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University of Southern California · Psychology
Active 2006–2026
Christopher Beam is an associate professor of psychology and gerontology at USC Dornsife. He is a clinical psychologist specializing in life-span development, behavioral genetics, and advanced quantitative methods. His research encompasses various areas of life-span development, with a current focus on collecting midlife data on twins aged 40 and older in the Louisville Twin Study. His work aims to investigate genetic and environmental processes that explain how early psychosocial and cognitive development predict midlife cognitive functioning and markers of preclinical Alzheimer's disease. Additionally, he examines how perceived social isolation, or loneliness, changes in the second half of the lifespan and how these changes relate to dementia risk. Clinically, Dr. Beam focuses on geropsychological interventions, primarily group-based interventions for complicated grief in older adults. He is also a faculty member in the Gerontological Workforce Enhancement Program at the USC Keck School of Medicine. His research addresses the biological and environmental mechanisms that explain differences in cognitive and psychological development across the lifespan, guided by broad questions about how social experiences earlier in life contribute to age-related cognitive changes, personality development, and the onset of psychopathology.
Research Square · 2026-03-16
Developmental Increases in the Reliability of Cognitive Assessment Bias G x Age Estimates
2025-06-26
NIH · $20k · 2014
NIH · $5.7M · 2019–2026
April D. Thames
Elissa C. McIntosh
University of Southern California
George M. Slavich
Neurobehavioral Systems
Chandler M. Spahr
University of California, Riverside
Eric Turkheimer
Beam LabPI
PhD, Psychology
University of Virginia
Predoctoral Psychology Resident, Psychiatry and Behavioral Sciences
University of Washington
MA, Psychology
University of Virginia
MA, Psychology
New York University
BA, Psychology
Seattle Pacific University
BA, Philosophy
Seattle Pacific University
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The heritability (G) of cognitive ability increases substantially across development. However, previous studies of G x Age interaction—also known as the Wilson Effect—have not controlled for developmental changes in the reliability of cognitive assessment. Unmodeled reliability changes may bias estimates of cognitive growth and G x Age interaction, obscuring the developmental etiology of cognitive ability, but this possibility has not been explored empirically due to a lack of appropriate data and statistical methods. Using an expanded version of the Louisville Twin Study data set in which Ronald Wilson (1983) originally documented G x Age interaction, we first replicated heritability increases between ages 3 months and 15 years. Then, we examined the extent to which unmodeled reliability changes biased estimates of G x Age interaction using continuous time dynamic modeling. Our-best fitting model, which corrected for reliability differences across test battery and age, estimated that heritability increased from .26 to .55. Reliability increased substantially across development, from less than .30 in infancy to approximately .80 at age 15. Models that did not control for developmental reliability increases yielded downwardly biased estimates of cognitive growth and differentiation, G x Age interaction, developmental decreases in shared environmental effects, and increases in non-shared environmental effects. Results indicated that a re-evaluation of previous G x Age estimates may be warranted, and that future studies should control for developmental fluctuations in reliability. Our continuous time dynamic models improved estimation of developmental change in cognitive ability and can be easily adapted to other psychological constructs.
European Journal of Epidemiology · 2025-12-01
Aging · 2025-07-23
DNA methylation age (DNAmAge) surpasses chronological age in its ability to predict age-related morbidities and mortality. This study analyzed data from 287 middle-aged twins in the Louisville Twin Study (mean age 51.9 years ± 7.03) to investigate the effect of DNAmAge acceleration on change in IQ (ΔIQ) between childhood and midlife, while testing childhood socioeconomic status (SES) as a moderator of the relationship. DNAmAge was estimated with five commonly used algorithms, or epigenetic clocks (Horvath, Horvath Skin and Blood, GrimAge, and PhenoAge). A factor analysis of these measures produced a two-factor structure which we identified as first generation and second generation measures. Results of genetically informed, quasi-causal regression models indicated that accelerated second generation DNAmAge predicted more negative ΔIQ from childhood to midlife, after accounting for genetic and environmental confounds shared by twins. The relationship between DNAmAge and ΔIQ was moderated by childhood SES, with a stronger effect observed among twins from low SES backgrounds. Second generation DNAmAge measures trained to estimate phenotypic biological age show promise in their predictive value for cognitive decline in midlife. Our genetically informed twin design suggested that epigenetic aging may represent a pathway through which early-life socioeconomic disadvantage impacts midlife cognitive health.
European Journal of Epidemiology · 2025-08-12 · 4 citations
Low educational attainment is recognized as a modifiable risk factor for dementia. Despite the commonly accepted notion that greater educational attainment confers lower dementia risk, few family-based studies have investigated the causal bases for the association. Using data from seven twin samples from Sweden, Denmark, Australia, and the US participating in the IGEMS (Interplay of Genes and Environment in Multiple Studies) consortium (N = 60,027, 10.92% with dementia), we tested whether twins who achieve higher education than their co-twins have lower risk of dementia. The primary analysis applied a multilevel between-within regression framework, supported by descriptive statistics of within-pair differences. Results confirmed an overall association between educational attainment and dementia risk, such that individuals with higher educational attainment had less likelihood of developing dementia (phenotypic regression coefficient = -0.68, p <.0001). Within twin pairs, however, twins who achieved greater education than their co-twins did not uniformly show lower dementia risk (within-family regression coefficient = -0.07, p =.0983, while between-family regression coefficient = -0.98, p <.0001). Taken together, the pattern of results shows that the effect of educational attainment on dementia risk is largely attributable to genetic influences in common to educational attainment and dementia, although there are also contributions from environmental influences shared between members of the same family. Results were similar in men and women. These findings add to the literature by using a co-twin control design to address possible reasons that low educational attainment is associated with greater dementia risk.
The Journals of Gerontology Series B · 2025-12-03
OBJECTIVES: Birth weight is a widely used indicator of prenatal experiences in models of the developmental origins of cognitive ability across the lifespan. This study aimed to examine the association between birth weight and cognitive ability using a community sample of twins followed prospectively from infancy to midlife. We leveraged the twin study design to identify phenotypic and biometric associations between the two constructs. METHODS: The sample consisted of 1,501 participants (387 dizygotic pairs, 360 monozygotic pairs, and 7 singletons; 53.1% female; 91.1% White) from the Louisville Twin Study. We modeled the change in the strength of the association between birth weight and cognitive ability using exponential decay functions. RESULTS: The magnitude of the association between birth weight and cognitive ability declined exponentially from infancy (β = .59, p < .05) to midlife (β = .27, p < .05). The lower asymptote of the exponential decay function was reached at about age 2.5 years of age, after which the association between birth weight and cognitive ability stabilized and remained constant up to midlife. A 1-kilogram increase in birth weight was associated with an 8.85-point increase in cognitive scores at 3 months and a 4.05-point advantage after about 2.5 years. Biometric regression models revealed that shared environmental factors accounted for the decline in the association between birth weight and cognitive ability. A small, positive within-pair association persisted into midlife. DISCUSSION: These findings suggest that prenatal experiences may have lasting effects on cognitive development across the lifespan, supporting developmental origin models of cognitive ability.
Person-Environment Transaction Underlying Personality Development in Middle and Late Adulthood
2025-11-06
The niche-picking principle has been proposed to explain stabilization in personality development and personality continuity of adult. The niche-picking principle posits that the reciprocal exchange between people and their environments -- person-environment transaction -- serve to maintain trait continuity, thereby preserving rank-order stability of trait differences. To date, however, no longitudinal twin study has directly tested whether reciprocal effects between people and their environments contribute to trait continuity in middle and older adulthood. Using a sample of twins from the Swedish Adoption/Twin Study of Aging (SATSA), we tested whether the niche-picking principle explained stability of longitudinal within-family differences in neuroticism, extraversion, and openness across two stages of adulthood development. Genetic simplex models that include a reciprocal effects (i.e., phenotype-environment covariance) parameter were fit to twins' longitudinal data. Results suggest that the niche-picking principle partly explains continuity of neuroticism and openness in middle adulthood whereas it partly explains continuity of neuroticism and extraversion in older adulthood. Stable genetic and unique environmental variance also explained continuity of each trait. Findings partially support lifespan developmental theories that posit that people adapt to and possibly optimize behaviors to sustain existing traits. We discuss the importance of the reciprocal exchange between people and their environments across the lifespan and how these exchanges might shift to support trait continuity.
2025-07-02
For decades, researchers have debated whether the magnitude of the Flynn Effect—intergenerational increases in mean IQ scores—varies across cognitive domains and subdomains, and whether the Flynn Effect reflects gains in general cognitive ability (g). We conducted a cross-domain, subtest-level investigation of the Flynn Effect across middle childhood and early adolescence (ages 7-15 years, N = 1187, 89% White, 9% Black, 52% female) in longitudinal cognitive ability data collected prospectively between 1957 and 1999 using three versions of the Wechsler Intelligence Scale for Children. Results provided clear evidence of the Flynn Effect as both increases in mean IQ score across generational cohort and decreases in mean IQ across test versions. Flynn Effect magnitude differed substantially across domains and subtests. Performance IQ gains were larger than full-scale and verbal IQ gains in cohort-based analyses, but test version-based estimates showed an opposite pattern (VIQ &gt; FSIQ &gt; PIQ). Variance in Flynn Effect magnitude across subtests did not follow a discernible pattern. The strength of the Flynn Effect on individual subtests was not strictly proportional to each subtest’s g-loading, with performance IQ subtests showing larger increases than would be expected given their g-loadings and verbal subtests showing smaller-than-expected gains.
Blood‐based Biomarkers for Alzheimer's Disease and Memory Function in Midlife
Alzheimer s & Dementia · 2025-12-01
BACKGROUND: Clarifying risk factors for Alzheimer's disease (AD) in midlife permits intervening earlier in the lifespan and delaying conversion to AD. Understanding the relationship between blood-based AD biomarkers and memory functioning during middle age may help clarify whether elevated levels correspond to poor memory performance in later life. Blood-based biomarkers, including amyloid-β42/amyloid-β40 and ptau181, are associated with AD diagnosis, but studies investigating the correlates of these biomarker levels in middle age are scarce (Li et al., 2022; Karikari et al., 2020). METHOD: Edition (CVLT-3) were collected from 154 midlife twins (78 complete families) as part of the Louisville Twin Study. Pearson correlations and mixed effects regression analysis were used to estimate between-family and within-family associations between AD biomarkers and four CVLT-3 subtests (immediate word recall, short-delay free recall, long-delay free recall, and recognition). RESULT: Correlations of amyloid-β42/amyloid-β40 and the CVLT3 subtests ranged from -.02 to .04 while correlations with ptau181 ranged from -.09 to -.04. Although no correlations were statistically significant, the pattern of associations between episodic memory and ptau181 at least suggested a reliable negative association. Neither between-family nor within-family correlations were observed. CONCLUSION: Although AD biomarker levels have been found to correlate with memory functioning in older adult samples, we did not observe these same effects in middle adulthood. Thus, the current results suggest that individual differences in blood-based AD biomarkers may not have predictive utility for observed memory functioning in middle adulthood.
Journal of Alzheimer s Disease · 2025-05-13 · 1 citations
Background Current methods to quantify blood biomarkers for Alzheimer's disease (AD) are expensive and are not widely available. Objective To develop a low-cost, sensitive, and accurate multiplex assay to quantify Aβ 40 , Aβ 42 , p181Tau, p217Tau, NfL, and GFAP biomarkers in plasma and serum based on a widely available technology. Methods We used commercial antibodies to Aβ 40 , Aβ 42 , p181Tau, p217Tau, NfL, and GFAP, and xMAP Luminex technology, and developed the multiplex 5ADCSI to quantify these biomarkers from plasma and serum. The utility of 5ADCSI was tested in matched cerebrospinal fluid (CSF) and plasma or serum of a cohort of cognitively normal (CN: n = 35), with mild cognitive impairment (MCI: n = 17), and with AD (n = 11) individuals. Results The 5ADCSI demonstrated high specificity and sensitivity, with excellent precision. In clinical samples, moderate to strong correlation is observed between CSF and plasma or serum for Aβ 42/40 ( r = 0.78 ), p181Tau/Aβ 42 ( r = 0.57 ), p217Tau/Aβ 42 ( r = 0.72 ), p181Tau ( r = 0.59 ), p217Tau ( r = 0.75 ), and GFAP ( r = 0.59 ). The AUC of receiver-operator characteristic curve for differentiating CN from AD for plasma/serum and CSF are 0.75, and 0.80 for Aβ 42/40 , 0.95, 0.91 for p217Tau, 0.76, 0.81 for p181Tau, and 0.73 and 0.78for GFAP, respectively. Conclusions The 5ADCSI assay is highly specific, sensitive, and accurate. The wide availability of the base technology of 5ADCSI is an advantage over other similar methods and would allow cost-effective large-scale studies for validation of blood biomarkers for early diagnosis of AD.
Deborah Winders Davis
University of Louisville
Margaret Gatz
University of Southern California
Deborah Finkel
University of Southern California