Mild Cognitive Decline Is a Risk Factor for Scam Vulnerability in Older Adults

Research on elderly financial exploitation has mostly focused on financial abuse that occurs in families and other types of trusted relationships. As such, little is known about financial frauds and scams perpetrated by strangers. Financial fraud and scam prevention activities for older adults must be promoted, for which the correlation between the psychological, social, and cognitive characteristics of their vulnerability needs to be determined. The present study aimed to determine whether cognitive decline is a risk factor for scam vulnerability in older adults. Thus, we created a scam vulnerability scale for older adults with cognitive decline and analyzed the data to reveal the correlation between them, including inhibition and executive function. We conducted an interview survey with 50 older adults with cognitive decline (average age: 79.42 years, SD: 5.44) and 51 older adults without cognitive decline (average age: 76.12 years, SD: 5.82). The interview survey included the scam vulnerability scale, psychosocial questionnaires, and neuropsychological tests. The scale included six items with a four-point Likert scale based on a previous study. Hierarchical multiple regression analysis revealed that lower scores on the Japanese version of the Alzheimer's Disease Assessment Scale–Cognitive Subscale (ADAS-Jcog; indicating higher general cognitive function) correlated with higher scam vulnerability in the cognitive decline group (β = −0.46, p < 0.001). In addition, men were found to be more vulnerable in both groups (cognitive decline group: β = −0.29, p = 0.015, cognitive non-decline group; β = −0.32, p = 0.018). Inhibition and executive function were found not to correlate significantly with scam vulnerability. These results suggest that mild cognitive decline correlates with higher scam vulnerability, whereas moderate to severe cognitive decline correlates with lower vulnerability, possibly because it makes understanding the scam attempt itself difficult. Older adults with mild cognitive decline and their families, particularly those visiting elderly care or outpatient facilities, should be notified of the scam vulnerability of older clients using the ADAS-Jcog score as an index to help them avoid victimization.

Evaluation of the Brain Function State During Mild Cognitive Impairment Based on Weighted Multiple Multiscale Entropy

The mild cognitive impairment (MCI) stage plays an essential role in preventing the progression of older adults to Alzheimer's disease. In this study, neurofeedback training (NFT) is applied to improve MCI brain cognitive function. To assess the improvement effect, a novel algorithm called Weighted Multiple Multiscale Entropy (WMMSE) is proposed to extract and analyze the electroencephalogram (EEG) features of patients with MCI. To overcome the information loss problem of traditional multiscale entropy (MSE), WMMSE fully considered the correlation of the sequence and the contribution of each sequence to the total entropy. The experimental group composed of 39 patients with MCI was subjected to NFT for 10 days during two sessions. The control group included 21 patients with MCI without any intervention. The Lempel-Ziv complexity (LZC) was used for primary assessment, and WMMSE was used to accurately analyze the effect of NFT. The results show that the WMMSE values of F4, C3, C4, O1, and T5 channels post-NFT are higher compared with pre-NFT and significant differences (P < 0.05). Moreover, the cognitive subscale of the Montreal Cognitive Assessment (MoCA) results shows that the post-NFT score is higher than the pre-NFT in the vast majority of the patients with MCI and significant differences (P < 0.05). When compared with the control group, the WMMSE values of the experimental group increased in each channel. Therefore, the NFT intervention method contributes to brain cognitive functional recovery, and WMMSE can be used as a biomarker to evaluate the state of MCI brain cognitive function.

The influence of anxiety sensitivity on mindfulness

Although many individuals who engage in mindfulness endorse less anxiety, others experience heightened anxiety when focusing on particular sensations. This study aimed to determine whether specific mindfulness items related to observing internally or externally differ in individuals with panic disorder (PD) or elevated anxiety sensitivity (AS). We examined a clinical sample of 1521 Japanese individuals who completed online self-report questionnaires. Several multiple indicator multiple cause (MIMIC) models investigated differential item functioning among the items in the Observe facet of the Five Facet Mindfulness Questionnaire (FFMQ), based on PD and/or AS. This process was repeated to examine the relationship between the Anxiety Sensitivity Index-3 (ASI-3) subscales and particular items of the Observe facet. Increased AS correlated with increased observing generally, and increased AS was associated with greater scores on observing internal items and lower scores on external items. When PD and AS were analyzed simultaneously, only AS remained significant. The cognitive subscale showed the same pattern of results as the total ASI-3 subscale. We conclude that AS modulates the mindfulness experience.

293 Predictive utility of a brief scale to identify U.S. Army Soldiers who are genetically vulnerable and resilient to sleep loss

Introduction Sleep loss that is inherent to military operations can lead to cognitive errors and potential mission failure. Single Nucleotide Polymorphisms (SNPs) allele variations of several genes (COMT, ADORA2A, TNFa, CLOCK, DAT1) have been linked with inter-individual cognitive resilience to sleep loss through various mechanisms. U.S. Army Soldiers with resilience-related alleles may be better-suited to perform cognitively-arduous duties under conditions of sleep loss than those without these alleles. However, military-wide genetic screening is costly, arduous, and infeasible. This study tested whether a brief survey of subjective resilience to sleep loss (1) can demarcate soldiers with and without resilience-related alleles, and, if so, (2) can predict cognitive performance under conditions of sleep loss. Methods Six SNPs from the aforementioned genes were sequenced from 75 male U.S. Army special operations Soldiers (age 25.7±4.1). Psychomotor vigilance, response inhibition, and decision-making were tested after a night of mission-driven total sleep deprivation. The Iowa Resilience to Sleeplessness Test (iREST) Cognitive Subscale, which measures subjective cognitive resilience to sleep loss, was administered after a week of recovery sleep. A receiver operating characteristic (ROC) curve was used to determine whether the iREST Cognitive Subscale can discriminate between gene carriers, and a cutoff score was determined. Cognitive performance after sleep deprivation was compared between those below/above the cutoff score using t-tests or Mann-Whitney U tests. Results The iREST discriminated between allele variations for COMT (ROC=.65,SE=.07,p=.03), with an optimal cutoff score of 3.03 out of 5, with 90% sensitivity and 51.4% specificity. Soldiers below the cutoff score had significantly poorer for psychomotor vigilance reaction time (t=-2.39,p=.02), response inhibition errors of commission (U=155.00,W=246.00,p=.04), and decision-making reaction time (t=2.13,p=.04) than Soldiers above the cutoff score. Conclusion The iREST Cognitive Subscale can discriminate between those with and without specific vulnerability/resilience-related genotypes. If these findings are replicated, the iREST Cognitive Subscale could be used to help military leaders make decisions about proper personnel placement when sleep loss is unavoidable. This would likely result in increased safety and improved performance during military missions. Support (if any) Support for this study came from the Military Operational Medicine Research Program of the United States Army Medical Research and Development Command.

326 Comparison of Psychological and Physiological Features Between Insomnia Patients with Short and Normal Objective Sleep Duration

Introduction Objective sleep duration has been suggested to be a novel biomarker in the phenotyping of insomnia (Vgontzas & Fernandez-Mendoza, 2013). It was hypothesized that insomnia phenotype with PSG-defined short sleep duration (< 6 hours) is associated with physiological hyperarousal, while the phenotype with normal sleep duration (≥ 6 hours), is associated with anxious-ruminative psychological profile and poor resources for coping with stress. The aim of this study was to assess whether these two insomnia phenotypes differ in terms of self-reported psychological and physiological features. Methods A total 45 (mean age=36.6, female=76%) insomnia patients underwent a polysomnographic evaluation, completed several self-rating scales (include ISI, BAI, BDI, FIRST, DBAS, and PSAS), and were split into two groups base on their objective sleep duration (cut-off 6 hours). Results When compared to the short sleep group using independent sample t-test, the normal sleep group showed a significant higher mean score on FIRST (t= -2.13; p< .05). The short sleep group showed non-significant trends to have higher mean scores on BDI and BAI. The scores on the other scales showed no significant differences between the two groups. The FIRST score correlated positively with the score of DBAS (r= 0.32; p< .05) and the total (r= 0.36; p< .05) and cognitive-subscale scores (r= 0.41; p< .01) on PSAS. The BAI score correlated positively with the score of the total (r= 0.53; p< .001) and somatic subscale (r= 0.59; p< .001) on PSAS. Conclusion These results support the hypotheses that the normal sleep phenotype tends to be more vulnerable to the impact of stress, especially on sleep, due to pre-sleep cognitive hyperarousal. Since the BAI scale contains more items regarding physiological symptoms of anxiety disorders, the tendency of higher BAI score in short sleep group may indicate that the short sleep phenotype has higher physiological arousal, which supports the phenotyping model proposed by Vgontzas and Fernandez-Mandoza. Support (if any):

Effects of Cariprazine on Cognition in Patients With Bipolar Mania or Mixed States: Post Hoc Analysis From 3 Randomized, Controlled Phase III Studies

IntroductionCariprazine, a dopamine D3-preferring D3/D2 and serotonin 5-HT1A receptor partial agonist, is approved for the treatment of schizophrenia and for depressive, manic, or mixed episodes associated with bipolar I disorder. Previous post hoc analyses have demonstrated that cariprazine was effective versus placebo for improving cognitive symptoms in patients with schizophrenia or bipolar depression. This post hoc analysis evaluated the effects of cariprazine on cognitive symptoms in patients with acute manic or mixed bipolar episodes.MethodsData from 3 phase II/III, randomized, double-blind, placebo-controlled studies in patients with manic or mixed episodes associated with bipolar I disorder (NCT00488618, NCT01058096, NCT01058668) were pooled and analyzed. Patients were randomized to placebo or flexibly dosed cariprazine (3-12 mg/d, 3-6 mg/d, or 6-12 mg/d [1 study only]) for 3 weeks of double-blind treatment; all dose groups were combined for the pooled analysis. Cognitive symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS) Cognitive subscale (sum of PANSS items P2, N5, N7, G10, G11); a score of 15 or greater at baseline indicated the presence of cognitive symptoms. Mean changes from baseline to week 3 in PANSS cognitive subscale/item scores and Young Mania Rating Scale (YMRS) total score were evaluated in the overall intent-to-treat (ITT) population and in the subgroup of patients with baseline cognitive symptoms. A mixed-effects model for repeated measures (MMRM) was used to impute missing values.ResultsOf the 1012 patients in the ITT population, 174 (placebo=71; cariprazine=103) had a PANSS Cognitive subscale score of 15 or greater at baseline. At week 3, the cariprazine group demonstrated significantly greater mean improvement than the placebo group on PANSS cognitive subscale scores in both the ITT population (−2.2 vs −1.3; P<.0001) and the subgroup with baseline cognitive symptoms (−4.0 vs −1.9; P=.0002). In patients with baseline cognitive symptoms, improvement was significantly greater for cariprazine- versus placebo-treated patients on YMRS total score (−16.7 vs −8.2; P<.0001) and the individual PANSS cognitive subscale items of conceptual disorganization (−1.1 vs −0.5; P=.0004), difficulty in abstract thinking (−0.8 vs −0.3; P=.0044), stereotyped thinking (−0.3 vs −0.1; P=.0350), and poor attention (−1.1 vs −0.6; P=.0043).ConclusionIn patients with manic or mixed episodes associated with bipolar I disorder, cariprazine versus placebo was effective in improving cognitive symptoms in the overall patient population as well as in patients with baseline cognitive symptoms. In addition, cariprazine versus placebo also demonstrated efficacy in improving manic symptoms in patients with baseline cognitive symptoms. These results suggest that cariprazine may provide benefits for the treatment of cognitive symptoms in patients with bipolar I mania.FundingAbbVie Inc.

Disease progression modelling from preclinical Alzheimer’s disease (AD) to AD dementia

To characterize the course of Alzheimer’s disease (AD) over a longer time interval, we aimed to construct a disease course model for the entire span of the disease using two separate cohorts ranging from preclinical AD to AD dementia. We modelled the progression course of 436 patients with AD continuum and investigated the effects of apolipoprotein E ε4 (APOE ε4) and sex on disease progression. To develop a model of progression from preclinical AD to AD dementia, we estimated Alzheimer’s Disease Assessment Scale-Cognitive Subscale 13 (ADAS-cog 13) scores. When calculated as the median of ADAS-cog 13 scores for each cohort, the estimated time from preclinical AD to MCI due to AD was 7.8 years and preclinical AD to AD dementia was 15.2 years. ADAS-cog 13 scores deteriorated most rapidly in women APOE ε4 carriers and most slowly in men APOE ε4 non-carriers (p < 0.001). Our results suggest that disease progression modelling from preclinical AD to AD dementia may help clinicians to estimate where patients are in the disease course and provide information on variation in the disease course by sex and APOE ε4 status.