The jury is still out on the extent to which severe stress in the form of CA has true negative sequelae on the development of memory and its function. Thus far, research has shown that children who have been abused perform as well as other children on basic memory tasks (Howe, Cicchetti, et al., 2006, Howe, Toth, et al., 2006). Global brain-volume differences that have been observed also have not been associated with differences in children's memory performance (De Bellis & Thomas, 2003). However, a growing body of evidence from adult studies suggests that memory deficits do exist for individuals with abuse histories, and that these deficiencies are related to neuroanatomical anomalies. One explanation for this discrepancy is that the effects of CA on neurodevelopment and the development of memory are delayed and become unmasked at a later point in maturation. Longitudinal studies would allow investigators to test this hypothesis by evaluating, over several time points, children who have been abused. Ornstein et al. (2004) cogently argued that such a study design is warranted to ascertain the mechanisms that drive the development of memory. Of course, this developmental approach to memory testing would necessitate that comprehensive, reliable, and valid measures be available for use that are developmentally sensitive as well.

Sex differences is another area that has been ignored in this line of research. For example, because the vast majority of patients diagnosed with BPD are women, the reported memory findings in BPD remain unclear as to whether the effects are specific to women. We believe that manifest sex-related differences in memory function stem from the interaction of three factors: (1) sex differences in the nature of adverse early experience, (2) sexually dimorphic effects of early experience on brain development, and (3) sex differences in brain laterality and hormonal milieu (Teicher, Feldman, et al., 2002). For instance, our findings that sexual abuse is associated with diminished corpus callosum size in girls, while diminished corpus callosum size in boys is associated with neglect (Teicher et al., 2004), underscore the possibility that memory abilities that rely on interhemispheric neurotransmission may be adversely affected differentially across sex.

Lastly, we strongly side with those investigators who take a develop-mentally grounded, hypothetico-deductive approach toward CA research. Such an approach is imperative to provide a logical, comprehensive, and structured framework for conducting studies that are both developmen-tally and clinically meaningful. One such example comes from Howe and colleagues (Howe, Cicchetti, et al., 2006, Howe, Toth, et al., 2006), who have proposed that retrieval, rather than encoding, storage/consolidation, and retention, is deficient in individuals with abuse histories and that memory processes differ only in how the information is semantically organized. Nelson and Carver (1998) hypothesized that deficient long-term potentiation is the mechanism whereby the development of the explicit memory system is impacted by exposure to high levels of cortisol. We provided above a neurobioevolutional model as to how CA might influence the development of memory and its neurobiology. Future models will be enhanced by incorporating the "gene-environment interplay" notions delineated by Rutter and colleagues (2006). For instance, evidence indicates that polymorphism of the monoamine oxidase A (MAOA) gene moderates the development of antisocial behavior after exposure to physical abuse and that this relationship is more robust in males with the genotype conferring low versus high MAOA activity (Kim-Cohen et al., 2006). Given such findings, one speculation is that CA effects on the expression of certain genes might lead to the types of memory impairments that have been documented in the literature. To conclude, this subject is "ripe for the pickin' "—how well we decipher the short- and long-term effects of CA on memory is in our hands.

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