Traumatic brain injury is one of several recognized risk factors for cognitive decline and neurodegenerative disease. Currently, risk scores involving modifiable risk/protective factors for dementia have not incorporated head injury history as part of their overall weighted risk calculation. We investigated the association between the LIfestyle for BRAin Health (LIBRA) risk score with odds of mild cognitive impairment (MCI) diagnosis and cognitive function in older former National Football League (NFL) players, both with and without the influence of concussion history.

Former NFL players, ages ≥ 50 (N=1050; mean age=61.1±5.4-years), completed a general health survey including self-reported medical history and ratings of function across several domains. LIBRA factors (weighted value) included cardiovascular disease (+1.0), hypertension (+1.6), hyperlipidemia (+1.4), diabetes (+1.3), kidney disease (+1.1), cigarette use history (+1.5), obesity (+1.6), depression (+2.1), social/cognitive activity (-3.2), physical inactivity (+1.1), low/moderate alcohol use (-1.0), healthy diet (-1.7). Within Group 1 (n=761), logistic regression models assessed the association of LIBRA scores and independent contribution of concussion history with the odds of MCI diagnosis. A modified-LIBRA score incorporated concussion history at the level planned contrasts showed significant associations across concussion history groups (0, 1-2, 3-5, 6-9, 10+). The weighted value for concussion history (+1.9) within the modified-LIBRA score was based on its proportional contribution to dementia relative to other LIBRA risk factors, as proposed by the 2020 Lancet Commission Report on Dementia Prevention. Associations of the modified-LIBRA score with odds of MCI and cognitive function were assessed via logistic and linear regression, respectively, in a subset of the sample (Group 2; n=289) who also completed the Brief Test of Adult Cognition by Telephone (BTACT). Race was included as a covariate in all models.

The median LIBRA score in the Group 1 was 1.6(IQR= -1, 3.6). Standard and modified-LIBRA median scores were 1.1(IQR= -1.3, 3.3) and 2(IQR= -0.4, 4.6), respectively, within Group 2. In Group 1, LIBRA score was significantly associated with odds of MCI diagnosis (odds ratio[95% confidence interval]=1.27[1.19, 1.28], p <.001). Concussion history provided additional information beyond LIBRA scores and was independently associated with odds of MCI; specifically, odds of MCI were higher among those with 6-9 (Odds Ratio[95% confidence interval]; OR=2.54[1.21, 5.32], p<.001), and 10+ (OR=4.55;[2.21, 9.36], p<.001) concussions, compared with those with no prior concussions. Within Group 2, the modified-LIBRA score was associated with higher odds of MCI (OR=1.61[1.15, 2.25]), and incrementally improved model information (0.04 increase in Nagelkerke R2) above standard LIBRA scores in the same model. Modified-LIBRA scores were inversely associated with BTACT Executive Function (B=-0.53[0.08], p=.002) and Episodic Memory scores (B=-0.53[0.08], p=.002).

Numerous modifiable risk/protective factors for dementia are reported in former professional football players, but incorporating concussion history may aid the multifactorial appraisal of cognitive decline risk and identification of areas for prevention and intervention. Integration of multi-modal biomarkers will advance this person-centered, holistic approach toward dementia reduction, detection, and intervention.

To describe cognitive impairment in out-of-hospital cardiac arrest (OHCA) survivors, with the hypothesis that OHCA survivors would perform significantly worse on neuropsychological tests of cognition than controls with acute myocardial infarction (MI). Another aim was to investigate the relationship between cognitive performance and the associated factors of emotional problems, fatigue, insomnia, and cardiovascular risk factors following OHCA.

This was a prospective case control sub-study of The Targeted Hypothermia versus Targeted Normothermia after Out-of-Hospital Cardiac Arrest (TTM2) trial. Eight of 61 TTM2-sites in Sweden, Denmark, and the United Kingdom included adults with OHCA of presumed cardiac or unknown cause. A matched non-arrest control group with acute MI was recruited. We administered an extensive neuropsychological assessment at approximately 7 months post-cardiac event, including a neuropsychological test battery and questionnaires on anxiety, depression, fatigue, and insomnia, and collected information on the cardiovascular risk factors hypertension and diabetes. Z-scores of individual tests were converted to neuropsychological composite scores per cognitive domain (verbal, visual/constructive, working memory, episodic memory, processing speed, executive functions). Between-group differences on the neuropsychological composite scores were investigated with linear regression. Associations between anxiety, depression, fatigue, insomnia, hypertension, diabetes, and the neuropsychological composite scores among OHCA survivors were calculated with Spearman’s rho.

Of 184 eligible OHCA survivors, 108 were included (mean age = 62, 88% male), with 92 MI controls enrolled (mean age = 64, 89% male). Amongst OHCA survivors, 29% performed z <-1 indicating at least borderline-mild impairment in >2 cognitive domains, and 14% performed z <-2 exhibiting major impairment in >1 cognitive domain. OHCA survivors performed significantly worse than MI controls in episodic memory (mean difference, MD = -0.37, 95% confidence intervals [-0.61, -0.12]), verbal (MD = -0.34 [-0.62, -0.07]), and visual/constructive functions (MD = -0.26 [-0.47, -0.04]) on linear regressions adjusted for educational attainment and sex. When additionally adjusting for anxiety, depression, fatigue, insomnia, hypertension, and diabetes, processing speed (MD = -0.41 [-0.74, -0.09]) and executive functions (MD = -0.69 [-1.13, -0.24]) were also worse following OHCA. Depressive symptoms were associated with worse executive functions (rs = -0.37, p <0.001) and worse processing speed (rs = -0.27, p = 0.01) post-OHCA. Anxiety symptoms (rs = -0.21, p = 0.01) and general fatigue (rs = -0.24, p = 0.01) were associated with worse executive functions. Diabetes was associated with worse processing speed (rs = -0.20, p = 0.03), visual/constructive (rs = -0.29, p <0.001) and executive functions (rs = -0.25, p = 0.02), while hypertension and insomnia were not significantly associated with neuropsychological test performance.

Cognitive impairment is generally mild following OHCA, but most pronounced in episodic memory, executive functions, and processing speed. OHCA survivors performed worse than MI controls. We suggest that a post-OHCA follow-up service should screen for cognitive impairment, emotional problems, and fatigue.

Alzheimer’s disease (AD) is expected to affect over 7 million older Americans by 2025. Development of fast and inexpensive screening measures for routine screening is critical for identifying those suffering from the earliest stages of AD including Mild Cognitive Impairment (MCI) and Subjective Cognitive Decline (SCD). Here we assess the validity and utility of a brief, 5-item SCD screener and its associations with neuropsychological performance as compared to an existing objective cognitive screener, the Mini Mental Status Exam (MMSE).

Development: A brief, 5-item SCD questionnaire was developed based on a more extensive 20-item version previously validated (Chapman et al. 2021). Participants: 27 cognitively diverse (MCI and cognitively normal) community dwelling older adults were recruited for this study. Mean age: 71.9 ± 7. Inclusion criteria include memory concerns. Exclusion criteria include no previous diagnoses of neurodegenerative diseases and/or major stroke. Administration: Participants completed a brief, 5-item SCD screener along with cognitive testing including the MMSE and a clinically validated list-learning test, the Selective Reminding Test (SRT). Statistical Methods: Spearman 2-tailed correlations were conducted to assess the relationship between the two screening measures, and their relationships to the SRT. Outcome measures on the SRT included total recall (max: 72) and delayed recall (max: 12). All cognitive measures were demographically adjusted with normative data.

The mean total for the SCD screener was 2.1 ±1.1, and the mean MMSE score was 29.2 ± 1.2. The SCD screener was associated with MMSE scores (r= -.39, p= .043), SRT Total Recall (r= -.43, p= .024) and Delayed Recall (r=-.42, p=.031) measures. MMSE scores did not associate with either SRT outcome (p>.05).

Results support the utility and validity of a brief subjective cognitive decline screener for identifying those who may be experiencing memory dysfunction. The brief SCD screener outperformed the MMSE, an existing and widely used objective screening measure. Associations between the SCD screener and SRT outcomes support the validity and utility of the brief screener and recapitulate previous findings with the more extensive version of the SCD questionnaire (Chapman et al. 2021). Ongoing research is focusing on the utility of the screener in frontline clinical settings and translation of the screener into Spanish.

Eliciting perceived cognitive complaints is a routine part of a clinical neuropsychological evaluation, presumably because complaints are informative of underlying pathology. However, there is no strong empirical support that subjective cognitive impairment (SCI) is actually related to objective cognitive impairment as measured by neurocognitive tests. Instead, internalizing psychopathology is thought to predominately influence the endorsement of SCI. Specifically, individuals with greater symptoms of depression and anxiety, when accounting for comorbidities, have a higher disposition to overestimate their degree of cognitive impairment as compared to objective testing. Yet, there are few existing studies that have determined which factors influence both SCI and the discrepancy between subjective and objective cognitive impairment in general outpatient populations. The current study examined the relationship between subjective and objective cognitive impairment in a clinically diverse sample of outpatients. We additionally explored the associations between SCI and relevant intrapersonal factors including internalizing psychopathology, number of medical comorbidities, and demographics. Finally, we quantified the degree of discrepancy between subjective and objective impairment and examined this discrepancy in relation to the intrapersonal factors.

The sample comprised 142 adult women and men (age range 18–79 years) seen in an outpatient neuropsychology clinic for a diverse range of referral questions. Scores on the cognition portion of the WHO Disability Assessment Schedule (WHODAS 2.0) were used to index SCI. A composite score from 14 measures across various domains of cognitive functioning served as an objective measure of cognitive functioning. Internalizing psychopathology was measured via a standardized composite of scores from screening measures of anxiety and depression. Medical comorbidities were indexed by the number of different ICD diagnostic categories documented in patients' medical records. Demographics included age, sex, race, and years of formal education. Objective-subjective discrepancy scores were computed by saving standardized residuals from a linear regression of neurocognitive test performance on the WHODAS 2.0 scores.

A hierarchical linear regression revealed that objective cognitive impairment was not significantly related to SCI (p > .05), explaining less than 2% of the variance in SCI ratings. Likewise, participants' demographics (age, sex, education, race) and number of comorbidities were not significantly related to their SCI ratings, explaining about 6% of the variance. However, participants' level of internalizing psychopathology was significantly associated with SCI (F[10, 131] = 4.99, p < .001), and explained approximately 20% of the variance in SCI ratings. Similarly, the degree of discrepancy between subjective and objective cognitive impairment was primarily influenced by internalizing psychopathology (F[9, 132] = 5.20, p < .001, R2 = 21%) and largely unrelated to demographics and number of comorbidities, which explained about 6% of the variance.

These findings are consistent with prior research suggesting that SCI may be more indicative of the extent of internalizing psychopathology rather than actual cognitive impairment. Taken together, these results illuminate potential treatment and diagnostic implications associated with assessing perceived cognitive complaints during a neuropsychological evaluation.

In the absence of treatments to halt or reverse symptoms of Alzheimer's disease, early detection may extend the window for meaningful treatment, advanced planning, and coping. Positron emission tomography (PET) scans for amyloid and tau are validated biomarkers of AD, yet results are rarely disclosed to participants due to concerns about negative impacts. While prior studies suggest limited anxiety, depression, or suicidality following biomarker disclosure, no study to date has examined broader psychological impacts of PET amyloid/tau disclosure to symptomatic individuals. Therefore, we explored post-disclosure changes in future time perspective (perceptions of limited time or possibilities left in the future), self-efficacy for managing symptoms, and perceived stigma as a function of result received.

Forty-three older adults (age = 72.0±6.2 years; education = 16.5±2.6; 88.4% White Non-Hispanic; 48.8% female) participated in the study, of whom 62.8% were diagnosed with mild cognitive impairment (MCI) and the remainder with Dementia of the Alzheimer's type. All participants underwent pre-disclosure biomarker education and decisional capacity assessment, followed by baseline measures. Participants demonstration decisional capacity completed an interactive disclosure session during which they received dichotomous results of their research positron emission tomography (PET) scans for amyloid and tau (elevated versus not elevated for each biomarker). Findings were discussed in relation to presence/absence of Alzheimer's disease, the etiology of their cognitive difficulties, and risk for conversion or further decline. At baseline, immediately following disclosure, and at 1-week follow-up, participants completed several questionnaires: the Future Time Perspective (FTP) scale, a measure of how much the participant sees time as limited, the Self Efficacy for Managing Chronic Disease scale (SECD), and the Stigma Scale for Chronic Illness (SSCI-8), all of which were modified to apply to Alzheimer's disease and associated experiences.

The main effects of time (F=1.10, p=.334, A?p2=.026), biomarker status (F(1)=3.10, p=.086, Ajp2=.070), and the time by biomarker status interaction (F=0.39, p=.661, Ajp2=.009) on FTP score was not significant. Though neither time (F=0.07, p=.933, A?p2=.002) nor the time by biomarker status interaction (F=2.16, p=.122, Ajp2=.050) effect on SECD was significant, being biomarker positive (A+T-/A+T+) was associated with lower self-efficacy (F(1)=5.641, p=.022, Ajp2=.121). Neither main effect for time (F=0.15, p=.853, Ajp2=.004) or biomarker status (F(1)=0.35, p=.558, A?p2=.009) on SSCI-8 was significant. The time by biomarker status interaction was significant (f=4.27, p=.018, =.096), such that biomarker negative participants experience a transient increase in perceived stigma directly after disclosure that resolves one week later, and biomarker negative participants experience the opposite pattern.

Findings suggest that individuals who receive biomarker positive results may feel less competent to manage their symptoms compared to those who are biomarker negative, emphasizing the need for post-disclosure interventions targeting self-efficacy. The effect of disclosure on perceptions of time being limited and on perceived stigma were minimal, even when those results indicate evidence of Alzheimer's disease and risk for clinical progression. These results further support the safety of biomarker disclosure procedures. Future studies should provide longer-term assessment of psychological, behavioral, and clinical outcomes following Alzheimer's disease biomarker disclosure.

Alterations in cerebral blood flow (CBF) are associated with risk of cognitive decline and Alzheimer’s disease (AD). Although apolipoprotein E (APOE) ε4 and greater vascular risk burden have both been linked to reduced CBF in older adults, less is known about how APOE ε4 status and vascular risk may interact to influence CBF. We aimed to determine whether the effect of vascular risk on CBF varies by gene dose of APOE ε4 alleles (i.e., number of e4 alleles) in older adults without dementia.

144 older adults without dementia from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) underwent arterial spin labeling (ASL) and T1-weighted MRI, APOE genotyping, fluorodeoxyglucose positron emission tomography (FDG-PET), lumbar puncture, and blood pressure assessment. Vascular risk was assessed using pulse pressure (systolic blood pressure -diastolic blood pressure), which is thought to be a proxy for arterial stiffening. Participants were classified by number of APOE ε4 alleles (n0 alleles = 87, m allele = 46, n2 alleles = 11). CBF in six FreeSurfer-derived a priori regions of interest (ROIs) vulnerable to AD were examined: entorhinal cortex, hippocampus, inferior temporal cortex, inferior parietal cortex, rostral middle frontal gyrus, and medial orbitofrontal cortex. Linear regression models tested the interaction between categorical APOE ε4 dose (0, 1, or 2 alleles) and continuous pulse pressure on CBF in each ROI, adjusting for age, sex, cognitive diagnosis (cognitively unimpaired vs. mild cognitive impairment), antihypertensive medication use, cerebral metabolism (FDG-PET composite), reference CBF region (precentral gyrus), and AD biomarker positivity defined using the ADNI-optimized phosphorylated tau/ß-amyloid ratio cut-off of > 0.0251 pg/ml.

A significant pulse pressure X APOE ε4 dose interaction was found on CBF in the entorhinal cortex, hippocampus, and inferior parietal cortex (ps < .005). Among participants with two e4 alleles, higher pulse pressure was significantly associated with lower CBF (ps < .001). However, among participants with zero or one ε4 allele, there was no significant association between pulse pressure and CBF (ps > .234). No significant pulse pressure X APOE ε4 dose interaction was found in the inferior temporal cortex, rostral middle frontal gyrus, or medial orbitofrontal cortex (ps > .109). Results remained unchanged when additionally controlling for general vascular risk assessed via the modified Hachinski Ischemic Scale.

These findings demonstrate that the cross-sectional association between pulse pressure and region-specific CBF differs by APOE ε4 dose. In particular, a detrimental effect of elevated pulse pressure on CBF in AD-vulnerable regions was found only among participants with the e4/e4 genotype. Our findings suggest that pulse pressure may play a mechanistic role in neurovascular unit dysregulation for those genetically at greater risk for AD. Given that pulse pressure is just one of many potentially modifiable vascular risk factors for AD, future studies should seek to examine how these other factors (e.g., diabetes, high cholesterol) may interact with APOE genotype to affect cerebrovascular dysfunction.

Depression is common in persons with MS (PwMS), substantially contributing to morbidity and mortality. Depression can dually impact PwMS as both a psychosocial reaction to living with the disease and a neurological effect of it. Cardinal features of depression include reduced ability to seek and experience pleasure, often attributed to dysregulation of the brain's reward system. People with depression exhibit atypical reward processing, as do fatigued PwMS. However, it is unclear whether MS itself affects reward processing, and whether it interacts with depression. The current study explored the associations of depression, MS, and their interaction on reward responsiveness. We hypothesized that depression and MS would independently be associated with poorer reward responsiveness and that they would interact synergistically to impair reward responsiveness.

Forty PwMS and 40 healthy age- and education-matched healthy controls (HC) participated in a computerized switching task with high- and low-reward manipulations. The Chicago Multiscale Depression Inventory (CMDI) Mood subscale measured depressive symptoms. The Behavioral Inhibition/Activation Scales (BIS/BAS) measured self-reported reward responsiveness and behavioral inhibition. Switching task performance was measured as response time (RT) and accuracy. Performance differences between the high- and low-reward conditions represented performance-based reward responsiveness. Linear mixed effects models were used to estimate the associations of MS and depression with reward responsiveness, behavioral inhibition, and task performance.

Depression, but not MS, was associated with higher BIS scores (p=.007). Neither depression nor MS was associated with BAS subscales. On the switching task, participants who reported lower depression responded to reward such that they were slightly faster in the high-reward condition compared to the low-reward condition (p=.07). By contrast, in participants who reported higher depression, there was no effect of reward on response time. Additionally, MS (p=.009) and depression (p=.018) were each associated with slower response times. Regarding accuracy, no effects of reward were observed; however, there was an interaction between MS and depression. Among HC participants, depression was not related to accuracy. In comparison, PwMS who reported higher depression were more accurate than PwMS who reported less depression (p=.043).

Consistent with hypotheses, higher depressive symptoms were associated with increased behavioral inhibition. Depression was not associated with self-reported reward responsiveness, but it was associated with reduced reward responsiveness on a cognitive task. Contrary to hypotheses, MS was not associated with reduced reward responsiveness. Additionally, higher depression and an MS diagnosis were related to slower response time, consistent with prior findings that psychomotor slowing is a hallmark feature of both disorders. Interestingly, we observed a unique behavioral trend in PwMS, such that PwMS with higher depressive symptoms were more accurate than PwMS with lower depressive symptoms, whereas this relationship was not present among HCs. Altogether, depression in both PwMS and cognitively healthy individuals may be associated with blunted reward responsiveness, but MS does not exacerbate this relationship. In fact, PwMS with depression may be more conscientious in their functioning and therefore perform better on cognitive task accuracy. Continued work should examine how reward processing and its underlying mechanisms may differ in depressed PwMS.

Cognitive impairment in depression could present as subjective and objective, but the intensity of subjective impairment is higher and is not correlated with the deficits measured by neuropsychological tests. Subjective cognitive impairment lowers quality of life and is associated with the severity of depression. Among depressive patients, negative emotional bias is present. It is better memory for negative or positive information than for neutral information. We hypothesized that rumination is associated with subjective cognitive impairment.

The study was performed through the online PsyToolkit platform. The study sample consisted of 168 healthy controls and 93 patients with depression were enrolled in the study. Participants completed questionnaires and performed a memory task that contained emotional words. The forty words were chosen from the Nencki Affective Word List. The list for memory test consists of 5 words from each Category: Happiness, Anger, Fear, Sad, Disgusting, and Neutral, and 10 words from category ‘Unclassified’ to balance the valence and arousal of the set. After 15 minutes, they recognized old words from the list of 80 words. Half of them were the same as in the first part, and other words were new, chosen with the same criteria. Depression symptoms were measured using the Beck Depression Inventory-II, subjective cognitive impairment with the Perceived Deficits Questionnaire-20, and intensity of rumination with the Polish Questionnaire of Rumination.

Subjective cognitive impairment and rumination were higher in patients with depression. They also had a higher error rate than healthy controls U = 6462.5; p = .021, especially in words from the neutral (U = 6292; p = .008) and happiness category (U = 6585; p = .031). However, there was no association between subjective cognitive impairment and performance in memory tasks. The regression analysis showed that depressive symptoms and intensity of rumination are better predictors of subjective cognitive deficits than objective performance on a memory task. The results of PDQ-20 were correlated with the error rate of words from categories: Happiness (r = -.162**), Sad (r = -.116*) and Neutral (r = -.145**). Words from categories Happiness, Disgust and Neutral were significantly better recognized than Unclassified, Fear or Sad group of words χ 2 F (6) = 132.685; p < .001. In MDD group recognition of Disgust words were statistically highest than Anger and Fear words χ 2 F (6) = 36.795; p < .001. The recognition of Happiness and Neutral word were not significantly different to other words.

Cognitive problems are common in depression and affect quality of life. Subjective cognitive impairment is more closely related to rumination than objective cognitive impairment among healthy participants and patients with major depressive disorder. Emotional bias among depressive patients has been partially confirmed. Emotional impact is important for memory of words and subjective perception of cognition.

Autonomic dysfunction is an important non-motor symptom of Parkinson’s disease (PD), with point prevalence estimates of approximately 50-70%. Common presentations include cardiovascular dysregulation, gastrointestinal dysfunction, impaired thermoregulation, and sexual dysfunction. In the present study, we sought to examine whether autonomic symptoms would predict trajectories of change in depression and anxiety over a 5-year period in newly diagnosed individuals with PD. Given that alterations in autonomic nervous system functioning (e.g., reduced heart rate variability, lower autonomic arousal) are frequently observed in individuals who have anxiety and depression, as well as the negative influence these symptoms can have on quality of life/functioning, we predicted that greater autonomic symptoms would be related to increased mood symptoms over time.

Participants included 414 individuals from the Parkinson’s Progression Markers Initiative, a prospective study of newly diagnosed and untreated individuals with PD. The PD participants (mean age=61.6+9.7, mean education=15.6+3.0, 92.5% non-Hispanic White) were followed annually for up to five years. Self-reported autonomic symptoms were measured using the Scales for Outcomes in Parkinson’s Disease-Autonomic Dysfunction (SCOPA-AUT), which consists of a total score and 6 subdomain scores (gastrointestinal, urinary, cardiovascular, thermoregulatory, pupillomotor, sexual). Mood measures included the Geriatric Depression Scale (GDS) and State-Trait Anxiety Inventory (STAI). Motor severity was assessed using the Unified Parkinson’s Disease Rating Scale (UPDRS) Part III. Bootstrapped linear regressions were performed to evaluate the relationship between autonomic symptoms (subdomains) and mood using data from the last visit (year 5). For longitudinal analyses, bootstrapped multilevel modeling was used to examine a) changes in SCOPA-AUT total over time (unconditional growth model only) and b) the relationship between mood and SCOPA-AUT total score over time, controlling for age/sex and motor severity.

Autonomic symptoms explained 28.2% of the total variance in trait anxiety, with unique predictors of gastrointestinal (/3=.266, p<.001) and thermoregulatory (ß=.202, p=.004) symptoms. For depression, autonomic symptoms explained 27.9% of the total variance, with unique predictors of gastrointestinal (ß=.225, p=.012), thermoregulatory (ß=.178, p=.013), and cardiovascular (ß=.154, p=.012) symptoms. There was a gradual linear increase in total autonomic symptoms over time (b=0.86, p<.001). Greater total autonomic symptoms were associated with higher average trait anxiety (b=0.54, p<.001), slightly greater increase in trait anxiety over time (b=0.04, p<.05), and occasion-to-occasion fluctuations in trait anxiety (b=0.24, p<.001). Similarly, increased total autonomic symptoms were associated with higher average depressive symptoms (b=0.14, p<.001), minimally greater increase in depressive symptoms over time (b=0.01, p<.05), and occasion-to-occasion fluctuations in depressive symptoms (b=0.08, p<.001). Motor severity did not explain individual differences or trajectories of change in depression or trait anxiety.

Autonomic symptoms, particularly gastrointestinal, cardiovascular, and thermoregulatory dysfunction, were related to increased mood symptoms in PD patients and predicted increases in depression/anxiety over time. Our findings do not distinguish between two theoretical possibilities - whether autonomic symptoms lead to depression/anxiety versus involvement of co-occurring neural systems underlying both. Regardless, our study highlights the importance of treating autonomic dysfunction in early PD, and future work should incorporate additional measures of autonomic dysfunction (e.g., physiological probes).

Deficits in visual-motor coordination and/or fine motor dexterity are often present in pediatric neurological and neurodevelopmental conditions and may adversely affect performance on tests with motor demands. This consideration is relevant when interpreting discrepant scores across Wechsler Intelligence Scale for Children, Fifth Edition (WISC-V) Processing Speed Index (PSI) subtests, specifically Symbol Search and the more motorically demanding Coding. Although test developers maintain that motor ability is unlikely to significantly impact Coding performances, clinicians often consider whether uneven WISC-V PSI subtest scores (Coding<Symbol Search) may in part be attributed to motor-related difficulties, when indicated. This has important clinical implications, as WISC-V Coding may then be omitted or substituted when calculating FSIQ. Thus, the present study aims to evaluate the role of motor task deficits in uneven PSI subtest scores in a sample of clinic-referred youth.

Participants were 238 children and adolescents (MAge=10.62 years; 65.5% male; 60.5% white) referred for neuropsychological assessment. All participants completed the Coding and Symbol Search subtests of the WISC-V and at least one of two motor tasks: the Beery-Buktenica Developmental Test of Visual-Motor Integration (VMI) and the Grooved Pegboard (GP). To evaluate patterns of functioning, we determined the frequencies of patients who demonstrated uneven PSI subtest performances (defined in this study as a Coding scaled score [ss] at least 3-points lower than that of Symbol Search) and/or normative weaknesses (i.e., Standard Score [SS] below 80, per recommendations from the American Academy of Clinical Neuropsychology) on motor tasks. A chi-square test of independence was used to evaluate associations between uneven PSI performance and the presence/absence of motor weaknesses. Among those with uneven PSI performance, a one-way ANOVA was used to examine whether PSI subtest difference scores varied as a function of motor performance group (No Weakness=0, VMI Weakness Only=1, GP Weakness Only=2, Weaknesses on Both=3).

Of the 238 participants, 28 (11.0%) displayed normative weaknesses on the VMI only, 43 (16.9%) displayed weaknesses on the dominant-GP only, and 18 (7.1%) displayed weaknesses on both tasks. On the WISC-V, 56 participants (23.5%) exhibited uneven PSI subtest performance (Coding<Symbol Search), with 21 (37.5%) of those participants displaying at least one normative motor weakness. Chi-square analyses indicated no significant association between the presence/absence of motor skill weakness and uneven PSI subtest performance, (X2 (3) = 5.79, p = .122). Among those with uneven PSI performance, Coding/Symbol Search difference scores were not significantly associated with motor performance group (F(3,55) = 1.26, p = .297).

These findings suggest that while patients with uneven WISC-V Coding and Symbol Search scores may also display motor task deficits, these deficits are not significantly associated with uneven performances overall. Additionally, of the participants with uneven PSI subtest scores, the majority did not exhibit normative weaknesses on motor tasks. Therefore, clinicians may be overcorrecting for a motoric cause of uneven performance and underappreciating the potential unevenness a child demonstrates in processing speed. Future studies should evaluate the role of other neurocognitive factors, such as working memory, in this score discrepancy pattern.

COVID-19 has significantly impacted society for over 2.5 years, and Long COVID is concerning for its long-term impact on the healthcare system. Further, cognitive and emotional functioning in Long COVID has limited research, but 2 recent studies (Whiteside et al., 2022a, Whiteside et al., 2022b) examined cognitive and emotional functioning in Long COVID patients approximately 6 months post-diagnosis. The studies found limited cognitive deficits, but significant depression and anxiety, which in turn were the best predictors of low average cognitive scores. Further, the mean Personality Assessment Inventory (PAI) profile included highest mean elevations on somatic preoccupation (SOM) and depression (DEP) subscales. To further explore personality functioning in Long COVID, this study compared PAI profiles of Long COVID patients with a potentially similar group with post-concussion syndrome (PCS) which has been shown to have a strong psychological component.

Participants included 44 consecutive outpatients (Mean age = 47.89, SD = 13.05, 84% Female, 75% Caucasian) referred from a Long COVID clinic with cognitive complaints related to COVID, while the comparison group of PCS patients included 50 consecutive referrals (Mean age = 38.82, SD = 16.24, 52% Female, 90% Caucasian) related to cognitive complaints attributed to PCS. A series of t-tests between the 2 groups was conducted on the PAI validity, clinical, interpersonal, and treatment consideration scales. PAI clinical subscales were also compared. To control for multiple comparisons, p < .01 was utilized and effect sizes were compared.

The results demonstrated that both Long COVID (SOM M = 68.66, SD = 12.56; DEP M = 63.39, SD = 12.70) and PCS groups (SOM M = 65.28, SD = 12.06; DEP M = 70.32, SD = 16.15) displayed the highest mean elevations on PAI SOM and DEP scales but no statistically significant differences in mean scale elevations between Long COVID and PCS groups on SOM (t [92] = 1.33, p = .80) and DEP (t [92] = -2.11, p = .097). However, results demonstrated statistically significant differences on the paranoia subscale (PAR; t [92] = -3.27, p = .009), antisocial features subscale (ANT; t [92] = -2.22, p = .01), stress subscale (STR; t [90] = -3.51, p = .006) and suicidal ideation subscale (SUI; t [92] = -2.73, p = .000) of the PAI. Specifically, the mean scores for the PCS group were higher across the paranoia (M = 57.30), antisocial features (M= 52.24), stress (M = 58.44), and suicidal ideation subscales (M = 57.82) of the PAI than the Long COVID group. While these patterns of reporting differed between groups, mean scores for both groups were in the normal range.

Results support the similarities in emotional/personality functioning across Long COVID and PCS patients and the importance of evaluating psychological functioning in these samples as a standard part of neuropsychological evaluations. Further, the results suggest that psychological treatment strategies utilized with PCS patients may be helpful for Long COVID patients, but more research is needed.

Alzheimer’s disease (AD) clinical trials lack diverse representation, limiting their generalizability. In addition, the clinical meaningfulness of observed changes during treatment may vary as a function of participant characteristics. Defining meaningful change in AD within diverse ethnoracial groups is therefore greatly needed. Meaningful change in AD trials can be assessed by three different anchors: participants, informants, or clinicians. Previous research has suggested that estimations of the minimal clinically important difference (MCID) vary by disease severity, choice of anchor, and anchor agreement. These relationships have been studied primarily within non-Hispanic white (NHW) samples. This project evaluates anchor-based MCID within and across the three most prevalent ethnoracial groups in the United States, non-Hispanic White (NHW), Hispanic/Latino (H/L), and Black/African-American (B/AA).

Data from the National Alzheimer’s Coordinating Center Uniform Dataset (NACC UDS) were used to investigate MCID within older adults (ages 50+) diagnosed as cognitively normal or cognitively impaired due to suspected AD. Data were taken from all versions of the UDS and consisted of all available participants with two consecutive annual visits. The identified sample (N=22,043) is approximately 83.6% NHW, 4.7% H/L, and 11.7% B/AA. Participant, informant, and clinician anchor variables were utilized to compare proportions of anchor agreement within and across ethnoracial groups. MCID on the Mini-Mental State Exam (MMSE) was estimated within each ethnoracial group and compared across the independent variables of anchor agreement and disease severity (cognitively normal (CN), mild cognitive impairment (MCI), and dementia) in 2x3 ANOVAs.

Participant age (M = 71.56, SD = 9.03) did not significantly differ across ethnoracial groups; years of education significantly differed across groups, p < .001, with NHW (M=15.83 SD=3.05), H/L (M=12.49, SD=5.01), and B/AA (M=14.42, SD=3.22). Across all three anchors (participant, informant, clinician), unanimous agreement about the presence or absence of a decline in functioning was present in about 75.1% of the full sample. To further explore agreement differences across groups, anchor agreement was classified into a 3-level variable: 1) agreement that the participant remained stable over time, 2) agreement that the participant declined, and 3) disagreement. The proportion of each level within each ethnoracial group was significantly different, (x2(4, n = 22,043) = 179.16, p < .001, phi = .09, NHW (34.5% agreement-stable, 41.4% agreement-declined, 24.1% disagreement), H/L (30.5%, 42.6%, 26.9%, respectively), and B/AA (42.2%, 28.1%, 29.7%, respectively). MCID estimates on the MMSE followed similar trends within each ethnoracial group. There was a significant main effect of disease severity, such that MCID estimates increased in magnitude with increasing disease severity. There were no significant main effects of anchor agreement for any ethnoracial group. Within the NHW sample only, an interaction effect between diagnostic severity and anchor agreement was significant (p = .007).

Across ethnoracial groups, MCID estimates on the MMSE are reliably influenced by the severity of disease. However, the benefit of anchor-based MCID estimates may vary by ethnoracial group with respect to both anchor choice and use of anchor agreement. The origins of anchor disagreement and perceived stability in functioning warrant further exploration.

We examined the use of pupillometry as an early risk marker of Alzheimer's disease (AD). Pupil dilation during a cognitive task has been shown to be an index of cognitive effort and may provide a marker of early change in cognition even before performance begins to decline. Individuals who require more effort to successfully perform a task may be closer to decline. We previously found greater compensatory effort to perform the digit span task in individuals with amnestic mild cognitive impairment (aMCI) who may be at greater risk for AD than individuals with non-amnestic MCI (naMCI). Task evoked pupil dilation is linked to increased norepinephrine output from the locus coeruleus (LC), a structure affected early in the AD pathological process. In this study, we measured pupil dilation during verbal fluency tasks in participants with aMCI or naMCI, and cognitively normal (CN) individuals. Based on our findings using the digit span task, we hypothesized that participants with aMCI would show greater compensatory cognitive effort than the other two groups.

This study included 101 older adults without dementia recruited from the UC San Diego Shiley-Marcos Alzheimer's Disease Research Center and San Diego community (mean [SD] age = 74.7 [5.8]; education = 16.6 [2.5]; N=58 female; N=92 White); 62 CN, 20 aMCI and 19 naMCI participants. Pupillary responses (change relative to baseline at the start of each trial) were recorded at 30 Hz using a Tobii X2-30 (Tobii, Stockholm, Sweden) during semantic (animals, fruits, vegetables) and phonemic (letters F, A, S) fluency tasks. Participants generated as many words as possible in a category (semantic) or starting with a given letter (phonemic) in 60 seconds.

Repeated measures ANOVA (3 groups X 2 fluency conditions) with age, education and sex as covariates showed a significant main effect of group (F(2,95)=3.64, p=.03), but no group X condition interaction (F<1). Pairwise comparisons showed significantly greater fluency task-evoked dilation for aMCI relative to CN (p=.015) and naMCI (p=.019) participants. When controlling for performance (total letter or category words produced), pupil dilation (cognitive effort) remained significantly greater in aMCI relative to the other two groups in both fluency conditions, suggesting pupil dilation informs risk beyond information provided by task performance.

In a previous sample of community-dwelling men who were an average of 13 years younger than the present sample, we found significantly greater pupil dilation during a digit span task in aMCI relative to naMCI and CN groups. In the present study, we replicated those findings in an older sample using a different cognitive task. Significantly greater pupil dilation was found in individuals with aMCI on verbal fluency tasks, indicating greater compensatory cognitive effort to maintain performance. Pupillometry provides a promising biomarker that might be used as an inexpensive and noninvasive additional screening tool for risk of AD.

Various forms of social media have been investigated as platforms for science and health communication, with a recent growing interest in TikTok. TikTok has more than one billion active users. Sixty-two percent of TikTok users are under the age of 29, making it a platform of particular interest when considering the impact of social media content dissemination in pediatric neuropsychology. Personal communication suggests that children, adolescents, and young adults internationally reference specific information from TikToks about attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), tic disorder, and specific learning disorders in the context of clinical neuropsychological assessment. Despite the emerging prevalence of TikTok observed clinically and discussed informally among clinicians, there has yet to be a synthesis of available empirical information of TikTok as a health communication platform for discussing neurodevelopmentally relevant conditions.

A systematic review of research regarding TikTok and neurodevelopmentally relevant conditions was conducted using PRISMA guidelines. The following databases were searched: Ovid MEDLINE (to 20 July 2022), PsycINFO (to 20 July 2022), and PubMed (to 20 July 2022) using search terms TikTok AND ADHD OR autism OR tic OR learning disorder. Searches using search terms TikTok AND learning disability OR dyslexia OR dysgraphia OR dyscalculia were also conducted but were excluded as they yielded no results. Articles were eligible for inclusion if they presented original data (e.g., case series, descriptive analyses, etc.) related to information about neurodevelopmentally relevant conditions on TikTok. A final sample of 5 original papers met criteria for inclusion.

The systematic review sample included a mixture of clinical case series and empirical analyses using primary data from TikTok. Across publications, there was an emphasis on the prevalence of misinformation about disorders on TikTok, the frequency of atypical presentations of neurodevelopmental disorders on TikTok, and the potential for an iatrogenic impact on children and adolescents who view TikTok videos.

Despite the increasing frequency with which patients access TikTok for health-related information, there is a relative dearth of published research on TikTok regarding neurodevelopmentally relevant conditions. This is in contrast to other health-related areas (e.g., there are a far greater number of published articles on TikTok and COVID-19 and dermatology compared to neuropsychological disorders). These findings suggest a missed opportunity for researchers and clinicians alike to engage with TikTok. Based on clinical experience and a review of the available literature, the following recommendations are provided and will be presented in-depth:

1. 1. Clinicians should gain familiarity with virally spread information via TikTok, particularly as it relates to symptoms and presentations of neuropsychological and neurodevelopmental conditions.

2. 2. Clinicians should explicitly assess for knowledge content and source regarding neuropsychological and neurodevelopmental conditions during intake and/or feedback in order to address misinformation and myths, validate lived experiences, and develop rapport with patients.

3. 3. Clinicians and researchers should consider a strengths-based approach to TikTok usage that highlights the value of sharing resources, building community, and decreasing stigma.

4. 4. Clinicians and researchers should be aware of information shared via TikTok as a potential concern for test security.

Mild decline in independent functioning is a core diagnostic criterion for Mild Cognitive Impairment. Performance-based assessments have been considered the gold standard to identify subtle deficits in functioning. Existing assessments were largely designed using demographically homogenous samples (white, highly educated, middle class) and often assume tasks are performed similarly across populations. The current study aimed to validate the utility of the Performance Assessment of Self-Care Skills (PASS) in determining cognitive status in a sample of predominantly African American, low-income older adults.

Cognition and functional capacity were measured in n=245 older participants (aged 50+ years) who were recruited from a larger community study located in Pittsburgh, PA. Cognitive status was defined by a mean split on the Modified Mini Mental Status Examination (3MS) score (84/100). Participants above the cutoff were classified as unlikely cognitive impairment (UCI) and those below classified as potential cognitive impairment (PCI). Functional capacity was assessed using the number of cues provided on three PASS subtasks: shopping, medication management, and critical information retrieval (higher score = worse functioning). Self-reported cognitive and functional decline was assessed via the Everyday Cognition (ECog) questionnaire (higher score = greater decline). Generalized linear models compared performance scores between groups adjusting for literacy (WRAT3), age, and education. Receiver operating characteristic curve (ROC) analyses were run for select functional performance scores to assess their predictive ability in discriminating between PCI and UCI.

Compared to the UCI group (N = 179), the PCI group (N = 66) was older (68 vs. 65 years, p = 0.05), less educated (11 years vs. 12 years, p < 0.01), had lower WRAT3 z-scores (0.19 vs. -0.55, p < .01), and required more cues on the shopping (4.33 vs. 8.54, p < 0.01) and medication management PASS subtasks (2.74 vs. 6.56, p < .01). Both groups reported elevated levels of subjective cognitive complaints on the ECog (1.46 vs. 1.56, p = .09) and performed similarly on the critical information retrieval PASS subtask (0.25 vs 0.54, p = .06). When discerning between UCI and PCI groups, the PASS Shopping subtask had an optimal cut-off score of 4, sensitivity of 0.86, specificity of 0.47, positive predictive value (PPV) of 0.37, and area under the curve (AUC) of 0.71. PASS Medication Management had an optimal cut-off score of 3, sensitivity of 0.77, specificity of 0.56, PPV of 0.39, and AUC of 0.74.

Subjective functional decline and performance on the critical information retrieval subtask were not associated with cognitive groups. PASS shopping and medication management had moderately high AUCs, suggesting they can reliably distinguish between groups. However, both tasks also exhibited low PPVs, low levels of specificity, and high levels of sensitivity, making them strong “rule-out” tests but poor “rule-in” tests in this sample. Because accurate assessment of functioning is useful for MCI and critical to dementia diagnosis, it is imperative we understand how these tasks function across different populations. Future work should 1) validate measures of functional ability across different populations and 2) develop population-appropriate assessments for use in clinical and research settings.

brain white matter integrity as a result of vascular burden is associated with a form of late-life depression, known as vascular depression (VaDep). Black older adults may be particularly vulnerable to developing VaDep due to a higher prevalence of vascular conditions compared to White older adults. The current study examined whether clinical and imaging markers of vascular burden predicted depressive symptoms in an older Black sample. Based on the literature in primarily White samples, we expected greater clinical vascular burden and white matter hyperintensity (WMH) volume to predict greater depressive symptoms both cross-sectionally and over 4-year follow-up. We additionally hypothesized that participants with operationally-defined VaDep would have worse cognitive performance and slower gait speed compared to those without VaDep. Exploratory analyses examined race (Black vs. White) as an additional predictor.

This study used publicly available data from 113 Black older adults who were followed for four years in the Healthy Brain Project (a substudy of the Health, Aging, and Body Composition Study). Clinical vascular burden was defined as the number of vascular conditions (e.g., hypertension, diabetes, stroke); total WMH volume and WMH volume in the uncinate fasciculus, superior longitudinal fasciculus, and cingulum were considered imaging markers of vascular burden. Clinical and imaging-defined vascular burden were used to predict baseline depressive symptoms and average depressive symptoms over follow-up as measured by the Center for Epidemiologic Studies Depression Scale (CES-D). We then formed groups based on cutoffs for vascular burden (two or more conditions) and depressive symptoms (upper tertile of CES-D scores) to compare cognitive (Digit Symbol Substitution Test and 15-Item Executive Interview) and gait speed performance at baseline and changes over four years in VaDep, non-vascular depression, vascular only, and healthy groups. Exploratory analyses included 179 White older adults from the Healthy Brain Project dataset to examine race differences.

Total WMH volume and WMH volume in the uncinate fasciculus predicted higher depressive symptoms both cross-sectionally and longitudinally. However, no similar pattern emerged when using clinically-defined vascular burden as the predictor. The VaDep group had the slowest processing speed but the trajectory of decline over time did not differ between groups. The non-vascular depression group’s executive performance improved over time while performance by the other groups remained stable. Both VaDep and non-vascular depression groups’ gait speed declined over time. There was a stronger association between depression and uncinate fasciculus WMH in Black compared to White individuals, and the Black VaDep group had the slowest baseline processing speed of all groups.

This research supports the validity of the VaDep framework in Black older adults by showing the impact of WMH, particularly in the uncinate fasciculus, on depressive symptoms and identifying cognitive risks associated with VaDep in this population. Moreover, results suggest WMH may confer a greater risk for depression in Black compared to White older adults, and that VaDep disproportionately impacts processing speed in Black older adults. This work addresses an important gap in the VaDep literature by examining a group that has historically been underserved.

Accurately interpreting cognitive change is an essential aspect of clinical care for older adults. Several approaches to identifying 'true’ cognitive change in a single cognitive measure are available (e.g., reliable change methods, regression-based norms); however, neuropsychologists in clinical settings often rely on simple score differences rather than advanced statistics, especially since multiple scores compose a typical battery. This study sought to establish quick-reference normative criteria to help neuropsychologists identify how frequently significant change occurs across multiple measures in cognitively normal older adults.

Data were obtained from the National Alzheimer’s Coordinating Center (NACC). Participants were 845 older adults who were classified as cognitively normal at baseline and at 24-month follow-up. In NACC, these clinical classifications are made separately from the assessment of cognitive performance, including cognitive change. The sample was 34.9% female, 83.5% White, 13.1% Black 2.3% Asian, and 1.1% other race with a mean age of 70.7 years (SD=10.2). Of the sample, 95.5% identified as non-Hispanic. Mean education was 16.1 years (SD=2.8). The cognitive battery entailed: Craft Story Immediate and Delayed Recall, Benson Copy and Delayed Recall, Number Span (Forward & Backward), Category Fluency (Animals & Vegetables), Trails A&B, Multilingual Naming Test, and Verbal Fluency (F&L). Change scores between baseline performance and follow-up were calculated for each measure. The natural distribution of change scores was examined for each measure and cut points representing the 5th and 10th percentile were applied to each distribution to classify participants who exhibited substantial declines in performance on each measure. We then examined the multivariate frequency of statistically rare change scores for each individual.

As expected in a normal sample, overall cognitive performance was generally stable between baseline and 24-month follow-up. Across cognitive measures, 81.9% of participants had at least one change score fall below the 10th percentile in the distribution of change scores, and 55.7% had at least one score below the 5th percentile, 49.3% of participants had two or more change scores that fell below the 10th percentile and 21.1% with two or more below the 5th percentile. There were 26.7% participants that had three or more change scores below the 10th percentile, and 6.4% of participants had three change scores below the 5th percentile.

Among cognitively normal older adults assessed twice at a 24-month interval with a battery of 13 measures, it was not uncommon for an individual to have at least one score fall below the 10th percentile (82% of the sample) or even the 5th percentile (56%) in the natural distribution of change scores. There were 27% participants that had three or more declines in test performance below the 10th percentile; in comparison, only 6% of the sample had three or more change scores at the 5th percentile. This suggests that individuals who exhibit more multivariate changes in performance than these standards are likely experiencing an abnormal rate of cognitive decline. Our findings provide a preliminary quick-reference approach to identifying clinically significant cognitive change. Future studies will explore additional batteries and examine multivariate frequencies of change in clinical populations.

Lateralization and localization of neuropathology helps determine the extent to which eloquent cortex and diseased brain tissue share loci, important information for neurosurgical decision-making, and predicting neurocognitive outcomes. Emerging data suggest that lateralization and localization can inform specific neurorehabilitation approaches following acquired brain injury (ABI). In recent years, computerized cognitive remediation (CCR) of attention and working memory (WM) has been included among treatment guidelines to enhance cognition in post-acute recovery following ABI. Although CCR has shown promise for improving attention and executive functioning in ABI, it is unknown how treatment response may be predicted by locus of ABI. Even less is known about the effects of CCR following neurosurgery. The current study explores neurosurgical lateralization and localization as potential variables for predicting treatment response to CCR.

Adult patients with a variety of neurological diagnoses (N = 17; ∼47% women) completed a full course of Cogmed Working Memory Training (CWMT) s/p neurosurgical intervention. All participants engaged in 30 sessions of CWMT over eight weeks, as well as neuropsychological (NP) assessment at pre-training baseline, immediate post-training, and at 3-month follow-up. Objective and subjective indices of attention, working memory, executive functioning, and emotional well-being were evaluated at three time-points. Neurosurgical loci included left-hemisphere frontal, temporal, and temporoparietal lobes, as well as right-hemisphere frontal, frontotemporal, and temporal lobes.

NP data were reviewed and yielded a clinical impression of cognitive and affective functioning for a cohort of patients with heterogeneous diagnoses (e.g., brain tumor, epilepsy, NPH). Preliminary NP findings suggested that treatment response to CCR for WM was consistent with extant literature on brain-behavior relationships according to lateralization and localization of neurosurgical intervention.

Neurosurgical patients experience neurocognitive and affective dysfunction that may respond well to cognitive rehabilitation (CR) that includes CCR. Additionally, it is possible that lateralization and localization of surgical intervention may contribute to individual differences in treatment response. Further neurorehabilitation research is warranted to identify patients most likely to benefit from CCR and better tailor CR modalities to optimize recovery s/p neurological surgery.

Metamemory is a component of metacognition that includes both the knowledge of factors that affect memory (i.e., declarative metamemory) and knowledge and application of factors in one's own learning and recall performance (i.e., procedural metamemory; Kreutzer et al., 1975). Previous researchers have examined children's metamemory through interviews and found that metamemory abilities are positively associated with age and performance on memory measures (see Godfrey et al., 2022 for review). However, there is not yet a standardized measure to evaluate children's metamemory. The current study aimed to examine the psychometric characteristics of a declarative metamemory questionnaire, the Measure of Metamemory (MoM-10), for children ages 6-12 years old. Based on previous research, we hypothesized that performance on the MoM-10 would not be associated with sex but would be positively associated with age and learning and memory performance.

A total of 75 English-speaking typically developing children between the ages of 6 to 12 years old were recruited for the current study (M age=9.1+1.92; females 49%). Participants completed the MoM-10 which assessed declarative metamemory via 10 multiple choice questions (accuracy score of 0 or 1 points per question) and required participants to provide an explanation for their multiple-choice answer (explanation score of 0, 1, or 2 points per question). The metamemory questionnaire provided two outcome variables: an Accuracy score of 10 possible points, and an Explanation score of 20 possible points. Additionally, participants completed a 3-trial pictorial learning/memory task which provided an Immediate Recall score and Delayed Recall score.

As hypothesized, there were no sex differences on the MoM-10 Accuracy scores (t(73)=0.71, p=0.48) or Explanation scores (t(73)=-73, p=0.47). Consistent with our hypothesis, age was significantly associated with Accuracy (r=0.31, p<0.01) and Explanation scores (r=0.79, p<0.001). Internal consistency of the MOM-10 was moderate for the Explanation score (Cronbach's alpha=0.68) and low for the Accuracy score (KR-20=0.54). Lastly, after controlling for age, participants' MoM-10 Accuracy score was significantly associated with Immediate Recall (r=0.32, p<0.01) on the learning/memory task and the Explanation scores were significantly associated with the Immediate Recall (r=0.36, p<0.01) and Delayed Recall scores (r=0.32, p<0.01) on the learning/memory task.

The current study presents an initial review of psychometric properties of a metamemory questionnaire for children ages 6 to 12 years old. Additionally, as hypothesized, these results suggest the MOM-10 performance is significantly positively associated with participants' age and immediate and delayed recall performance on a pictorial learning/memory task. These associations provide lines of evidence for convergent validity given the expected maturation of metamemory with both age and with improvements in actual memory performance. However, based on the low internal consistency of the accuracy scores, further refinement will be explored including possibly rephrasing questions from the current item set or perhaps excluding current items in future use of the scale.

Stroke is a prevalent disease and often produces cognitive impairment. Post-stroke cognitive impairment has been associated with challenges returning to interpersonal and occupational activities. Knowing what factors are associated with cognitive impairment post-stroke can be useful for predicting outcomes and guiding rehabilitation strategies. One such factor is gender. Previous research has not led to definitive conclusions as to whether there are gender differences in cognitive outcomes following stroke. This may be because other factors, including age at stroke onset, years of education, premorbid intelligence, and lesion volume, may account for apparent gender differences in cognitive outcomes of stroke. Here, we sought to examine whether there are gender differences in general and specific cognitive functions following stroke, beyond what can be accounted for by age at stroke onset, years of education, premorbid intelligence, and lesion volume.

Participants were 237 individuals in the chronic epoch (> 3 months) following ischemic stroke. Using multivariate linear regression, we examined gender as a predictor of overall cognitive functioning and specific cognitive functions, while controlling for age at stroke onset, years of education, premorbid intelligence, and lesion volume. To quantify overall cognitive functioning, we used a measure of general cognitive ability (g) and Full Scale IQ score from the WAIS. To quantify specific cognitive functions, we used scores from 16 individual neuropsychological tests.

After controlling for demographic and lesion factors, men and women did not show any significant differences in overall cognitive functioning following stroke as measured by g (ß = -0.01, 95% CI: -0.14 - 0.12, p = .887) or Full Scale IQ (ß = -0.01, 95% CI: -2.93 - 2.27, p = .801). There were some significant gender differences on specific cognitive tests after controlling for demographic and lesion factors. Specifically, women performed better than men on the Rey Auditory Verbal Learning Test (ps < .001) and men performed better than women on the WAIS Information subtest (ß = -.65, 95% CI: -0.97 - -0.33, p < .001).

Our findings suggest that although men and women have similar overall cognitive functioning after stroke, they show some differences in specific cognitive functions even after accounting for demographic and lesion factors. Namely, women demonstrated better performance on a test of learning while men demonstrated better performance on a test of verbal knowledge/comprehension. This information is important for clinicians as they assess cognitive outcomes in patients post-stroke and plan rehabilitation strategies.