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Conclusions 465The above model assumes that adolescence is a risk period for the emergenceof mood disorder because the neural circuits that subserve socioemotional reactionscome “online” following puberty. In other words, a normal neuromaturationalprocess, interacting with environmental factors, sets the stage for the expressionof anxiety and depression. Focusing on the cognitive manifestations of adolescentbrain development, Lauren Alloy and Lyn Abramson (chapter 13) make thisassumption in their biocognitive vulnerability-transactional stress model of depression,and posit that growth in cognitive competence during adolescence canset the stage for cognitive vulnerability to depression.Other contributors to this volume make similar assumptions about adolescentonsetsubstance abuse (O’Brien, chapter 17), interpersonal problems (Tucker &Moller, chapter 4), and conduct problems (Greenberg, Riggs, & Blair, chapter 20).Along the same lines, in chapter 1, Linda Spear reviews evidence to suggest thatadolescence is a period of increased risk taking and stress sensitivity because neuralpathways that subserve responses to both reward and stress are undergoing maturation.For this reason, the postpubertal developmental period is associated withheightened risk for sensation-seeking behaviors, such as substance abuse.Abnormal Adolescent Brain DevelopmentIn contrast to the focus on normative processes, some models posit that, for certaindisorders, adolescence is a period of increased risk when neuromaturationalprocesses go awry. Again, Sowell, Thompson, and Toga (chapter 3) elegantlydescribe several adolescent neuromaturational processes that could deviate, innature or timing, from the normal trajectory. The notion of adolescent neuromaturationalabnormalities has played a central role in the literature on psychoticdisorders. Several authors have suggested that disturbances in the processes associatedwith normal adolescent brain maturation may be associated with schizophrenia.Other authors have pointed out that some of the neural processes occurringduring adolescence involve a reduction in neuronal interconnections, referred toas synaptic pruning, which is presumed to make brain function more efficient.Based on this evidence, it has been suggested that the prodromal signs of schizophreniatend to have their origins during adolescence because the pruning processexceeds normal levels and results in an aberrant pattern of interconnectionsthat disrupts brain function (Keshavan & Hogarty, 1999).The Interaction Between Constitutional Vulnerabilityand Adolescent Brain MaturationOf course, many disorders that typically begin in adolescence are known to be linkedwith earlier indicators of behavioral dysfunction. Retrospective and prospectivestudies have shown that individuals who succumb to affective and psychotic disordersin late adolescence/young adulthood often manifest developmental delays andbehavioral problems in early childhood. These abnormalities are apparent in the