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Magnetic resonance spectroscopy (MRS) and spectroscopic imaging (MRSI) enable the noninvasive regional assessment of major metabolites in the human brain including: N-acetyl aspartate (NAA), glutamate, gamma amino butyric acid (GABA) and phosphocreatine (PCr). In epilepsy, neuronal impairment and bioenergetic alterations result in decreased levels of NAA and PCr in both the primary focus and networks involved in seizure propagation. The alterations in NAA and PCr are not due solely to neuronal loss, but are correlated with functional decline and hiostologic changes at a cellular level, suggesting a significant role for bioenergetic impairment in the pathophysiology of epilepsy. Alterations in brain GABA levels have been used to titrate and evaluate the effectiveness of antiepileptic medications targeting the GABAergic system.

This chapter describes and elaborates on the energy coupling processes of living systems. First, equilibrium and nonequilibrium systems are discussed, introducing living systems as open, nonequilibrium, and dissipative structures continuously interacting with their surroundings. The roles of thermodynamics and Gibbs free energy as they apply to energy coupling phenomena are then summarized, followed by a discussion of protein structures as playing a crucial role in information processes and energy couplings. The “well-informed” character of living systems and the control of free energy, or exergy, by information are also briefly discussed. Finally, using the linear nonequilibrium thermodynamic approach, energy couplings in ATP production through oxidative phosphorylation and active transport of ions by chemical pumps are discussed as a part of bioenergetics.

This chapter comprises a detailed case history on the emergence of what was to become a model of a molecular “pump,” the photoactive protein bacteriorhodopsin. The surge of research on this brand-new research object is part of the early 1970s’ “membrane moment,” which rapidly transformed the field. The unfolding of research at the University of San Francisco, the Max Planck Institute of Biochemistry, and Cambridge’s Laboratory of Molecular Biology shows a coalescence of concepts and methods from enzymology, organic chemistry, physiology, and structural biology around the concrete materialization of a membrane and its active protein. Thereby, this chapter provides a history of active matter avant la lettre, highlighting the field’s manifold connections to chemistry. Laboratory notebooks reveal transformative steps and the impact of materiality on this research project from an analysis of membrane structures to the study of an exemplary molecular machine. This chapter provides insight into the work style and topics of a novel, influential generation of molecular biologists, which changed the scope of these sciences, and it can be read as an element in a prehistory of optogenetics, a current approach that makes use of such molecular machinery to modify neuronal activity.

Physiologists and evolutionary biologists have traditionally investigated different but complementary aspects of biological phenomena. Homeostasis, the maintenance of approximately constant conditions in bodily fluids, has been the purview of physiology. Evolutionary insights can, however, deepen our knowledge of homeostatic regulatory mechanisms. Bioenergetics has been of central concern to both physiology and evolution. Physiologists have been interested in the energetic content of foods, in the metabolic transformations of the energy derived from foods, and in the energetic costs of physiological processes, while evolutionary life history theory addresses the ways that organisms have evolved to acquire and allocate metabolic energy throughout their life course. Engineering control theory highlights the limitations as well as the benefits of different regulatory mechanisms and so helps to explain why we have evolved multiple integrated and cooperative homeostatic mechanisms. The physiological responses to pregnancy illustrate the ways in which an evolutionary perspective enriches our understanding of homeostasis.

Models of individual growth commonly used in fisheries and ecological research can be built around simple allometric functions representing the build-up of body mass (anabolism) and metabolic loss terms incorporating the effects of respiration, egestion, and excretion. From a bioenergetic perspective, body weight is a natural choice for the response variable in these models because it can be readily recast in terms of energy. Temperature affects virtually every dimension of the biology and ecology of aquatic organisms. Modifications of traditional models of individual growth can be augmented to account for temperature effects. The development of ‘full’ bioenergetic models considering each of the individual elements of production is a natural culmination of the issues described above. By invoking mass-balance constraints the bioenergetic approach offers important avenues for estimating elements of production that can be difficult to otherwise obtain.

Alzheimer’s disease (AD) is an intriguing and still unsolved puzzle that has attracted, over the last decades, the interest of the scientific community. Despite the limited knowledge regarding the initial cause(s) of AD, mitochondrial abnormalities have been pinpointed as one of the earliest and strongest events related with the pathological course of this complex neurodegenerative disease. In this sense, the present chapter addresses three distinct but connected pieces of the AD puzzle: (a) how could defects of mitochondrial bioenergetics and dynamics contribute to AD pathology? (b) Could mitochondrial defects promote the disease-defining amyloid-β‎ and tau pathologies, and vice versa? and (c) Are mitochondria feasible therapeutic targets to postpone AD symptomatology and neuropathology, and, if so, how and when? The understanding and connection of these puzzle pieces provide a more comprehensive picture about the fundamental role of mitochondrial (mal)function in the neurodegenerative processes that occur in AD and propels future research interventions aimed to forestall AD-related pathological phenotype by bolstering mitochondrial “health.”