, allowing for sieve effects operating as intermediates of the physical open system. The dissipative energy potential is controlled within astrocytes by decreasing the number of H-bonds through rapid circulation. This is made possible by decreasing the number of H-bonds to reach the vapor state associated with air breathing, which could also operate through the vomeronasal organ that experiences direct contact with the brain. The breakdown of MgATP by the Na+/K+ ATPase of MgATP is involved in the release of ADP3-, and Pi2- and nascent Mg2+ that decrease ATP4-. Mg2+ could be the generator of an action potential via the activation of a Na+/K+ ATPase pump, which opens the gates for Na+ in and K+. The free [Mg2+] up-regulates responsiveness of the post synaptic AC (adenylyl cyclase) NA (noradrenaline) released by the long axons of the corpus coerellus into the synaptic junctions, and also contributes to additional up-regulation by increasing the CAMP. The up-regulation of AC by Mg2+ is turned off by Ca+2. Stressors trigger the Mg2+ response, which results in emotional pain. The zipping-out of DNA by the CAMP results in an Mg2+-CAMP-DNA complex that up-regulates gene expression for every participant in the synthesis of proteins during development, and eventually the formation of long-term memory occurs. Genes that relate to the synthesis of microtubules may participate in the formation of short-term memory. The regenerative capacity of CAMP could be involved in Alzheimer’s treatment by using the vomeronasal pathway to reach specific brain areas.