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Objectives: As a complex, polygenic trait, brain size has likely been influenced by a range of direct and indirect selection pressures for both cognitive and non‐cognitive functions and capabilities. It has been hypothesized that hominin brain expansion was, in part, a correlated response to selection acting on aerobic capacity (Raichlen & Polk, 2013). According to this hypothesis, selection for aerobic capacity increased the activity of various signaling molecules, including those involved in brain growth. One key molecule is brain‐derived neurotrophic factor (BDNF), a protein that regulates neuronal development, survival, and plasticity in mammals. This review updates, partially tests, and expands Raichlen and Polk's (2013) hypothesis by evaluating evidence for BDNF as a mediator of brain size. Discussion: We contend that selection for endurance capabilities in a hot climate favored changes to muscle composition, mitochondrial dynamics and increased energy budget through pathways involving regulation of PGC‐1α and MEF2 genes, both of which promote BDNF activity. In addition, the evolution of hairlessness and the skin's thermoregulatory response provide other molecular pathways that promote both BDNF activity and neurotransmitter synthesis. We discuss how these pathways contributed to the evolution of brain size and function in human evolution and propose avenues for future research. Our results support Raichlen and Polk's contention that selection for non‐cognitive functions has direct mechanistic linkages to the evolution of brain size in hominins. [ABSTRACT FROM AUTHOR] more...

Brain-derived neurotrophic factor ( BDNF) serves as a vital regulator of neuronal proliferation and survival, and has been shown to regulate energy homeostasis, glucose metabolism and body weight maintenance. Elevated concentrations of plasma BDNF have been associated with obesity and type 2 diabetes mellitus. Acute aerobic exercise transiently increases circulating BDNF, potentially correcting obesity-related metabolic impairment. The present study aimed to compare acute aerobic exercise elicited BDNF responses in obese and normal-weight subjects. Furthermore, we aimed to investigate whether acute exercise-induced plasma BDNF elevations would be associated with improved indices of insulin resistance, as well as substrate utilization [carbohydrate oxidation ( CHOoxi) and fat oxidation ( FAToxi)]. Twenty-two healthy, untrained subjects [11 obese (four men and seven women; age = 22.91 ± 4.44 years; body mass index = 35.72 ± 4.17 kg/m2) and 11 normal-weight (five men and six women; age = 23.27 ± 2.24 years; body mass index = 21.89 ± 1.63 kg/m2)] performed 30 min of continuous submaximal aerobic exercise at 75% maximal oxygen consumption. Our analyses showed that the BDNF response to acute aerobic exercise was similar in obese and normal-weight subjects across time (time: P = 0.015; group: P = not significant) and was not associated with indices of IR. Although no differences in the rates of CHOoxi and FAToxi were found between both groups, total relative energy expenditure was significantly lower in obese subjects compared to normal-weight subjects (3.53 ± 0.25 versus 5.59 ± 0.85; P < 0.001). These findings suggest that acute exercise-elicited BDNF elevation may not be sufficient to modulate indices of IR or the utilization of either carbohydrates or fats in obese individuals. [ABSTRACT FROM AUTHOR] more...

Depression is increasingly present in the population, and its pathophysiology and treatment have been investigated with several animal models, including olfactory bulbectomy ( Obx). Fish oil ( FO) supplementation during the prenatal and postnatal periods decreases depression-like and anxiety-like behaviors. The present study evaluated the effect of FO supplementation on Obx-induced depressive-like behavior and cognitive impairment. Female rats received supplementation with FO during habituation, mating, gestation, and lactation, and their pups were subjected to Obx in adulthood; after the recovery period, the adult offspring were subjected to behavioral tests, and the hippocampal levels of brain-derived neurotrophic factor ( BDNF), serotonin (5- HT) and the metabolite 5-hydroxyindoleacetic (5- HIAA) were determined. Obx led to increased anxiety-like and depressive-like behaviors, and impairment in the object location task. All behavioral changes were reversed by FO supplementation. Obx caused reductions in the levels of hippocampal BDNF and 5- HT, whereas FO supplementation restored these levels to normal values. In control rats, FO increased the hippocampal level of 5- HT and reduced that of 5- HIAA, indicating low 5- HT metabolism in this brain region. The present results indicate that FO supplementation during critical periods of brain development attenuated anxiety-like and depressive-like behaviors and cognitive dysfunction induced by Obx. These results may be explained by increased levels of hippocampal BDNF and 5- HT, two major regulators of neuronal survival and long-term plasticity in this brain structure. [ABSTRACT FROM AUTHOR] more...