ArticlePsychology and aging2014
IDE (rs6583817) polymorphism and pulse pressure are independently and interactively associated with level and change in executive function in older adults.
Article in Psychology and aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- The unity and diversity of executive functions: A systematic review and re-analysis of latent variable studies.Psychological bulletin · 2018Pooled it
- Association between arterial stiffness, cerebral small vessel disease and cognitive impairment: A systematic review and meta-analysis.Neuroscience and biobehavioral reviews · 2015Pooled it
- Data-driven approaches to executive function performance and structure in aging: Integrating person-centered analyses and machine learning risk prediction.Neuropsychology · 2021Article
- Integrating Three Characteristics of Executive Function in Non-Demented Aging: Trajectories, Classification, and Biomarker Predictors.Journal of the International Neuropsychological Society : JINS · 2021Article
- A Multimodal Risk Network Predicts Executive Function Trajectories in Non-demented Aging.Frontiers in aging neuroscience · 2021Article
- Frailty effects on non-demented cognitive trajectories are moderated by sex and Alzheimer's genetic risk.Alzheimer's research & therapy · 2019Article
- Prospective associations between pulse pressure and cognitive performance in Chinese middle-aged and older population across a 5-year study period.Alzheimer's research & therapy · 2018Article
- A Network of Genetic Effects on Non-Demented Cognitive Aging: Alzheimer's Genetic Risk (CLU + CR1 + PICALM) Intensifies Cognitive Aging Genetic Risk (COMT + BDNF) Selectively for APOEɛ4 Carriers.Journal of Alzheimer's disease : JAD · 2018Article
- Executive function performance and change in aging is predicted by apolipoprotein E, intensified by catechol-O-methyltransferase and brain-derived neurotrophic factor, and moderated by age and lifestyle.Neurobiology of aging · 2017Article
- Cognitive activity mediates the association between social activity and cognitive performance: A longitudinal study.Psychology and aging · 2016Article
- Vascular Health and Genetic Risk Affect Mild Cognitive Impairment Status and 4-Year Stability: Evidence From the Victoria Longitudinal Study.The journals of gerontology. Series B, Psychological sciences and social sciences · 2016Article
- Risk-reducing Apolipoprotein E and Clusterin genotypes protect against the consequences of poor vascular health on executive function performance and change in nondemented older adults.Neurobiology of aging · 2016Article
- Apolipoprotein E and Clusterin can magnify effects of personality vulnerability on declarative memory performance in non-demented older adults.International journal of geriatric psychiatry · 2016Article
- Genetic factors moderate everyday physical activity effects on executive functions in aging: Evidence from the Victoria Longitudinal Study.Neuropsychology · 2016Article
- Alzheimer's Genetic Risk Intensifies Neurocognitive Slowing Associated with Diabetes in Non-Demented Older Adults.Alzheimer's & dementia (Amsterdam, Netherlands) · 2015Article
- ApoE and pulse pressure interactively influence level and change in the aging of episodic memory: Protective effects among ε2 carriers.Neuropsychology · 2015Article
- Synergistic associations of catechol-O-methyltransferase and brain-derived neurotrophic factor with executive function in aging are selective and modified by apolipoprotein E.Neurobiology of aging · 2015Article
- APOE moderates the association between lifestyle activities and cognitive performance: evidence of genetic plasticity in aging.Journal of the International Neuropsychological Society : JINS · 2014Article
- APOE and COMT polymorphisms are complementary biomarkers of status, stability, and transitions in normal aging and early mild cognitive impairment.Frontiers in aging neuroscience · 2014Article
- Cognitively elite, cognitively normal, and cognitively impaired aging: neurocognitive status and stability moderate memory performance.Journal of clinical and experimental neuropsychology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWe report a gene × environment (health) study focusing on concurrent performance and longitudinal change in a latent-variable executive function (EF) phenotype. Specifically, we tested the independent and interactive effects of a recently identified insulin degrading enzyme genetic polymorphism (IDE rs6583817) and pulse pressure (PP; one prominent aging-related vascular health indicator) across up to 9 years of EF data in a sample of older adults from the Victoria Longitudinal Study. Both factors vary across a continuum of risk-elevating to risk-reducing and have been recently linked to normal and impaired cognitive aging.
methodWe assembled a genotyped and typically aging group of older adults (n = 599, M age = 66 years at baseline), following them for up to 3 longitudinal waves (M interval = 4.4 years). We used confirmatory factor analyses, latent growth modeling, and path analyses to pursue 3 main research goals.
resultsFirst, the EF single factor model was confirmed comprising 4 executive function tasks and it demonstrated measurement invariance across the waves. Second, older adults with the major IDE G allele exhibited better EF outcomes than homozygotes for the minor A allele at the centering age of 75 years. Adults with higher PP performed more poorly on EF tasks at age 75 years and exhibited greater EF longitudinal decline. Third, gene × health interaction analyses showed that worsening vascular health (higher PP) differentially affected EF performance in older adults with the IDE G allele.
conclusionGenetic interaction analyses can reveal differential and magnifying effects on cognitive phenotypes in aging. In the present case, pulse pressure is confirmed as a risk factor for concurrent and changing cognitive health in aging, but the effects operate differently across the risk and protective allelic distribution of this IDE gene.
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