Cue-utilization in the imagination inflation effect paradigm in older adults with mild cognitive impairment.

OBJECTIVE: We investigated the imagination inflation effect in healthy older adults and older adults with mild cognitive impairment (MCI) to determine whether an intervention can reduce susceptibility to these distortions, with implications for daily functioning. METHOD: Fifty-seven older adults aged 69-90 participated. In Session 1, participants either: listened to an action statement being read, performed the action, or imagined performing the action. Actions were either functional (encountered actions of daily life; e.g., "fill the pillbox") or nonfunctional (not routinely encountered; e.g., "put the toy duck on a plate"). During Session 2, participants imagined action statements from the first session. In Session 3, participants were asked to determine whether action statements were performed during the first session. Intervention participants were instructed before the first and third sessions to attend various sensory aspects of their experience using a cue-utilization technique. RESULTS: Memory was worse for functional compared to nonfunctional actions. For older adults with MCI, the intervention increased correct identifications of functional actions that were performed. For healthy older adults, the intervention increased source memory of functional actions that were imagined. The intervention did not impact the accuracy of nonfunctional actions or the rates of misremembering an action as having been performed. CONCLUSIONS: These initial findings supported the efficacy of a cue-utilization intervention to improve memory for functional actions in an imagination inflation effect paradigm in community-dwelling older adults. The use of such strategies represents an important first step in designing interventions that are applicable to daily life. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

The Rey 15-Item Memory Test in US veterans.

INTRODUCTION: The Rey 15-item Test is a public-domain, memory-based performance validity test, frequently used in clinical settings. Various efforts have been made to modify the test to make it more sensitive and more robust to effects of lower education and intelligence. The most promising of these is the addition of a recognition trial to the existing free recall paradigm. METHOD: The present study explored the use of the Rey-15 + Recognition Trial in a sample of 155 younger U.S. military veterans seen for evaluation of mild traumatic brain injury or attention deficit hyperactivity disorder (50 cases classified as invalid, 105 classified as valid). RESULTS: Optimal classification accuracy was obtained on the Combination index (cutoff ≤23, sensitivity = 50%, specificity = 95%) and the Recognition Hits score (cutoff ≤11, sensitivity = 52%, specificity = 93%). The Free Recall score had somewhat lower sensitivity when a similar 95% specificity threshold was set (cutoff ≤11, 38% sensitivity). A qualitative error score used in previous studies did not improve classification accuracy. CONCLUSIONS: The Rey-15 + Recognition Trial proved to be effective, with particular advantage bestowed by the recognition trial. Implications of these findings in the context of the study's clinical sample of military veterans and in the broader literature are discussed.

Cognitive Impairment and Predicting Response to Treatment in an Intensive Clinical Program for Post-9/11 Veterans With Posttraumatic Stress Disorder.

OBJECTIVE: This study examined whether objectively measured pretreatment cognitive impairment predicted worse response to treatment for posttraumatic stress disorder. Participants were 113 veterans and active duty service members who participated in a new multidisciplinary 2-week intensive clinical program that included individual trauma-focused cognitive-behavioral therapy, group psychotherapy, psychoeducation, skills-building groups, and complementary and alternative medicine treatments (mean age: 39.7 years [SD=8.5]; 20% women). METHODS: Prior to treatment, participants completed a brief computerized cognitive battery (CNS Vital Signs) and were operationalized as having cognitive impairment if they scored in the ≤5th percentile on two or more of five core cognitive domains. Participants completed measures of traumatic stress, depression, cognitive self-efficacy, and satisfaction with their ability to participate in social roles before and after treatment. RESULTS: There were no significant correlations between pretreatment individual cognitive test scores and change in the clinical outcome measures. One-half of the study sample (49.6%) met criteria for cognitive impairment. In a mixed multivariate analysis of variance, the interaction between cognitive impairment and time was not significant (F=0.83, df=4, 108, p=0.51), indicating that the pre- to posttreatment changes in outcome scores were not significantly different for the cognitively impaired group compared with the cognitively intact group. The multivariate main effect for time was significant (F=36.75, df=4, 108, p<0.001). Follow-up univariate tests revealed significant improvement in traumatic stress, depression, cognitive self-efficacy, and satisfaction with social roles after treatment. CONCLUSIONS: Cognitive impairment was not associated with worse response to treatment in veterans with severe and complex mental health problems. Veterans with and without cognitive impairment reported large improvements in symptoms and functioning after treatment.

The Aging Well through Interaction and Scientific Education (AgeWISE) Program.

OBJECTIVE: We conducted a randomized controlled trial of the Aging Well through Interaction and Scientific Education (AgeWISE) program, a 12-week manualized cognitive rehabilitation program designed to provide psychoeducation to older adults about the aging brain, lifestyle factors associated with successful brain aging, and strategies to compensate for age related cognitive decline. METHODS: Forty-nine cognitively intact participants ≥ 60 years old were randomly assigned to the AgeWISE program (n = 25) or a no-treatment control group (n = 24). Questionnaire data were collected prior to group assignment and post intervention. Two-factor repeated-measures analyses of covariance (ANCOVAs) were used to compare group outcomes. RESULTS: Upon completion, participants in the AgeWISE program reported increases in memory contentment and their sense of control in improving memory; no significant changes were observed in the control group. Surprisingly, participation in the group was not associated with significant changes in knowledge of memory aging, perception of memory ability, or greater use of strategies. CONCLUSIONS: The AgeWISE program was successfully implemented and increased participants' memory contentment and their sense of control in improving memory in advancing age. CLINICAL IMPLICATIONS: This study supports the use of AgeWISE to improve perspectives on healthy cognitive aging.

Performance validity and processing speed in a VA Polytrauma sample.

OBJECTIVE: While recognition memory has been the primary tool for the assessment of performance validity in neuropsychological evaluations, some consideration has also been given to embedded measures from other cognitive domains, including processing speed. The present study evaluated the classification accuracy of several speed-based measures in a Veterans Affairs Medical Center Polytrauma sample. METHOD: The present sample consisted of 114 military veterans (Mean age = 35.5, SD = 9.4) referred for a suspected history of mild traumatic brain injury who were administered a full neuropsychological protocol that included several validity checks. Veterans were assigned to Valid (n = 80) or Invalid (n = 34) groups based on outcomes of performance validity measures (PVMs). RESULTS: Several processing speed measures yielded acceptable or excellent classification accuracy; sensitivity values ranged from 29 to 53% with specificity values above 90%. Efforts to identify an improved algorithm that would collapse across multiple processing speed PVMs were unsuccessful compared to classification based on single measures. CONCLUSIONS: Processing speed measures can serve as efficient performance validity assessment tools.

Orexin receptor 2 expression in the posterior hypothalamus rescues sleepiness in narcoleptic mice.

Narcolepsy is caused by a loss of orexin/hypocretin signaling, resulting in chronic sleepiness, fragmented non-rapid eye movement sleep, and cataplexy. To identify the neuronal circuits underlying narcolepsy, we produced a mouse model in which a loxP-flanked gene cassette disrupts production of the orexin receptor type 2 (OX2R; also known as HCRTR2), but normal OX2R expression can be restored by Cre recombinase. Mice lacking OX2R signaling had poor maintenance of wakefulness indicative of sleepiness and fragmented sleep and lacked any electrophysiological response to orexin-A in the wake-promoting neurons of the tuberomammillary nucleus. These defects were completely recovered by crossing them with mice that express Cre in the female germline, thus globally deleting the transcription-disrupter cassette. Then, by using an adeno-associated viral vector coding for Cre recombinase, we found that focal restoration of OX2R in neurons of the tuberomammillary nucleus and adjacent parts of the posterior hypothalamus completely rescued the sleepiness of these mice, but their fragmented sleep was unimproved. These observations demonstrate that the tuberomammillary region plays an essential role in the wake-promoting effects of orexins, but orexins must stabilize sleep through other targets.

Do enteric neurons make hypocretin?

Hypocretins (orexins) are wake-promoting neuropeptides produced by hypothalamic neurons. These hypocretin-producing cells are lost in people with narcolepsy, possibly due to an autoimmune attack. Prior studies described hypocretin neurons in the enteric nervous system, and these cells could be an additional target of an autoimmune process. We sought to determine whether enteric hypocretin neurons are lost in narcoleptic subjects. Even though we tried several methods (including whole mounts, sectioned tissue, pre-treatment of mice with colchicine, and the use of various primary antisera), we could not identify hypocretin-producing cells in enteric nervous tissue collected from mice or normal human subjects. These results raise doubts about whether enteric neurons produce hypocretin.