Browsing by Subject "Cognitive functioning"

Now showing 1 - 4 of 4
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    Childhood Socioeconomic Status Interacts with Cognitive Function to Impact Scam Susceptibility Among Community-Dwelling Older Adults
    (Taylor & Francis, 2023) Glover, Crystal M.; Yu, Lei; Stewart, Christopher C.; Wilson, Robert S.; Bennett, David A.; Lamar, Melissa; Boyle, Patricia A.; Neurology, School of Medicine
    Objectives: We examined whether childhood socioeconomic status (SES) is related to scam susceptibility in old age and tested the hypothesis that childhood SES interacts with cognitive function to impact scam susceptibility. Methods: This study employed a cross-sectional design. All data were collected in participants' community-based residences. Participants were 1071 older adults (mean age = 81.05 years, SD = 7.53) without dementia (median MMSE score = 28.29, IQR = 27.86-30.00). Participants completed assessments of childhood SES, cognitive function, and scam susceptibility. We used linear regression models to examine the associations of childhood SES and cognitive function with scam susceptibility. Results: In a regression model adjusted for age, gender, and education, poorer cognitive function was associated with higher scam susceptibility, but childhood SES was not. However, in an additional model that included the interaction of childhood SES and cognitive function, the interaction was significant, such that lower childhood SES was associated with higher scam susceptibility among participants with lower cognitive function. Conclusion: Lower childhood SES is associated with higher scam susceptibility among older adults with lower levels of cognitive function. Thus, older adults who experienced limited resources in childhood and have lower cognitive function may represent a specific group for interventions to increase scam awareness and prevent financial exploitation.
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    Genetic architecture of age-related cognitive decline in African Americans
    (American Academy of Neurology, 2016-12-21) Raj, Towfique; Chibnik, Lori B.; McCabe, Cristin; Wong, Andus; Replogle, Joseph M.; Yu, Lei; Gao, Sujuan; Unverzagt, Frederick W.; Stranger, Barbara; Murrell, Jill; Barnes, Lisa; Hendrie, Hugh C.; Foroud, Tatiana; Krichevsky, Anna; Bennett, David A.; Hall, Kathleen S.; Evans, Denis A.; De Jager, Philip L.; Department of Biostatistics, Richard M. Fairbanks School of Public Health
    OBJECTIVE: To identify genetic risk factors associated with susceptibility to age-related cognitive decline in African Americans (AAs). METHODS: We performed a genome-wide association study (GWAS) and an admixture-mapping scan in 3,964 older AAs from 5 longitudinal cohorts; for each participant, we calculated a slope of an individual's global cognitive change from neuropsychological evaluations. We also performed a pathway-based analysis of the age-related cognitive decline GWAS. RESULTS: We found no evidence to support the existence of a genomic region which has a strongly different contribution to age-related cognitive decline in African and European genomes. Known Alzheimer disease (AD) susceptibility variants in the ABCA7 and MS4A loci do influence this trait in AAs. Of interest, our pathway-based analyses returned statistically significant results highlighting a shared risk from lipid/metabolism and protein tyrosine signaling pathways between cognitive decline and AD, but the role of inflammatory pathways is polarized, being limited to AD susceptibility. CONCLUSIONS: The genetic architecture of aging-related cognitive in AA individuals is largely similar to that of individuals of European descent. In both populations, we note a surprising lack of enrichment for immune pathways in the genetic risk for cognitive decline, despite strong enrichment of these pathways among genetic risk factors for AD.
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    Postnatal Depressive Symptoms Among Mothers and Fathers of Infants Born Preterm: Prevalence and Impacts on Children's Early Cognitive Function
    (Wolters Kluwer, 2016-01) Cheng, Erika R.; Kotelchuck, Milton; Gerstein, Emily D.; Taveras, Elsie M.; Poehlmann-Tynan, Julie; Department of Pediatrics, IU School of Medicine
    OBJECTIVE: Preterm birth is associated with lower cognitive functioning. One potential pathway is postnatal parental depression. The authors assessed depressive symptoms in mothers and fathers after preterm birth, and identified the impacts of both prematurity and parental depressive symptoms on children's early cognitive function. METHOD: Data were from the nationally representative Early Childhood Longitudinal Study, Birth Cohort (n = 5350). Depressive symptoms at 9 months were assessed by the Center for Epidemiologic Studies Depression Scale (CESD) and children's cognitive function at 24 months by the Bayley Short Form, Research Edition. Weighted generalized estimating equation models examined the extent to which preterm birth, and mothers' and fathers' postnatal depressive symptoms impacted children's cognitive function at 24 months, and whether the association between preterm birth and 24-month cognitive function was mediated by parental depressive symptoms. RESULTS: At 9 months, fathers of very preterm (<32 weeks gestation) and moderate/late preterm (32-37 weeks gestation) infants had higher CESD scores than fathers of term-born (≥37 weeks gestation) infants (p value = .02); preterm birth was not associated with maternal depressive symptoms. In multivariable analyses, preterm birth was associated with lower cognitive function at 24 months; this association was unaffected by adjustment for parental depressive symptoms. Fathers', but not mothers', postnatal depressive symptoms predicted lower cognitive function in the fully adjusted model (β = -0.11, 95% confidence interval, -0.18 to -0.03). CONCLUSION: Fathers of preterm infants have more postnatal depressive symptomology than fathers of term-born infants. Fathers' depressive symptoms also negatively impact children's early cognitive function. The national findings support early identification and treatment of fathers of preterm infants with depressive symptoms.
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    Unraveling The Ambiguity Between Cognition And Depression: A Longitudinal Analysis Of Older Adults
    (Oxford University Press, 2022) Roessler, Meghann; Manchella, Mohit; Singh, Anmoldeep; Coleman, Max; Francis, Heather; Saykin, Andrew; Risacher, Shannon; Apostolova, Liana; Radiology and Imaging Sciences, School of Medicine
    Research on directionality of the relationship between cognitive functioning and depression is ambiguous, especially when considering implications for patients with mild cognitive impairment or Alzheimer disease (AD). Previous research suggests that depression in late life could be a pre-clinical manifestation of AD before other cognitive symptoms are detectable. Some research supports the hypothesis that level of depression can independently predict level of cognition. Other research suggests that depression is a risk factor for developing dementia or AD late in life. Further research on the impact of subjective cognitive decline versus objective cognitive performance in association with depressive symptoms is a critical area to explore. Using data from the Social Networks in Alzheimer Disease (SNAD) study and the Indiana Alzheimer Disease Research Center (IADRC), we conducted a preliminary longitudinal analysis of 196 focal subjects (Mage = 71.6 years, Pfemale = 63%). Interviews conducted one year apart were leveraged to elucidate the bidirectional relationship between depressive symptomology and cognition. Using a lagged dependent variable approach controlling for age, sex, race, and education, the results indicate that only executive function predicts depression at timepoint 2 (-0.31 SD, p< 0.001). However, depression predicts focal Cognitive Change Index (CCI) (0.06 SD, p< 0.05), processing speed (-0.04 SD, p< 0.05), and episodic memory (-0.04 SD, p< 0.05). Other cognitive domains examined, including attention, language, visual/spatial skills, MoCA score, and informant-rated CCI, were not significant as predictors or as outcomes. These results suggest that depression may be a more robust predictor of cognition than cognition is of depression.