The vulnerability to coaching across measures of malingering

Neuropsychologists are increasingly called upon to conduct evaluations with individuals involved in personal injury litigation. While the inclusion of malingering measures within a test battery may help clinicians determine whether a client has put forth full effort, attorney coaching may allow dishonest clients to circumvent these efforts. The purpose of this study was to determine the degree to which frequently used measures of effort are susceptible to coaching as well as to explore and classify strategies undertaken by coached analogue malingerers. Additionally, potential improvements in the external validity of the simulation design were explored

Are we honestly studying malingering?: a profile and comparison of simulated suspected malingerers

Malingering research typically uses analog simulation designs or the differential prevalence design among real patients. Both have been criticized for methodological limitations in external and internal validity, respectively. Samples of simulated malingerers were compared to suspected malingerers to examine generalizability of analog findings. Overall results support the use of simulation designs. Furthermore, it was demonstrated that stringent selection of suspected malingerers maintains internal validity of the differential prevalence design. A second focus, to determine if demographic matching of simulated malingerers is necessary, showed that matching on age and race is not necessary

D-β-Hydroxybutyrate Is Protective in Mouse Models of Huntington's Disease

Abnormalities in mitochondrial function and epigenetic regulation are thought to be instrumental in Huntington's disease (HD), a fatal genetic disorder caused by an expanded polyglutamine track in the protein huntingtin. Given the lack of effective therapies for HD, we sought to assess the neuroprotective properties of the mitochondrial energizing ketone body, D-β-hydroxybutyrate (DβHB), in the 3-nitropropionic acid (3-NP) toxic and the R6/2 genetic model of HD. In mice treated with 3-NP, a complex II inhibitor, infusion of DβHB attenuates motor deficits, striatal lesions, and microgliosis in this model of toxin induced-striatal neurodegeneration. In transgenic R6/2 mice, infusion of DβHB extends life span, attenuates motor deficits, and prevents striatal histone deacetylation. In PC12 cells with inducible expression of mutant huntingtin protein, we further demonstrate that DβHB prevents histone deacetylation via a mechanism independent of its mitochondrial effects and independent of histone deacetylase inhibition. These pre-clinical findings suggest that by simultaneously targeting the mitochondrial and the epigenetic abnormalities associated with mutant huntingtin, DβHB may be a valuable therapeutic agent for HD