It has been known for over 40 years that there are two fundamentally different kinds of detection tasks in the theory of signal detectability. The Type 1 task is to distinguish between events defined independently of the observer; the Type 2 task is to distinguish between one's own correct and incorrect decisions about those Type 1 events. For the Type 1 task, the behavior of the detector can be summarized by the traditional receiver operating characteristic (ROC) curve. This curve can be compared with a theoretical ROC curve, which can be generated from overlapping probability functions conditional on the Type 1 events on an appropriate decision axis. We show how to derive the probability functions underlying Type 2 decisions from those for the Type 1 task. ROC curves and the usual measures of performance are readily obtained from those Type 2 functions, and some relationships among various Type 1 and Type 2 performance measures are presented. We discuss the relationship between Type 1 and Type 2 confidence ratings and caution against the practice of presenting transformed Type 2 ratings as empirical Type 1 ratings.

The authors review the literature on the 2 main models of the placebo effect: expectancy theory and classical conditioning. A path is suggested to dissolving the theoretical impasse that has long plagued this issue. The key is to make a clear distinction between 2 questions: What factors shape placebo effects? and What learning mediates the placebo effect? The reviewed literature suggests that classical conditioning procedures are one shaping factor but that verbal information can also shape placebo effects. The literature also suggests that conditioning procedures and other sources of information sometimes shape conscious expectancies and that these expectancies mediate some placebo effects; however, in other cases conditioning procedures appear to shape placebo effects that are not mediated by conscious cognition.

DHA supplementation improved memory and the RT of memory in healthy, young adults whose habitual diets were low in DHA. The response was modulated by sex. This trial was registered at the New Zealand Clinical Trials Registry (http://www.anzctr.org.au/default.aspx) as ACTRN12610000212055.

In the present study, we investigated age-related decline in face recognition memory and whether this decline is moderated by the age of the target faces and by the number of faces that the participant must learn (memory load). Thirty-two participants in each of three age groups (18-39 years, 60-75 years, and 76-96 years) completed a face recognition task. Signal detection analyses confirmed that face recognition accuracy declined with age. However, this finding was qualified by an interaction between participant age and target age, which revealed that the age-related decline in face recognition accuracy occurred only for young target faces. Increased memory load was associated with comparable performance decrements across all age groups. However, memory load appears not to be the cause of these decrements. Instead, they appear to be a product of recognition load (the number of stimuli presented in the recognition phase).

Contrary findings notwithstanding, the prevailing notion is that recognition memory is little affected by Parkinson's disease (PD). Both a power analysis and a meta-analysis were conducted to help clarify the degree of recognition memory deficit associated with PD. The power analysis confirmed that, in general, memory studies of PD participants have been underpowered. This analysis indicated the need to pool study results in a subsequent meta-analysis, the main finding of which was that recognition memory deficits do occur with PD. The largest deficit occurs in PD participants with dementia. Nevertheless, deficits also occur in PD participants without dementia on medication, but nondopaminergic central nervous system abnormalities are more likely to underlie this deficit than PD medication itself. Future development of a theory of cognitive dysfunction in PD should take into account these recognition memory deficits, which may increase with disease progression.