Differences In Cognitive Changes Research Articles

Cognitive function in patients with HR+ advanced breast cancer treated with endocrine therapy with or without CDK4/6 inhibitors in the SONIA trial.

1016 Background: Given the important role of estrogen in normal neuronal function, endocrine treatment for breast cancer may adversely affect cognition, including memory, planning and attention. Previous studies showed mixed results but were often underpowered. It is unknown whether CDK4/6 inhibitors have cognitive side effects. SONIA-EfFECT is a side-study of the SONIA trial that investigates cognitive functioning in HR+ advanced breast cancer patients treated with endocrine therapy with or without CDK4/6 inhibitors. Methods: Patients randomized in the SONIA trial to receive first-line treatment with aromatase inhibitors with (Arm A) or without (Arm B) CDK4/6 inhibition were approached to participate in the SONIA-EfFECT side-study. Patients were asked to identify a female relative or friend without cancer to serve as a cancer-free control. Both patients and controls were asked to complete the Amsterdam Cognition Scan, an online neuropsychological test battery, at baseline and after 9 months. Patients who switched to second-line treatment within nine months were not retested. To prevent confounding effects of imbalance in age, education, and computer use between patient groups and controls, propensity score matching was performed. Baseline cognitive function was assessed by converting raw test scores to standardized Z-scores adjusted for computer use, based on baseline performance in the matched control group. To investigate the effect of endocrine therapy ±CDK4/6 inhibitors over time, standardized regression-based change scores were computed based on baseline and follow-up performance in the matched control group. One-way analyses of variance were conducted to compare baseline performance and cognitive change between the two arms and the matched control group. Results: 260 patients (130 Arm A/130 Arm B) and 196 controls completed baseline assessments. A matched sample of 130 controls was selected. 199 patients (108 Arm A/91 Arm B) and 119 matched controls had complete follow-up assessments. Patients in both study arms performed significantly worse than the controls on the domains of verbal memory, working memory, processing speed, executive function, and motor function. In both patient arms and the controls, standardized regression-based change scores showed limited decline in cognitive function over the 9-month interval. Moreover, minimal differences in cognitive change were observed between the patients treated with and without CDK4/6 inhibitors, and between patients and the controls. Conclusions: HR+ advanced breast cancer patients show worse cognitive function on all cognitive domains compared to a control group without cancer. Nine months of treatment with endocrine therapy with or without CDK4/6 inhibitors does not further worsen cognitive function in this study. Clinical trial information: NCT03425838 .

Estimation of Differences in Work Attitudes by National Character from Psychological Change Points

More and more foreign workers work in Japan year by year. However, there is a problem that a few foreign workers keep working in Japan. One of the reasons is the work attitudes of foreign workers is different from those of Japanese companies. Japanese companies want to fully understand their work attitudes so that they can develop foreign workers’ human resources appropriately. This study proposes a method for estimating the differences in the work attitudes from physiological characteristics during video watching. The method uses videos to collect psychological change points during the viewing. Pupil diameter is measured to estimate cognitive change while EDA is measured to estimate emotional change. Change points are detected from time series of the physiological characteristics to know the scene causing the changes. The work attitudes are also examined from questionnaires. An experiment reveals differences in cognitive change indicating that Japanese and Vietnamese have different views on work. It also showed that Japanese and Vietnamese have different attitudes towards work difficulties and responsibilities. Differences in emotional change indicated that Japanese and Vietnamese differ in the factors that cause emotional change. The findings can be used for human resource development to assign suitable work to foreign workers.

THE RELATIONSHIP OF COGNITIVE CONTROL BELIEFS TO 10 YEAR CHANGES IN COGNITIVE PERFORMANCE

Abstract Past work has shown that older adults who believe they have control over their cognitive performance (i.e., higher cognitive control beliefs) have better cognitive performance than those with lower cognitive control beliefs. However, it is unclear whether cognitive control beliefs are related to individual differences in cognitive change among middle-aged and older adults. The current study examined longitudinal associations between cognitive control beliefs and 10-year cognitive changes using data from waves 2 and 3 of the Midlife in the United States study (MIDUS; N=2,509, Ages 33 to 83 at wave 2). We predicted that higher baseline cognitive control beliefs would be related to greater maintenance of episodic memory and executive functioning over 10 years. Age was tested as a moderator of these relationships and each analysis controlled for baseline performance, age, sex, education, and self-rated physical health. Multiple linear regression models revealed that higher baseline control beliefs were related to less decline in episodic memory (p<.001) and executive functioning (p<.05); however, age did not moderate these relationships. Taken together, these results suggest that across age, cognitive control beliefs are associated with greater maintenance of episodic memory and executive functioning over 10 years in middle-aged and older adults. As such, cognitive control beliefs may represent a promising modifiable mechanism to help minimize cognitive declines starting in midlife.

Depression symptoms and cognition in multiple sclerosis: Longitudinal evidence of a specific link to executive control

Background: Depression symptoms are prevalent in multiple sclerosis (MS) and associated with poorer cognition in cross-sectional studies; it is unknown whether changes in depression symptoms track with cognitive changes longitudinally. Objective: Investigate whether changes in depression symptoms correspond with cognitive changes over time in MS, and identify specific cognitive functions related to depression symptoms. Method: Persons with early relapse-onset MS (n = 165) completed a depression questionnaire (Beck Depression Inventory FastScreen) and tests of cognitive speed, executive control, and memory at baseline and 3-year follow-up. One-way ANOVAs assessed differences in cognitive change across participants with worsened, stable, or improved depression symptoms from baseline to year 3. Results: Change in depression symptoms was related to change in executive control (p = 0.001, ηp2 = 0.08; worsened mood with worsened executive control; improved mood with improved executive control), even when adjusting for cognitive speed (p = 0.002, ηp2 = 0.08). There were no links to cognitive speed (p = 0.826) or memory (p = 0.243). Regarding individual depression symptoms, executive control was related to loss of pleasure and suicidal thoughts. Conclusions: Executive control tracks with depression symptoms, raising hope that management of mood may improve executive control. The specific link between executive control and anhedonia implicates dysfunctional reward processing as a key component of MS depression.

0885 Alzheimer’s disease progression risk in Cognitive Normal Older Adults with Obstructive Sleep Apnea using NIA-AA Research Framework

Abstract Introduction We determined risk profiles of strata-specific cognitive-normal (NL) older-adults with obstructive sleep apnea (OSA) characterized by their Aβ, P-Tau & T-tau (ATN) burden, on prospective AD stage-transition Methods Longitudinal study utilizing data from 167 community-dwelling NL older-adults participating in NYU studies on memory, sleep and aging. Subjects had baseline CSF AD-biomarker data and at least two follow-up clinical and neuropsychological data. OSA was defined using AHI4%. Using the NIA-AA Research Framework, data-driven, clinically relevant thresholds for CSF-Aβ42 (≤375pg/ml), P-tau (≥53.7pg/ml) and T-tau (≥367 pg/ml) indicated ATN status respectively. Twenty-four participants with suspected non-AD pathologic change defined as A-T+ were excluded leaving 143 for the analysis. Main outcome was AD stage-transition (i.e., change from Global Deterioration Scale (GDS) 1 or 2 [NL] at baseline to ≥3 [≥ MCI] during follow-up). Logistic mixed-effects models with random intercept and slope were used to assess associations between ATN characterized OSA subjects, and longitudinal AD stage transition, controlling for age-at-baseline, sex, APOE4-status, years-of-education, and their interactions with time. Results Of the 143 participants, 91 (63.8%) were women. The mean (SD) age was 69.6 (7.3) years and follow-up time was 4.73 (3.45) years. Sixteen (11.2%) were OSA+/A+/TN-, and 21 (14.7%) were OSA-/A+/TN-. Ninety-two (64.3%) had normal AD biomarkers (OSA+/A-/T- [n=45] and OSA-/A-/T- [N=47]). To generate strata-specific risks, subjects were combined into groups: (i) OSA subjects with AD pathologic change OSA+/A+/TN [n=25] consisting of OSA+/A+/TN+ [n=9] plus OSA+/A+/TN- [n=16] (ii) non-OSA subjects with AD pathologic change OSA-/A+/TN [n=26]) consisting of OSA-/A+/TN+ [n=5] and OSA-/A+/TN- [n=21] Fourteen subjects (9.8%) transitioned from NL to MCI (i.e., OSA+/A+/TN [6/25], OSA-/A+/TN [3/26], OSA+/A-/TN- [4/45] and OSA-/A-/TN- [3/47]). OSA+/A+/TN subjects were at higher risk of AD stage-transition relative to OSA-/A-/TN- (β = 1.31, 95%CI, 1.02, 1.62); OSA+/A-/TN- (β = 0.89, 95%CI, 0.42, 1.37); and OSA-/A+/TN subjects, (β = 0.71, 95%CI, 0.38, 1.04); P < .01 for all. OSA+/A-/T- vs. OSA-/A-/T- participants did not show differences in cognitive change over time (β = 0.22, 95%CI, -0.15, 0.39, P =.17). Conclusion Among ATN characterized NL older-adults with OSA, those with evidence of AD pathologic change have the greatest risk of developing AD. Support (if any) AASMBTS#231-BS-20, NIAK23AG068534A, AARG-D- 21-848397, BFFA2022033S

Journal Digest: CBT With Cardiac Rehab, PMDD Neurochemistry, and More

Journal Digest: CBT With Cardiac Rehab, PMDD Neurochemistry, and More

Dopaminergic medication normalizes aberrant cognitive control circuit signalling in Parkinson's disease.

Dopaminergic medication is widely used to alleviate motor symptoms of Parkinson's disease, but these medications also impact cognition with significant variability across patients. It is hypothesized that dopaminergic medication impacts cognition and working memory in Parkinson's disease by modulating frontoparietal-basal ganglia cognitive control circuits, but little is known about the underlying causal signalling mechanisms and their relation to individual differences in response to dopaminergic medication. Here we use a novel state-space computational model with ultra-fast (490 ms resolution) functional MRI to investigate dynamic causal signalling in frontoparietal-basal ganglia circuits associated with working memory in 44 Parkinson's disease patients ON and OFF dopaminergic medication, as well as matched 36 healthy controls. Our analysis revealed aberrant causal signalling in frontoparietal-basal ganglia circuits in Parkinson's disease patients OFF medication. Importantly, aberrant signalling was normalized by dopaminergic medication and a novel quantitative distance measure predicted individual differences in cognitive change associated with medication in Parkinson's disease patients. These findings were specific to causal signalling measures, as no such effects were detected with conventional non-causal connectivity measures. Our analysis also identified a specific frontoparietal causal signalling pathway from right middle frontal gyrus to right posterior parietal cortex that is impaired in Parkinson's disease. Unlike in healthy controls, the strength of causal interactions in this pathway did not increase with working memory load and the strength of load-dependent causal weights was not related to individual differences in working memory task performance in Parkinson's disease patients OFF medication. However, dopaminergic medication in Parkinson's disease patients reinstated the relation with working memory performance. Our findings provide new insights into aberrant causal brain circuit dynamics during working memory and identify mechanisms by which dopaminergic medication normalizes cognitive control circuits.

Sex Differences in the Relationship between Exercise and the Brain

IntroductionExercise is an effective, non‐pharmacological therapy to promote brain health. Sex differences in cognitive changes through the lifespan and in response to exercise training are documented, yet more information is needed to characterize these disparities. We hypothesized that aerobic exercise training would improve memory, coordination, and muscular strength in female rats and have no significant effect in male rats.MethodsThirty‐two Fisher 344 animals (16 males and 16 females) were housed 2 per cage, on a 12:12 light:dark cycle with food and water ad libitum. At two months old, following a 1‐week acclimatization period where the non‐compliant runners were identified, they were randomly assigned to sedentary or exercise training groups. Those in the exercise training group completed a 10 week treadmill training protocol. The protocol was administered during the animal’s dark cycle and began at 15 cm/s for 15 minutes and increased up to 35 cm/s for 60 minutes. Animals in the sedentary group were restricted to cage activity. Memory (Morris water maze), coordination (Rotarod) and muscular strength (grip strength) were assessed following the exercise intervention.ResultsA significant exercise training effect was seen in females but absent in males. Female runners showed greater performance in the Morris water maze (9.2 sec. vs 32.7, p <.05) and in the Rotarod (69 sec. vs 47.5, p <.05). No significant training effect was documented in the male groups. Also, no training effect was documented in grip strength in either males or females.ConclusionIn the present study, memory and coordination improvements as a result of aerobic exercise training were seen in female but not male rats. This work adds to existing literature which investigates sex differences in cognitive health and adaptations to exercise training.

Transforming Aging: Increased Access to Care Minimizes Rural and Urban Differences in Cognitive Change

Rural-urban disparities in cognitive health outcomes, such as greater prevalence of cognitive decline among rural-dwelling older adults, have been linked to inequity in access to care. However, few studies have demonstrated whether longitudinal increased access to care may mitigate such disparities. This paper presents data from ongoing systematically collected behavioral health data on new and returning patients at an interdisciplinary geriatrics clinic at the University of Alabama Medical Center. The aim of this study was to determine baseline predictors of cognitive change across three annual visits (n = 42, mean age of 75.63 years (SD = 9.15)). Adjusting for baseline cognitive status, baseline subjective health literacy, and baseline depression and anxiety, results from a univariate ANCOVA showed that age at first visit (B = -.024, 95% CI [-.041, -.008], t(35) = -2.990, p = .005) and rural-urban status (B = .555, 95% CI [.123, .988], t(35) = 2.608, p = .013) predicted cognitive change at timepoint three (T3). Specifically, individuals from rural areas were less likely to experience cognitive decline and scored .555 points better than individuals from urban areas on cognitive screeners at T3 compared with baseline cognitive status. These results suggest that increased access to and utilization of care may ameliorate traditional disparate rates of cognitive decline between rural- and urban-dwelling older adults. Moreover, behavioral health screenings in primary geriatrics clinic care may help identify patient cognitive needs and facilitate integrated care through combined medical, pharmacological, and behavioral interventions to promote positive cognitive health outcomes.

Instrumental variable meta‐analysis of the effect of systolic blood pressure reduction on cognitive change: Evidence from randomized trials of antihypertensive therapies

AbstractBackgroundPrevious meta‐analyses of trials of antihypertensive drugs have only evaluated the effect of randomization to treatment on cognition, without accounting for duration of treatment or degree to which treatment decreased blood pressure. We assumed that any cognitive benefit of antihypertensive treatment would be proportional to the magnitude of change in systolic blood pressure (SBP) achieved and the duration of follow‐up during which a lower SBP was sustained.MethodWe aggregated data from randomized trials of antihypertensive drugs which reported data on change in both SBP and the Mini Mental Status Exam (MMSE). We estimated the effect of decreasing SBP on annual cognitive change for each trial using an instrumental‐variable approach. This was determined for each trial separately using maximum‐likelihood estimation, assuming differences in cognitive change between treatment arms was proportional to the difference in SBP between the groups and the duration of follow‐up. For interpretability, we expressed effects as difference in MMSE per 10mmHg change in SBP per year. Results were combined using a fixed‐effects meta‐analysis.ResultOut of 8 trials (N=70,734; follow‐up: 2.3 to 6 years), 7 suggested benefit of SBP reduction on cognitive change, with 2 of these 8 trials reaching statistical significance. No trials showed statistically significant cognitive harm. The pooled estimate suggested that a 10mmHg decrease in blood pressure slowed MMSE decline by 0.033 (95% CI: 0.023 to 0.044) points per year.ConclusionRandomized‐controlled trials of antihypertensives indicate that decreases in SBP slow cognitive decline. Even with a clinically substantial decrease in blood pressure, the average long‐term effect appears likely to be modest. Instrumental‐variable meta‐analysis can be used to provide an estimated annual benefit per change in SBP, allowing results from trials of heterogeneous treatments to be put on the same scale. Such estimates have more clinical relevance than standard intent‐to‐treat estimates.

Cognitive change after DBS in refractory epilepsy: A randomized-controlled trial.

Deep brain stimulation of the anterior thalamic nucleus (ANT-DBS) reduces seizure frequency in patients with refractory epilepsy. There are, however, few studies on treatment-related changes in cognitive functions. The main objective of this study was to investigate cognitive changes in patients receiving ANT-DBS. We also explored whether possible effects were related to stimulation duration and whether change in seizure frequency was associated with cognitive changes. Bilateral ANT electrodes were implanted in 18 patients with refractory epilepsy, aged 18-52years. Immediately after implantation, patients were randomized to stimulation ON (n=8) or OFF (n=10) for the first 6months (blinded phase). During the following 6-month open phase, both groups received stimulation. Neuropsychological assessments were conducted before implantation (T1), at the end of the blinded period (T2), and 1year after implantation (T3). Groupwise comparisons across the three time points revealed changes in performance in two of 22 cognitive test scores: motor speed and sustained attention. We found no significant group differences in cognitive change from T1 to T2. Patients reported fewer symptoms of executive dysfunction after 12months of stimulation. Patients showing significant improvement in seizure frequency had better performance in a measure of verbal learning. Our results indicate that ANT-DBS has very limited effects on cognitive functioning, as measured by formal tests after 6- or 12-month stimulation. ANT-DBS may have a positive influence on executive function. Our findings provide limited support for an association between change in seizure frequency and cognitive functioning.

Cognitive Decline in Parkinson's Disease: A Subgroup of Extreme Decliners Revealed by a Data-Driven Analysis of Longitudinal Progression.

Cognitive impairment is an important symptom of Parkinson’s disease (PD) and predicting future cognitive decline is crucial for clinical practice. Here, we aim to identify latent sub-groups of longitudinal trajectories of cognitive change in PD patients, and explore predictors of differences in cognitive change. Longitudinal cognitive performance data from 349 newly diagnosed PD patients and 145 healthy controls from the Parkinson Progression Marker Initiative were modeled using a multivariate latent class linear mixed model. Resultant latent classes were compared on a number of baseline demographics and clinical variables, as well as cerebrospinal fluid (CSF) biomarkers and striatal dopamine transporter (DAT) density markers of neuropathology. Trajectories of cognitive change in PD were best described by two latent classes. A large subgroup (90%), which showed a subtle impairment in cognitive performance compared to controls but remained stable over the course of the study, and a small subgroup (10%) which rapidly declined in all cognitive performance measures. Rapid decliners did not differ significantly from the larger group in terms of disease duration, severity, or motor symptoms at baseline. However, rapid decliners had lower CSF amyloidß42 levels, a higher prevalence of sleep disorder and pronounced loss of caudate DAT density at baseline. These data suggest the existence of a distinct minority sub-type of PD in which rapid cognitive change in PD can occur uncoupled from motor symptoms or disease severity, likely reflecting early pathological change that extends from motor areas of the striatum into associative compartments and cortex.

Cognitive change and antipsychotic medications: Results from a pragmatic rater-blind RCT

Cognitive impairment is a core aspect of psychotic disorders and difficult to treat. Atypical antipsychotics (AAs) might have differential effects on cognitive impairment, but rigid study designs and selective sampling limit the generalizability of existing findings. This pragmatic, semi-randomized, industry-independent study aimed to investigate and compare the effect of amisulpride, aripiprazole and olanzapine on cognitive performance in psychosis over a 12-month period controlling for diagnostic group.This sub study of the BeSt InTro study recruited adults with ongoing psychosis in the schizophrenia spectrum of disorders (ICD-10 diagnoses F20-F23, F25, F28 or F29; n = 104) from Bergen and Stavanger, Norway; and Innsbruck, Austria. Participants were randomized to amisulpride, aripiprazole, or olanzapine and they completed neuropsychological assessments at baseline, 6 weeks, 6 and 12 months. The test battery targeted working memory, verbal ability, and processing speed. We used Longitudinal mixed effect (LME) models to assess cognitive change for intention to treat (ITT) and per protocol (PP) medication groups, as well as comparing cognitive performance between F20 and non-F20 participants.The sample baseline global cognitive performance t-score was 42.20. Global performance improved significantly to every follow-up, including for the F20 group. There were however no significant differences in cognitive change over time between neither ITT nor PP medication groups.

Managing ECT related cognitive side effects: An individual approach

Electroconvulsive brain stimulation may represent the strongest manipulation available to study brain plasticity in humans. Brain plasticity induced by electroconvulsive brain stimulation, profoundly improves disturbed emotion and motivation in patients with depression. Electroconvulsive therapy (ECT) is a highly effective and safe treatment for psychiatric disorders like severe depression. However, there is ongoing concern about the negative impact of ECT on brain function and cognition that is, surprisingly, only seen in a part of the treated patients. After 80 years of research on ECT, virtually nothing is known about the mechanisms underlying these strong individual differences in cognitive changes induced by ECT. A first step would be to better quantify the pattern and severity of the adverse cognitive outcomes in order to better distinguish patients that suffer from adverse cognitive outcomes from those that do not or even improve. By better distinguishing of these subgroups, a second step towards understanding can be taken: to identify the factors that predict adverse cognitive outcomes. Our research aims to advance understanding of the mechanisms of cognitive plasticity and reveal the pre-treatment profiles that render a patient cognitive vulnerable or resilient.DisclosureNo significant relationships.

The Role of Cilostazol and Inflammation in Cognitive Impairment After Ischemic Stroke.

The aim of this study is to examine the potential effect of cilostazol and inflammation on cognitive impairment after stroke in an Asian population. Forty-five patients with cognitive impairment after ischemic stroke using cilostazol were enrolled as the study group and 45 patients using aspirin or clopidogrel were enrolled as the control group. Neuropsychiatric assessments were administered at the start of the study and after 6 months. Multiple logistic regression analysis was used to estimate the association between the cognitive change and cilostazol use. Macrophage polarization were assessed using flow cytometry in 7 patients. There were a significantly higher number of patients with peripheral arterial occlusive disease in the cilostazol group. No significant differences were observed in the cognitive change between the cilostazol and control groups. M1 macrophage subset increment were observed in the patient having a declined cognitive change. Cilostazol did not make a significant difference in cognitive change after ischemic stroke. M1 macrophage subset increment may indicate post stroke cognitive decline. Due to limited number of subjects, these findings should be examined further in large-scale randomized clinical trials.

A longitudinal study of the post-stroke immune response and cognitive functioning: the StrokeCog study protocol

BackgroundStroke increases the risk of cognitive impairment even several years after the stroke event. The exact mechanisms of post-stroke cognitive decline are unclear, but the immunological response to stroke might play a role. The aims of the StrokeCog study are to examine the associations between immunological responses and long-term post-stroke cognitive trajectories in individuals with ischemic stroke.MethodsStrokeCog is a single-center, prospective, observational, cohort study. Starting 6–12 months after stroke, comprehensive neuropsychological assessment, plasma and serum, and psychosocial variables will be collected at up to 4 annual visits. Single cell sequencing of peripheral blood monocytes and plasma proteomics will be conducted. The primary outcome will be the change in global and domain-specific neuropsychological performance across annual evaluations. To explain the differences in cognitive change amongst participants, we will examine the relationships between comprehensive immunological measures and these cognitive trajectories. It is anticipated that 210 participants will be enrolled during the first 3 years of this 4-year study. Accounting for attrition, an anticipated final sample size of 158 participants with an average of 3 annual study visits will be available at the completion of the study. Power analyses indicate that this sample size will provide 90% power to detect an average cognitive change of at least 0.23 standard deviations in either direction.DiscussionStrokeCog will provide novel insight into the relationships between immune events and cognitive change late after stroke.

Sex Differences in Cognitive Changes in De Novo Parkinson's Disease.

To evaluate the sex differences in cognitive course over 4 years in Parkinson's disease (PD) patients with and without mild cognitive impairment (MCI) compared to controls. Four-year longitudinal cognitive scores of 257 cognitively intact PD, 167 PD-MCI, and 140 controls from the Parkinson's Progression Markers Initiative were included. Longitudinal scores of men and women, and PD with and without MCI were compared. Women had better verbal memory, men had better visuospatial function. There was no interaction between sex, diagnostic group, and/or time (4-year follow-up period). Sex differences in cognitive course in de novo PD are similar to healthy aging. Cognitive decline rates in PD with and without MCI are similar for the first 4 years of PD.

How specific is cognitive change? A randomized controlled trial comparing brief cognitive and mindfulness interventions for depression

Objective: There is a debate in psychotherapy research as to whether different kinds of psychotherapy work through specific mechanisms of change. Particularly, it is questioned whether cognitive change is specific to cognitive therapy. This study aimed to answer this question by comparing a brief cognitive intervention with an active comparison intervention (i.e., brief mindfulness-based intervention) and by following strict methodological guidelines. Method: 72 currently depressed outpatients were randomized to either cognitive intervention (n = 39) or mindfulness-based intervention (n = 33). Automatic thoughts (negative self-statements, well-being, and self-confidence), dysfunctional attitudes (performance evaluation and approval by others) and depressive symptoms were assessed before and six times during treatment. Within-person and between-person mediation effects were analyzed using multilevel structural equation modeling. Results: There was no difference in cognitive change between the interventions. Negative self-statements and performance evaluations were significant mediators of the within-person effect of time on depressive symptoms, while the three other cognitive variables did not change. Conversely, change in depressive symptoms also mediated within-person cognitive change. Conclusion: Cognitive change seems to be a general rather than a specific mechanism of change. However, the mutual impact of cognitive and depressive change does not support a unidirectional causal model.

Relationship of Cigarette Smoking and Time of Quitting with Incident Dementia and Cognitive Decline.

Understanding how dementia risk is impacted by timing of smoking cessation has public health implications for prevention efforts. We investigated the relationship of cigarette smoking and cessation with dementia risk and cognitive decline in the Atherosclerosis Risk in Communities (ARIC) study. Ongoing prospective cohort study. Begun in 1987-1989, ARIC was conducted in four US communities. A total of 13 002 men and women (25% African American) aged 52 to 75 years. All-cause dementia was defined using standardized algorithms incorporating longitudinal cognitive data, proxy report, and hospital and death certificate dementia codes. Cognitive decline was measured using a composite cognitive score created from three tests measured at two time points (1996-1998 and 2011-2013). Smoking and cessation status were defined by self-report using data from 1987-1989 (visit 1) and 1996-1998 (visit 4). Incident dementia risk and differences in cognitive change by smoking status were estimated with Cox proportional hazards and linear regression models, respectively. To address smoking-related attrition, cognitive scores were imputed for living participants with incomplete cognitive testing. The proportion of never, former, and current smokers was 44%, 41%, and 14%; 79% of former smokers quit 9 years or more before baseline. A total of 1347 participants developed dementia. After adjustment, compared with never smoking, the hazard ratio for all-cause dementia for current smoking was 1.33 (95% confidence interval [CI] = 1.12-1.59) and for recent quitting (<9 y before baseline) was 1.24 (95% CI = 1.01-1.52). Quitting 9 years or more before baseline was not associated with dementia. We found no differences in rates of cognitive decline by smoking status. Although quitting at any time suggested benefit, dementia risk depended on time since smoking cessation. Our study highlights the importance of early midlife cessation to decrease dementia risk. J Am Geriatr Soc 68:337-345, 2020.

Associations between education and age-related cognitive changes from early adulthood to late midlife.

The aims of the study were to explore general trends and individual differences in cognitive changes from early adulthood to late midlife and to investigate associations between education and cognitive changes. We used data from the Lifestyle and Cognition Follow-Up Study 2015 on 1,543 Danish men born in 1950-1961. Test scores on the 78-item intelligence test used by the Danish conscription authorities, Børge Priens Prøve (BPP), completed at draft board examination (baseline, mean age = 20 years) and at follow-up (mean age = 61 years) were used to measure cognitive changes. The mean change in BPP scores was -2.94 (SD = 5.57), and a retest correlation of 0.81 between the baseline and follow-up BPP scores was observed. In spite of the substantial retest correlations, the 8.3% of the sample with statistically reliable change had a mean decline in BPP scores of -13.41 (SD = 2.56). In latent change score models adjusted for year of birth and retest interval, more years of education was associated with larger decline in BPP scores, but the association was reversed when further adjusting for baseline BPP scores. Moreover, significant interactions indicated that more years of education was associated with less cognitive decline in men with relatively low or average BPP scores at baseline, whereas no influence of education was found in men with high baseline scores. Hence, more years of education may compensate for low or average intelligence by increasing cognitive reserve in these individuals or by influencing mediating lifestyle and occupational factors. (PsycINFO Database Record (c) 2019 APA, all rights reserved).