Memory-related default-executive coupling across the lifespan and associations with changes in cognitive control.

Decision making is a fundamental neurocognitive capacity that often depends on processing the uncertainty and risk associated with available choice options (; ; ). To examine how risk is incorporated in the decision-making process, participants are typically asked to choose between options that differ in reward probability and magnitude (; ). Such risky choice paradigms usually entail an optimal solution. Multiplying the reward magnitude by the probability yields an option’s expected value ; the best option has the highest expected value. However, according to (PT) by , it is in the apparent simple calculation of expected value that people deviate from optimality. An alternative model that is frequently used to account for suboptimal risky decision making is the (HPDM; ; ). is the reduction of the subjective outcome value as a function of the probability with which it occurs (; ). While HPDM is strong in its simplicity, PT might better account for risk attitudes (). Previous research employing different paradigms to study risky decision making has identified several neural systems involved in risky decision making (; ; ). Risk taking is linked to increased activity in regions associated with the neural representation of subjective reward value (; , ; ; ), including the posterior cingulate cortex (PCC), ventromedial prefrontal cortex (vmPFC), dorsolateral prefrontal cortex (dlPFC), and ventral striatum, in particular the nucleus accumbens (NAc; ; ; ; ). Moreover, the anterior insula, anterior cingulate cortex (ACC), and dorsomedial prefrontal cortex (dmPFC) are important for conflict monitoring and exhibit activation increases during risk taking (; ; ). Several previous studies linked homeostatic state changes to the extent to which context modulates risk taking. For example, individuals may act more risk averse shortly after having a meal () and make riskier choices when hungry (; ; ), perhaps as a survival mechanism to foster exploratory behaviour and prioritise quick food acquisition (). Hunger and satiety are the interoceptive reports of energy deficit or surplus, respectively. Rodent models suggest that both are tightly controlled by well-defined neurocircuitry interactions (; ; ; ; ), including foremost hypothalamic areas () and the hippocampus (; ; ), amongst others, which strongly interact with the dopaminergic mesoaccumbens pathway (; ). Support for these interactions has been observed in human participants as well (; ; ). Hunger is signalled in the hypothalamus (arcuate nucleus and paraventricular hypothalamic nucleus) in rodents (; ; ; ). While hunger is operationally difficult to define, physiological proxies linking hunger state to metabolic signals may be relevant in informing state-adaptive processes. To that end we considered ghrelin as a critical peptide which signals the state of hunger, which in turn drives hunger-related behaviour (; ; ).