Fear of falling is an anxiety-related phenomenon that is associated with increased risk of morbidity and mortality in older adults. Furthermore, a growing body of research has established the relationship between fear of falling and decreased cognitive functioning within various populations (i.e., older adult, multiple sclerosis, stroke survivors). Yet there is little information on the relationship between fear of falling and cognition outside of a geriatric context, with no publications investigating this relationship within informal caregivers. It is important to understand this relationship within caregiver populations because fear of falling may negatively impact caregivers’ ability to take care of themselves and their care recipients. The present study examines the relationship between fear of falling and cognitive function in informal caregivers.

Fifty informal caregivers (86% female; 58% White; 10% Hispanic or Latino; 82% married; 53% with at least a bachelor’s degree; mean age = 57.76 ± 16.60 years) were assessed at the VA Palo Alto Health Care System in Palo Alto, CA. Fear of falling was measured via the Short Falls Efficacy Scale. Areas of cognitive functioning included verbal attention (Rey Auditory Verbal Learning Task [RAVLT] Trial 1), learning and memory (RAVLT Trials 1-5), delayed memory (RAVLT Delayed Recall), visual attention (Stroop Color, Stroop Word), and executive function (Stroop Color Word). Analyses included linear regressions with age as a covariate in all models.

Analyses revealed that fear of falling was significantly associated with decreased verbal attention (RAVLT Trial 1: ß=-0.34, p = 0.02, t = -2.35, CI = [-0.659, -0.051]) and with decreased executive functioning (Stroop Color Word: ß = -0.35, p < 0.001, t = -3.10, CI = [-4.097, -0.874]). Fear of falling was not significantly associated with learning and memory or visual attention.

Fear of falling negatively impacts verbal attention and executive functioning, regardless of age. To our knowledge, this is the first study to examine the relationship between fear of falling and cognition outside of a geriatric population and within a caregiver sample. Findings suggest a need for additional assessment, research, and treatment of fear of falling within informal caregivers. Caregivers may need to be assessed for anxiety-related symptoms such as fear of falling on a more regular basis. A caregiver experiencing fear of falling, as well as difficulties with attention and executive functioning, can result in increased risk of functional and cognitive decline for both the caregiver and their care recipient. It is integral that future research investigates this relationship longitudinally to identify if the negative impact of fear of falling on cognition is reversible.

There is limited and mixed research describing the memory performance of boys with Duchenne muscular dystrophy (DMD), a progressive disorder that affects the muscle and the brain, presumably due to the absence of dystrophin; however, the literature indicates either the existence of a selective deficit in verbal working memory, or more generalized impairment in both verbal and visual memory. Far less is documented about the neurocognitive profile of boys with Becker muscular dystrophy (BMD), a closely related neuromuscular disorder which allows for at least some functional dystrophin protein to circulate. The Child and Adolescent Memory Profile (ChAMP) is a valid and widely used memory battery that has not been studied in either DMD or BMD. This study aimed to assess the verbal and visual memory performance in boys having either a DMD or a BMD diagnosis using the ChAMP. A working memory measure, the Digit Span subtest from the Wechsler Intelligence Scale for Children-Fifth Edition, was also included for comparison.

Twenty-one patients (Age M = 12.19 ± 3.60; 100% male; 76% DMD, 24% Becker) were selected from retrospective data collection of neuropsychological performance in children with neuromuscular disorders. Patients were recruited and assessed as part of a larger scale IRB-approved research study designed to better understand the neurocognitive and behavioral trajectories of boys with DMD or BMD with a complete neuropsychological battery.

Independent samples f-tests revealed no significant differences between groups across verbal (DMD M = 88.71; BMD M = 100.80; p = .08), visual (DMD M =90.36; BMD M 93.60; p = .33), and working memory (DMD M = 84.69; BMD: M 82.60; p = .40) domains. In additional analyses, a one sample f-test comparing verbal and visual memory within DMD children revealed significantly worse verbal than visual memory scores (verbal memory M = 88.71; visual memory M = 90.36; p = <.001).

There were no significant differences between groups in verbal, visual, and working memory performance, though sample size was a significant limitation. However, based on a comparison of means, children with BMD appear to have stronger verbal memory skills than children with DMD. Furthermore, significant differences between verbal and visual memory within DMD children were observed, such that verbal memory skills were weaker. These findings add to the absence of literature on verbal and visual memory outcomes in children with DMD and BMD.

The current research framework recommends using biomarkers to further understand Alzheimer’s disease (AD) pathogenesis, including other contributing factors like cerebrovascular disease. In longitudinal studies of people with neuropathological examination after death, baseline loneliness was associated with lower cognition, faster cognitive decline, and future AD risk, independent of AD pathology. Examination of memory impairment along with AD and cerebrovascular biomarkers, could aid risk reduction efforts earlier in the lifecourse and among populations with more exposure to loneliness. We hypothesized that loneliness is associated with amyloid, vascular, and neurodegeneration biomarkers; with worse memory; and that loneliness increases the susceptibility to biomarker-related memory impairment.

A subset of cognitively unimpaired older adults with available amyloid PET, vascular MRI (white matter hyperintensity volume, WMH), structural MRI (cortical thickness in AD signature regions), neuropsychological testing (memory factor score), dichotomized loneliness data (one item from CES-D), and relevant medical data were drawn from the community-based Washington Heights-Inwood Columbia Aging Project (WHICAP; n=169; covariates included age=81±6 years; 63% women; 49/31/20% Non-Hispanic Black/Non-Hispanic White/Hispanic; education=13±4 years; 32% APOE-e4 carriers). General linear models in the overall sample and stratified by race and ethnicity tested the association between loneliness and AD and cerebrovascular biomarkers, loneliness and memory, and the interaction of loneliness and biomarkers on memory, adjusting for covariates.

Loneliness was endorsed in 18% of participants, marginally associated with older age (2.1 [-0.2, 4.4], p=0.08), was more likely in those with untreated diabetes (13/0.1% lonely/not lonely, p=0.001), associated with lower cortical thickness (-0.05 [-0.09, -0.02], p=0.01), and associated with lower memory (0.3 [-0.6, -0.001], p=0.05). In Non-Hispanic White participants, loneliness was associated with greater WMH volume (0.5 [0.07, 0.82], p=0.03), while in Hispanic participants, loneliness was associated with lower cortical thickness (-0.16 [-0.24, -0.08], p=0.0006). In Non-Hispanic Black participants, loneliness was associated with lower memory (-13 [-26, -0.5], p=0.05), and the association between lower cortical thickness and lower memory was stronger in those that endorse loneliness (5 [0.2, 10], p=0.05). In Hispanic participants, loneliness was associated with higher memory (13 [4, 22], p=0.009), but the association between higher amyloid burden and lower memory was stronger in those that endorse loneliness (-12 [-20, -4], p=0.006); further, loneliness was marginally associated with lower memory (-0.7 [-1.4, 0.1], p=0.09), independently of WMH.

Associations between loneliness and biomarkers may relate to health seeking behavior, reported as treatment status for diabetes, for cerebrovascular burden and general neurodegeneration, but might be more complex for amyloid. The degree to which loneliness increased the susceptibility to amyloid and neurodegeneration-related, but not cerebrovascular-related, memory impairment, specifically, may suggest that domains beyond memory should be considered. Future work should be longitudinal to disentangle the effects of loneliness from related constructs like depression and anxiety, incorporate other AD biomarkers such as hyperphosphorylated tau, and incorporate biological mechanisms (e.g., stress, inflammation) into models of loneliness and AD pathogenesis. Older adults from all backgrounds may be more susceptible to loneliness, which was associated with lower memory; culturally-humble, social support-based interventions may reduce the risk of cognitive impairment.

Non-Hispanic Black older adults experience a disproportionate burden of Alzheimer’s Disease and related dementias (ADRD) risk compared to non-Hispanic White older adults. It is necessary to identify mechanisms that may be contributing to inequities in cognitive aging. Psychosocial stressors that disproportionately affect Black adults (e.g., discrimination) have the potential to impact brain health through stress pathways. The brain’s white matter, which appears to be particularly important for ADRD risk among Black older adults, may be uniquely vulnerable to stress-related physiological dysfunction. To further understand whether and how discrimination can affect ADRD risk, this study aimed to examine associations between multiple forms of racial discrimination and white matter integrity, operationalized through diffusion tensor imaging.

Cross-sectional data were obtained from 190 non-Hispanic Black residents aged 65+ without dementia in northern Manhattan. Racial discrimination was self-reported using the Everyday Discrimination and Major Experiences of Lifetime Discrimination scales. Example items from the Everyday Discrimination Scale include: “You are treated with less respect than other people”; “You are called names or insulted.” Example items from the Major Experiences of Lifetime Discrimination Scale include: “At any time in your life, have you ever been unfairly fired from a job?”; “Have you ever been unfairly denied a bank loan?” Racial discrimination was operationalized as experiences attributed to “race” or “skin color.” White matter integrity was assessed using fractional anisotropy (FA) via diffusion tensor imaging. Multivariable regression models evaluated the unique effects of everyday and major experiences of lifetime racial discrimination on mean FA in the whole brain and specific regions. Initial models controlled for age, sex/gender, intracranial volume, and white matter hyperintensities. Subsequent models additionally controlled for socioeconomic and health factors to consider potential confounders or mediators of the relationship between discrimination and white matter integrity.

Major experiences of lifetime discrimination were negatively associated with mean FA within the left cingulum cingulate gyrus and the right inferior fronto-occipital fasciculus. These associations persisted when controlling for additional covariates (i.e., education, depression, and cardiovascular diseases). In contrast, major experiences of lifetime discrimination were positively associated with mean FA within the right superior longitudinal fasciculus (temporal part). This association was attenuated when controlling for additional covariates. Everyday racial discrimination was not associated with mean FA in any regions.

These results extend prior work linking racial discrimination to brain health and provide evidence for both risk and resilience among Black older adults. Major experiences of lifetime racial discrimination, a proxy for institutional racism, may have a stronger effect on white matter integrity than everyday racial discrimination, a proxy for interpersonal racism. Educational opportunities and cardiovascular risk factors may represent mediators between racial discrimination and white matter integrity. White matter integrity within specific brain regions may be a mechanism through which racially patterned social stressors contribute to racial disparities in ADRD. Future research should characterize within-group heterogeneity in order to identify factors that promote resilience among Black older adults.

Neuronal dysfunction of the locus coeruleus (LC), the primary producer of norepinephrine, has been identified as a biomarker of early Alzheimer's disease (AD) pathophysiology. Norepinephrine has been implicated in attentional control, and its reduced cortical circulation in AD may be associated with selective attentional difficulties. Additionally, greater pupil dilation indicates greater effort needed to perform a cognitive task, and greater compensatory effort to perform the digit span task has been found in individuals at risk for AD. In this study, we examined associations between a neuroimaging biomarker of the LC and pupil dilation during the Stroop task as a sensitive measure of attentional control.

64 older adults without dementia were recruited from the San Diego community (mean [SD] age = 74.3 [6.3]; 39 cognitively unimpaired and 25 with mild cognitive impairment). All participants underwent magnetic resonance imaging of the LC and generated behavioral data from a computerized Stroop task that included 36 incongruent trials (e.g., GREEN presented in red ink), 36 congruent trials (e.g., GREEN presented in green ink), and 32 neutral trials (e.g., LEGAL presented in green ink) in a randomized presentation. Mean pupil dilation for each trial (change relative to baseline at the start of each trial) was measured at 30 Hz using the Tobii X2-30 system (Tobii, Stockholm, Sweden) and averaged within each Stroop condition. Paired t-tests assessed for differences in mean pupil dilation across incongruent and congruent Stroop conditions. Iterative re-weighted least squares regression was used to assess the association between a rostral LC contrast ratio measure derived from manually marked ROIs and mean pupil dilation during incongruent trials divided by congruent trials, adjusting for age, sex, and education. Follow-up analyses also assessed the association of these variables with mean reaction time (RT) for incongruent trials divided by congruent trials.

Mean pupil dilation significantly differed across conditions (t = 3.74, mean difference = .13, 95% CI [.06, .20]) such that dilation was higher during the incongruent condition (mean [SD] dilation = .18 [.38] mm) relative to the congruent condition (mean [SD] dilation = .05 [.35] mm). A significant association was observed between pupil dilation and LC contrast ratio, such that increased levels of mean dilation during incongruent trials relative to congruent trials were observed at lower levels of LC contrast ratio (i.e., lower LC integrity; r = -.37, 95% CI [-.55, -.13]). This association was not observed for mean dilation during only congruent trials (r = -.08, 95% CI [-.31, .18]). Additionally, neither LC contrast ratio [r = .24, 95% CI [-.02, .46]) nor mean incongruent/congruent pupil dilation (r = .14, 95% CI [-.13, .37]) were associated with incongruent/congruent RT.

Findings suggest that increased pupil dilation during a demanding attentional task is indicative of increased compensatory effort needed to achieve the same level of performance for individuals with reduced LC biomarker integrity. Pupillometry assessment offers a low-cost, non-invasive, and scalable biomarker of LC dysfunction that may be indicative of preclinical AD.

Norrie disease is a rare, x-linked recessive genetic disorder associated with an NDP gene mutation. Males are predominantly affected. Typical symptoms include vision loss around the time of birth and progressive hearing loss. Cognitive and behavioral abnormalities also occur in 30-50% of individuals, including developmental delays, intellectual disability, cognitive regression, psychosis, and aggression. There is limited research, however, examining the neuropsychological deficits in adulthood resulting from Norrie disease, especially with neuropsychological data and in individuals without other neurological manifestations of the disease, such as seizures. Here, we present the neurocognitive profile of a patient with Norrie disease who presented for a cognitive evaluation in adulthood due to report of more recent memory decline.

Mr. Smith is a Caucasian male in his mid-40's who previously underwent genetic testing and was subsequently diagnosed with Norrie disease. As a result of his diagnosis, he experienced complete vision loss since birth and bilateral hearing loss that began in childhood and gradually worsened in adolescence. Medical history was otherwise unremarkable. Developmental milestones were met on time. Historical intelligence testing conducted in elementary school revealed borderline on one intelligence test to high average performance on other intelligence tests. However, he was retained grades several times due to factors such as behavioral disruptions and academic difficulties. He had been employed as an assembly line worker for many years, but had not worked for 10 years prior to the neuropsychological evaluation. Emotionally, he had a longstanding history of anxiety and endorsed mild anxiety and depression at the time of the evaluation. The patient first noticed memory difficulties in adolescence then noticed further decline four years prior to the neuropsychological evaluation (around when he received a left-ear cochlear implant), which had remained stable since onset.

In the context of low average premorbid intellectual functioning, Mr. Smith's neurocognitive profile was notable for difficulties with alphanumeric set-shifting and abstract thinking, with otherwise preserved cognitive functioning. Weaknesses observed on testing may have represented longstanding weaknesses and did not rise to the level of a cognitive disorder. Affective distress was also suspected to have accounted for some of the cognitive lapses the patient reported experiencing with day-to-day functioning.

The current poster aims to contribute to the limited body of literature examining neuropsychological deficits in adulthood resulting from Norrie disease. This is especially critical given that the long-term cognitive dysfunction of this disorder is relatively unknown and could negatively impact patients' quality of life over time.

Agitation is a common neuropsychiatric symptom within the dementia spectrum, experienced by 70 percent of individuals with cognitive decline. Prior literature demonstrates a strong association between care recipient agitation and burden in caregivers of individuals with dementia, as these symptoms are often difficult to manage and predict. Understanding how agitation symptoms in the person with dementia may influence caregiver burden is imperative given these strong associations; however, both agitation and burden are complex, multidimensional constructs. Agitation in dementia involves a range of behaviors including increased motor activity, emotional distress, and aggressive behaviors. Caregiver burden is also multi-faceted and often incorporates dimensions of social/relationship, emotional, and physical health strain. The current study sought to determine whether specific presentations of agitation differentially relate to distinct patterns of caregiver burden.

Medical record data from an outpatient memory clinic were extracted for 609 persons with dementia and their caregivers. Caregivers completed the Zarit Burden Interview (ZBI) to assess caregiver burden and the Cohen-Mansfield Agitation Inventory (CMAI) to assess care recipient agitation behaviors. At their initial outpatient appointment, care recipients were also administered a measure of global cognitive functioning (either the Montreal Cognitive Assessment or the Mini-Mental State Examination). Demographic information was extracted from medical records. Exploratory factor analysis was used to determine ZBI and CMAI factor structures. Hierarchical multiple regression analyses then examined whether factors of the CMAI differentially predicted ZBI factors, controlling for dementia severity and demographic variables.

Exploratory factor analysis yielded three domains of agitation on the CMAI ("Physically Aggressive," "Physically NonAggressive," "Verbally Agitated") and four domains of burden on the ZBI ("Impact on Life," "Guilt/Uncertainty," "Embarrassed/Frustrated," and "Overwhelm"). Regression analyses demonstrated all domains of agitation positively predicted overall burden. Regarding specific aspects of burden, Physically Aggressive behaviors predicted only Embarrassment/Frustration (B=.41, SE=.10, ß=.16, p<.001). Non-Aggressive behaviors predicted Impact on Life (B=.14, SE=.05, ß=.13, p<.01) and Guilt/Uncertainty (B=.05, SE=.02, ß=.10, p<.05). Verbally Agitated behaviors predicted all burden dimensions: Impact on Life (B=.35, SE=.06, ß=.32, p<.001), Guilt/Uncertainty (B=.12, SE=.03, ß=.22, p<.001), Embarrassment/Frustration (B=.17, SE=.02, ß=.38, p<.001), and Overwhelm (B=.16, SE=.02, ß=.40, p<.001).

Findings enhance understanding of the relationships between specific agitation symptoms and distinctive aspects of caregiver burden, suggesting that targeted interventions for aspects of caregiver burden based on agitation symptoms may be useful in alleviating burden. Interventions focused on caregivers' feelings of guilt, personal health decline, lack of time for themselves, and fear and uncertainty about the future may be effective when care recipients present with physically nonaggressive behaviors (e.g., pacing, restlessness, inappropriate dress or disrobing). When a care recipient presents with physically aggressive behaviors, helping the caregiver cope with embarrassment or anger may be of benefit. When a care recipient presents with verbally agitated behaviors, interventions targeting burden globally may be most useful. Future work should seek to replicate the current findings and explore such interventions.

Both Apolipoprotein z4 (APOz4) and Brain-Derived Neurotropic Factor val66met (BDNF-met) have been implicated as cognitive risk polymorphisms and may signal a more rapid trajectory of cognitive decline (Boots et al., 2017; Lim et al., 2015). The presence of both risk alleles may additively result in greater cognitive difficulties (Cechova et al., 2020), specifically executive functioning (Sapkota et al., 2017). As executive functioning difficulties can be associated with Posttraumatic Stress Disorder (PTSD; Woon et al., 2017), individuals with PTSD who carry these polymorphisms may be at higher risk for decline in executive functioning. In this study, we examined the cross-sectional and longitudinal impact of these alleles on executive functioning performance in Veterans with PTSD.

Seventy community-dwelling male Veterans were enrolled as part of a larger study at VAPAHCS and consented to genetic analysis. A current or lifetime history of PTSD (score > 40 on the CAPS-IV; Blake et al., 1995) was required for study participation. Trail Making Test B (TMT-B; Army Individual Test Battery, 1994) was used to assess executive functioning. TMT-B was part of a comprehensive neuropsychological battery administered at baseline and yearly over the following three years. Mean age and education were 61 years old (SD = 4.5; range = 55-78) and 14 years (SD = 2.3; range = 8-20), respectively.

The majority of the sample was White (71%) and were from the Korean and Vietnam War eras.

APOz4 and BDNF-met were present in 29% and 27% of the sample, respectively; both were present in six participants. Regression models were fitted separately for TMT-B raw time-to-complete and number of errors, both cross-sectionally at screening and then longitudinally. The presence of BDNF-met was a significant predictor of TMT-B time and number of errors in both models (Time: ß = 0.09, p = 0.03 and ß = 0.11, p < 0.01; Errors: IRR = 2.4, p = 0.01 and IRR = 1.9, p = 0.01), while APOz4 only predicted errors longitudinally (IRR = 1.8, p = 0.03). There was no significant allelic interaction; however, the presence of both alleles additively multiplied TMT-B errors by approximately 3.7 times at screening (IRR = 3.7; p = 0.01) and 3.3 times longitudinally (IRR = 3.3; p < 0.01).

Altogether, these results are suggestive of an adverse, additive, effect of the APOz4 and BDNF-met polymorphisms on executive functioning, in particular error-proneness, with their combined presence tripling the errors made on TMT-B cross-sectionally and longitudinally. Consistent with previous research, the TMT-B error analysis increases detection of cognitive impairment, similar to other clinical samples (Varjacic et al., 2018). While TMT-B errors are typically interpreted qualitatively, the strong effect of these established risk alleles on error rates further support this metric as a clinically useful indicator of executive dysfunction in a PTSD population. In keeping with the Boston Process approach, these findings support the importance of error analysis in clinical interpretation of neuropsychological performance.

Metamemory is an aspect of metacognition that is one's knowledge of memory and understanding of their own memory performance (Kreutzer et al., 1975). Executive function skills are foundational skills required for the development of metamemory in early school-age children (Lockl & Schneider, 2007; Lecce et al., 2015). Previous studies have suggested children with Attention-Deficit/Hyperactivity Disorder (ADHD) may have weaker study and organizational strategies, suggesting weaker metamemory skills (O'Neill & Douglas, 1991; Voelker et al., 1989). The current study aimed to examine the metamemory knowledge of typically developing (TD) children and children with ADHD on a novel declarative metamemory questionnaire. We hypothesized that the ADHD group would have worse metamemory performance than the TD group and that executive functioning skills would be significantly associated with metamemory for all groups.

The current study recruited a total of 93 English-speaking children between the ages of 6 to 12 years old, including 70 typically developing (TD) children (M age=9.1+1.92; females 49%), and 23 children with diagnoses of ADHD (M age=9.56+1.27; females 57%). Fifty-seven percent of the ADHD group reported daily use of stimulant medication, but no participants took medication on the day of testing. The participant groups did not significantly differ regarding age or sex. Participants completed the Measure of Metamemory (MoM-10) which included 10 multiple choice questions (i.e., Accuracy) and asked participants to explain their multiple-choice answer (i.e., Explanation). This provided three scores: Accuracy (max 10 points), Explanation (max 20 points), and Total (max 30 points). Additionally, participants' parents completed the 12-item Behavior Rating Inventory of Executive Function, 2nd Edition (BRIEF-2) Screening form, evaluating the child's executive functioning, which provided a percentile based on age and sex.

Within the ADHD group, BRIEF-2 percentiles and MoM-10 scores did not differ between those who were medicated and those who were not. As previous literature has shown, the TD and ADHD groups significantly differed on the BRIEF-2 screening score percentiles (t(91)=-5.78, p<0.001; TD M=52.89+26.1; ADHD M=85.26+13.82). The TD and ADHD groups did not significantly differ on either the MoM-10 Accuracy (p=0.13; TD M=7.22+1.84; ADHD M=7.87+1.32), the Explanation (p=0.08; TD M=9.34+3.80; ADHD M=10.57+2.92), or Total (p=0.13). There was a trend towards a significant correlation between the Explanation scores and BRIEF-2 for TD participants (r=-0.23, p=0.06), but there was no significant correlation between Explanation, Accuracy, or Total scores and the BRIEF-2 for the ADHD group.

Our results tentatively suggest a possible association between metamemory and parent reported executive functioning for TD children, supporting the expected association between the development of executive functioning and the development of metamemory. However, there was no association between metamemory and executive functioning for children with ADHD, likely due to the restricted range of executive functioning scores for this group (i.e., M=85.25+13.82; Range 55-99). Additionally, metamemory did not significantly differ between diagnostic groups. Children with ADHD may have comparable metamemory knowledge to TD children as a result of executive functioning instruction and support they have received. Rather, there may be group differences in the application of metamemory judgement and strategies.

Verbal memory deficits are present in multiple sclerosis (MS), but neither inflammatory T2 lesion volume nor cerebral atrophy (generalized or localized hippocampal atrophy) fully explain disease-related verbal memory changes. Importantly, the hippocampus does not function in a vacuum; memory encoding and retrieval requires interactions between the hippocampus and cortical areas where information is processed and represented. Indeed, we have previously shown that lexical access speed (a language function assessed by rapid automatized naming) independently predicted delayed recall of verbal information (word list) for persons with MS, even when controlling for total learning. Informed by this work and recent ultra high field (7.0 Tesla) MRI research reporting high cortical lesion count in regions associated with phonological processing (e.g., plenum temporale, superior temporal gyrus), we assessed whether phonological processing independently explains verbal memory deficits in persons with MS.

Analyses were performed on a clinical sample of persons withMS aged 18 to 59 years (n=60: 49 relapsing, 11 progressive). Word-list memory was assessed by the Hopkins Verbal Learning Test, Revised (HVLT-R), which yielded scores for Total Learning (TL) and Delayed Recall (DR). Phonological processing was assessed with WIAT-4 Phonemic Proficiency. WIAT-4 Sentence Repetition was utilized as a non-phonological language control task, and WIAT-4 Word Reading was administered to control for premorbid verbal ability. CANTAB Paired Associate Learning served as a nonverbal memory comparison. Performance on tasks was standardized using published age-adjusted norms. Primary analyses used partial correlations to assess relationships between Phonemic Proficiency and (a) HVLT-R TL and DR controlling for WIAT-4 Word Reading, and (b) HVLT-R DR controlling for WIAT-4 Word Reading and HVLT-R TL. To assess specificity to phonological processing, the same partial correlations assessed relationships between Sentence Repetition and HVLT-R variables, and between Phonemic Proficiency and nonverbal memory (CANTAB PAL).

When controlling for premorbid verbal ability, Phonemic Proficiency performance accounted for 7.8% of the variance in HVLT-R TL (rpartial=0.28, p=0.031) and 16% of the variance in HVLT-R DR (rpartial=0.40, p=0.002). Moreover, when additionally controlling for HVLT-R TL, Phonemic Proficiency still accounted for 10% of the variance in HVLT-R DR (r partial— 0.32, p=0.016). Showing specificity to phonological processing ability, performance on Sentence Repetition was not significantly related to HVLT-R DR when controlling for premorbid verbal ability (WIAT-4 Word Reading) and HVLT-R TL (rpartial=0.09, p=0.510). Showing specificity to verbal memory, neither Phonemic Proficiency nor Sentence Repetition performance were reliably related to CANTAB PAL for any variance in performance in nonverbal memory (Ps>0.9).

Results suggest that language ability, specifically phonological processing, contributes to delayed recall of word lists independent of premorbid verbal ability and initial total learning scores in persons with MS. These findings demonstrate contributions of language ability to verbal memory and highlight the need for further research into language ability changes in persons with MS. This may have implications for verbal memory rehabilitation in MS.

Set-shifting/switching tasks, among other measures of executive functioning, are typically thought to represent frontal lobe functioning. However, the neuroanatomical correlates of these tests are not fully established. The aim of this study was to examine associations between individual measures of set-shifting/switching and cortical thickness. We hypothesized that performance on each switching measure would strongly correlate with aggregated cortical thickness within the frontal lobe.

Measures of interest included set-shifting subtests of the Delis-Kaplan Executive Function System (DKEFS): Color-Word Inhibition Switching, Category Switching, and Trail Making Test Number-Letter Switching. Archival data from an outpatient memory disorders clinic were reviewed to identify individuals whose neuropsychological evaluations included the measures of interest and had quality-assessed, volumetric MRI data available (n=243; 53.1% male, 81.9% Caucasian, Mage=72.4, SDage=6.7). Cortical thickness values were generated by FreeSurfer and averages were calculated for both frontal and temporal lobes, separately. Using partial correlations, controlling for age, we explored associations between each switching trial separately with right and left, frontal and temporal cortical thickness. The strength of associations within each lobe were then compared using Fisher's r-to-z transformations.

Category Switching was significantly correlated with left and right hemisphere temporal thickness (r=0.38 and 0.31, respectively), but was not significantly correlated with left or right frontal lobe cortical thickness (r=.12 and .07, respectively). Fisher's r-to-z transformations revealed significantly stronger relationships between Category Switching and temporal thickness, rather than frontal thicknesses. Trails Switching was also significantly correlated with left and right temporal cortical thickness (r=-0.28, and =-0.23, respectively) and bore weaker associations with frontal cortical thickness (r=-.13 and r = -.14 for left and right hemispheres, respectively). In contrast, Color-Word Inhibition-Switching did not show a significant relationship with frontal or temporal cortical thickness.

Contrary to our hypothesis, stronger associations were observed with temporal lobe cortical thickness for Category Switching. Category Switching involves a language production component which could explain the strong association with temporal cortical thickness compared to frontal cortical thickness. Additionally, the pattern of associations between Trails Switching and frontal and temporal thickness was non-specific. Perhaps most striking is the lack of association between each switching measure and frontal cortical thickness, which was unexpected, given that these measures are used to assess executive functioning, broadly localized to the frontal lobe. Future directions involve examining the associations of these measure with subcortical structures and replicating these findings in larger datasets.

Autism is a neurodevelopmental disorder characterized by impairments in social communication and the presence of restricted and repetitive behaviors (RRBs). Clinical diagnosis of autism is often complicated by heterogeneity in core autism traits and other individual characteristics (e.g., cognition). Previous literature suggests that degree of autism characteristics, cognitive ability, and age contribute to identifying homogenous subgroups of autism, which facilitates prognosis and treatment planning. The present study extends these findings by examining profiles of cognition, age, and autism characteristics (measured by the Autism Diagnostic Observation Schedule, Second Edition [ADOS-2]) in a clinical sample of school-aged children presenting with concern for possible autism. Profiles are also described according to whether children received an autism diagnosis and clinician ratings of emotional/behavioral problems, which have been shown to influence diagnostic clarity when assessing for autism.

We conducted a retrospective chart review of 188 children (68% male) ages 4-17 years (M=8.9) who were referred for an autism evaluation. Latent profile analysis was conducted using age, ADOS-2 Social Affect (SA) and RRB scores, and verbal and non-verbal intelligence quotients (VIQ/NVIQ). Model fit comparing 2, 3, 4, and 5-class models was assessed using log-likelihood, AIC, BIC, SABIC, entropy, and Lo, Mendell, and Rubin (LMR) and bootstrap likelihood ratio (BLRT) tests. The frequency of clinical autism diagnosis and ADOS-2 emotional/behavioral problems were calculated across profiles in the best-fitting model.

The 5-class model demonstrated the best fit. The following characteristics were observed across five profiles: 1) mean age = 9.5 years, Low Average VIQ/NVIQ, and low SA (M=5.2) and RRB (M=0.7) scores; 2) mean age = 7.3 years, Average VIQ/NVIQ, and low SA (M=3.1) and RRB (M=0.8) scores; 3) mean age = 10.1 years, Low Average VIQ/NVIQ, and high SA (M=11.3) and RRB (M=4.2) scores; 4) mean age = 8.8 years, Average VIQ/NVIQ, and moderately high SA (M=9.6) and RRB (M=3.4) scores; and 5) Exceptionally High VIQ, Above Average NVIQ, and comparatively mid-level SA (M=6.6) and RRB (M=3.6) scores. Autism diagnosis and emotional/behavioral problems varied across profiles. Profiles 1 and 2 contained lower diagnosis rates (33% and 10%, respectively). Profiles 3 and 4 contained the highest diagnosis rates (97% in both), followed by profile 5 (75%). In terms of emotional/behavioral problems, Profile 2 exhibited the highest overactivity (56%). Profile 3 demonstrated the highest rate of tantrums/disruptive behaviors (20%).

Findings revealed distinct profiles of IQ and autism characteristics within a clinical sample of school-aged children referred for possible autism. Children with the highest scoring ADOS profile were older compared to other profiles. Higher and lower scoring ADOS profiles exhibited both lower and higher IQ scores. Descriptive analyses suggested that the frequency of autism diagnosis was notably higher in moderate and high-scoring ADOS profiles; however, emotional/behavioral problems were salient in only one low and one high-scoring ADOS profile. The findings suggest that higher-scoring ADOS profiles consistently demonstrated high autism diagnosis rates but varied across IQ and behavioral problems. These results have implications for interpreting these characteristics during clinical autism diagnosis.

Timing, or the decision of when to act, is essential to mammalian behaviors from escaping predators to driving a car. It requires cognitive functions such as working memory for time-based rules and attention to the passing of time. Thus, it can be used as a proxy for higher order executive functions that are difficult to measure but are impaired in many neurological disorders. Therefore, insights from studies of interval timing, tasks which require estimating time intervals of several seconds, have great value for our understanding of human disease. Crucial to timing is the basal ganglia, which integrates cortical activity with midbrain dopamine signals and sends out signals to the spinal cord that regulate movement, motivation, and other behaviors. We have previously found that within the basal ganglia, medium spiny neurons of the striatum exhibit ramping activity in time-related tasks. In other words, they gradually increase or decrease firing frequency across a timed interval, and this is thought to encode time. Yet it is still unknown how the encoding of time is translated into time-based motor responses. To answer this question, we turned to the external globus pallidus (GPe) because it is a regulatory hub within the basal ganglia and is thus well positioned to regulate timing behavior. We sought to examine how the GPe functions in response to time-based demands.

We recorded from neuronal ensembles using 16 channel electrode arrays implanted in the GPe of five mice while they performed an interval timing task called the switch interval timing task. Spike sorting was then used to identify signal from individual neurons.

Data were compiled from 43 neurons over several trials. Principal component analysis of neural firing activity was then conducted and revealed a downward ramping pattern in GPe neurons during interval timing trials. Data were then separated based on trials in which mice made correct decisions and those in which mice made a mistake. We found that when mice make correct timing decisions, there is downward ramping activity in the GPe, yet when mice make timing mistakes, this ramping pattern is lost.

Our findings suggest that the GPe processes timing signals through ramping activity, before projecting to the output nuclei of the basal ganglia. This is a novel finding and contributes to a growing understanding of the temporal code of the basal ganglia. The full extent of this code is still unknown, but this insight contributes to a better understanding of how the globus pallidus represents cognition. If we can better explain the neural correlates of timing, we can use this knowledge to inform therapeutic interventions for basal ganglia dysfunction, which could have profound implications for diseases like Parkinson’s disease, which affects millions around the world.

CI Cognitive Therapy (CICT) is a combination of behavioral techniques derived from CI Movement Therapy (CIMT) modified to apply to the cognitive domain, and Speed of (Cognitive) Processing Training (SOPT). SOPT is effective in improving cognitive function in the treatment setting and driving ability in everyday situations. The data concerning the effect of SOPT on other cognition-based instrumental activities of daily living (IADL) in everyday situations is incomplete. The strengths of CIMT, based on its Transfer Package (TP), are to facilitate 1) transfer of improved function from the treatment setting to IADL in everyday settings, and 2) long-term retention of the improved performance of IADL. This study sought to determine in a preliminary case series whether the TP of CI Movement Therapy combined with SOPT would have the same effect on a wide range of impaired cognition-based ADL.

Participants were 6 adults with chronic stroke: mean chronicity = 36.2 months, (range, 16-56 months); mean age = 59.7 years, (range, 47-55); 1 female; 3 African American and 3 European American. Five had mild cognitive impairment, while one had moderate impairment. Participants received 35 hours of outpatient treatment in 10-15 sessions distributed over 2-6 weeks, depending on the participants’ availability. Sessions began with 1 hour of SOPT training followed by training of cognition-based ADL by the process of shaping, a common method in the behavior analysis field. Other behavior analysis methods employed in the TP of CI Movement Therapy were used, including: 1) behavior contracting, daily assignment of homework, participation of a family member in the training and monitoring process, daily administration of a structured interview assessing amount and quality of performance of 30 IADL, problem solving to overcome perceived (or real) barriers to performance of IADL. Participants were given daily homework assignments in follow-up and were contacted in periodic, pre-arranged phone calls to determine status, compliance and problem-solve.

All six participants showed marked improvement on the SOPT test similar to that in the Ball et al studies. However, here transfer to IADL outside the treatment setting was substantial. On the main real-world outcome, the Canadian Occupational Performance Measure (COPM), there were increases of 2.7±1.3 and 2.1±1.6 on the two scales (d’s = 1.9 & 1.3, respectively). (Changes on the COPM > 2 points are considered clinically meaningful and changes in d’ >.8 are considered large). On two other real-word measures, the Cognitive Task Activity Log (CTAL) and inventory of Improved and New Cognitive Activities (INCA), there was a marked increase during the acquisition phase of training. There was no loss in retention over the 6-16 months (mean = 12.2) of follow-up to date. Instead, the INCA showed strong further improvement after the end of treatment-setting training, especially in the New Activities Not Performed Since Before Stroke Onset category, going from a mean of 8.2 after training to 14.6 at the end of follow-up.

These very preliminary results suggest that CICT may be an efficacious therapy for mild to moderate cognitive impairment in chronic stroke and possibly other disorders.

A commonly used confrontation naming task used in the United States is The Boston Naming Test (BNT). Performance differences has been found in Caucasian and ethnic minorities on the BNT. The Cordoba Naming Test (CNT) is a 30-item confrontation naming task developed in Argentina. Past research has shown acculturation levels can influence cognitive performance. Furthermore, one study evaluated geriatric gender differences on CNT performance in Spanish. Researchers reported that older male participants outperformed female participants on the CNT. To our knowledge, researchers have not evaluated ethnic differences on the CNT using a geriatric sample. The purpose of the present study was to examined CNT performance and acculturation in a Latinx and Caucasian geriatric sample. It was predicted the Caucasian group would outperform the Latinx group on the CNT. Moreover, the Caucasian group would report higher acculturation levels on the Abbreviated Multidimensional Acculturation Scale (AMAS) compared to the Latinx group.

The sample consisted of 9 Latinx and 11 Caucasian participants with a mean age of 66.80 (SD =6.10), with an average of 14.30 (SD = 2.00) years of education. All participants were neurologically and psychologically healthy and completed the CNT and the AMAS in English. Acculturation was measured via the AMAS English subscales (i.e., English Language, United States. Identity, United States, Competency). A series of ANCOVAs, controlling for years of education completed and gender, was used to evaluate CNT performance and acculturation.

The ethnic groups were not well demographically matched (i.e., years of education and gender).We found that the Caucasian group outperformed the Latinx group on CNT performance p = .012, ηp 2 = .34. Furthermore, the Caucasian group reported higher acculturation levels (i.e., English Language, United States, Identity, United States, Competency) compared to the Latinx group p’s < .05, ηps2 = .42-.64.

To our knowledge, this is the first study to evaluate CNT performance between ethnic groups with a geriatric sample. As expected the Caucasian group outperformed the Latinx group on the CNT. Also, as expected the Caucasian group reported higher English acculturation levels compared to the Latinx group. Our findings are consistent with past studies showing ethnic differences on confrontational naming performance (i.e., The Boston Naming Test), favoring Caucasians. A possible explanation for group differences could have been linguistic factors (e.g., speaking multiple languages) in our Latinx group. Therefore, since our Latinx group reported lower levels of English Language, United States identity, and United States competency the Latinx group assimilation towards United States culture might of influence their CNT performance. Future studies with different ethnic groups (e.g., African-Americans) and a larger sample size should examine if ethnic differences continue to cross-validate in a geriatric sample.

Many individuals with COVID-19 develop mild to moderate physical symptoms that can last days to months. In addition to physical symptoms, individuals with COVID-19 have reported depressive symptoms and cognitive decline, posing a long-term threat to mental health and functional outcomes. Few studies have examined the presence of co-occurring depression and subjective cognitive decline in individuals who tested positive for COVID-19. The current study examined whether having COVID-19 is subsequently associated with greater depressive symptoms and subjective cognitive decline when compared to healthy individuals. Our study also examined differential associations between symptoms of depression and subjective cognitive decline between individuals who have and have never had COVID-19.

Adults (N = 104; mean age = 37 years, 69% female) were recruited online from Ontario and British Columbia, Canada. Participants were categorized into two groups: (1) persons who tested positive for COVID-19 at least three months prior, had been symptomatic, and had not been ventilated (N = 50); and (2) persons who have never been suspected of having COVID-19 (N = 54). The Center for Epidemiological Studies Depression Scale (CES-D) and the Subjective Cognitive Decline Questionnaire (SCD-Q) were administered to both groups as part of a larger clinical neuropsychological evaluation. Two separate linear regression analyses were conducted to examine the association of COVID-19 with depressive symptoms and subjective cognitive decline. A moderation analysis was performed to examine whether depressive symptoms were associated with subjective cognitive decline and the extent to which this differed by group (COVID-19 and controls). Participants’ age, self-reported sex, and history of depression were included as covariates.

The first regression model explained 17.2% of the variance in CES-D scores. It was found that the COVID-19 group had significantly higher CES-D scores (ß = .20, p = .03). The second regression model explained 35.9% of the variance in SCD-Q scores. Similar to the previous model, it was found that the COVID-19 group had significantly higher SCD-Q scores compared to healthy controls (ß = .22 p = .01). Lastly, the moderation model indicated that higher CES-D scores were associated with higher SCD-Q scores (ß = .43, p < .01), but there was no statistically significant group X CES-D score interaction.

These findings suggest that individuals who previously experienced a mild to moderate symptomatic COVID-19 infection report greater depressive symptom severity as well as greater subjective cognitive decline. Additionally, while more severe depressive symptoms predicted greater subjective cognitive decline in our sample, the magnitude of this association did not vary between those with and without a previous COVID-19 infection. While the underlying neurobiological and social mechanisms of cognitive difficulties and depressive symptoms in persons who have had COVID-19 have yet to be fully elucidated, our findings highlight treatment for depression and cognitive rehabilitation as potentially useful intervention targets for the post COVID-19 condition.

The purpose of this study using archival data was to examine processing speed (PS) and its relation with academic fluencies in children who were diagnosed with, and treated with chemotherapy for, acute lymphoblastic leukemia (ALL) before vs. after five years of age. Chemotherapy is the first-line treatment for childhood leukemias, and the impact of cancer treatment on academic and global functioning may include a steady decline in functions over time (Baron & Rey-Casserly, 2013). Specifically, this research initiative examined age and gender factors in PS and academic fluencies in this population.

Sixty-eight participants (39 M, 29 F; mean age 10.6 years) diagnosed with ALL and who were previously treated with chemotherapy were included. Thirty-seven participants (23 M, 14 F) were <5 years of age at the time of diagnosis and onset of chemotherapy, while 31 participants (16M, 15 F) were >5 years of age at diagnosis and treatment. Participants ranged in age from 6 to 17 years at the time of their neuropsychological evaluation. Participants were given the WISC-V (PS subtests) and WJ-IV academic fluencies (math and reading). To evaluate research questions and hypotheses, correlational tests, independent samples t-tests, and analyses of variance (ANOVA) were used. Results at the p< .05 level are reported.

There were significant correlations between PS and WJ math fluency (r=.510) and reading fluency (r=.392). Independent samples t-test analyses revealed that children who scored below 85 (standard score) on PS composite score demonstrated poorer performance on WJ math fluency (t(60)=-3.971, p=.000, d=1.065) and reading fluency (t(56)=-3.041, p=.004, d=0.896) compared to children whose PS scores were > 85. For children whose PS scores were <85, mean scores were in the low average range for WJ-IV math fluency (M=81.05) and reading fluency (M=84.50). No significant differences were found for age or gender in relation to PS and academic fluencies.

Findings are important in highlighting the need for school accommodations in pediatric survivors of ALL. Processing speed is one of the most vulnerable functions impacted by cancer therapies and was positively correlated with reading and math fluencies in this study. Mean scores for math and reading fluencies were low average for age. In terms of academic accommodations, due to the slow processing speed of these boys and girls, regardless of their age at diagnosis and onset of chemotherapy, the provision for extra time for ALL survivors is recommended to ensure they are given the opportunity to maximize their learning potential and demonstrate their true academic abilities. Parents are encouraged to practice basic fluencies at home as early as possible. Inhospital and home-bound schooling supports are recommended to maintain educational progress. For children at higher risk for late effects and neurocognitive decline, rehabilitation similar to that which TBI survivors receive can be effective, as well. Future prospective research, including longitudinal tracking, with more homogeneous samples of pediatric survivors of ALL is expected to extend and refine findings of the present study.