Fear extinction learning is a highly adaptive process that involves the integrity of frontolimbic circuitry. Its disruption has been associated with emotional dysregulation in stress and anxiety disorders. The most common behavioral approach to treating stress and anxiety disorders is based on the principles of fear extinction learning, that of exposure therapy. Many individuals don't respond well to this therapeutic approach, however, and why some individuals respond favorably to exposure-based therapies, and others don't, is not well understood. This thesis seeks to consider how developmental and individual differences influence the capacity to regulate fear, as well as to test a behavioral method that leads to enhanced fear regulation (i.e., attenuation of fear memory). Chapter 1 provides an overview of the relevant humans and rodent literatures on individual and developmental differences in cued-fear regulation. Chapter 2 presents the first evidence for adolescent-specific diminished cued-fear extinction learning in humans, paralleling results previously observed only in rodents. In Chapter 3, a common single nucleotide polymorphism in fatty acid amide hydrolase (FAAH), encoding an enzyme that plays an important role in the endocannabinoid system, is highlighted for its role in altering cued- fear extinction learning. Chapter 4 tests a novel behavioral method for enhancing cued-?fear regulation based on the principles of memory reconsolidation in adolescent and adult humans. Collectively, these studies point to markers that could potentially be used to identify patients for whom exposure therapy may not be effective and suggests an alternative approach that could lead to more efficacious treatments for these individuals.