Predictive Value of Odor Identification for Incident Dementia: The Shanghai Aging Study

Ding, Ding; Xiao, Zhenxu; Liang, Xiaoniu; Wu, Wanqing; Zhao, Qianhua; Cao, Yang

doi:10.3389/fnagi.2020.00266

Cited by 5 publications

(2 citation statements)

References 62 publications

(86 reference statements)

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“…Consequently, a large number of proposed risk factors with consistent empirical support of predicting dementia were not included in any index (e.g. poor sleep, 45,46 poor sense of smell, [47][48][49] disadvantageous personality traits, 50,51 etc.). Despite their inclusion of different, conceptually distinct risk factors, there was moderate to high correlation among the risk indexes (Pearson's r's between 0.55 and 0.80, P-values < 0.001) (Fig.…”

Section: What Is the Population Distribution Of Risk As Measured By P...mentioning

confidence: 99%

Improving risk indexes for Alzheimer’s disease and related dementias for use in midlife

Reuben

Moffitt

Abraham

et al. 2022

Brain Communications

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Knowledge of a person’s risk for Alzheimer’s disease and related dementias (ADRDs) is required to triage candidates for preventive interventions, surveillance, and treatment trials. ADRD risk indexes exist for this purpose, but each includes only a subset of known risk factors. Information missing from published indexes could improve risk prediction. In the Dunedin Study of a population-representative New Zealand-based birth cohort followed to midlife (N = 938, 49.5% female), we compared associations of four leading risk indexes with midlife antecedents of ADRD against a novel benchmark index comprised of nearly all known ADRD risk factors, the Dunedin ADRD Risk Benchmark (DunedinARB). Existing indexes included the Cardiovascular Risk Factors, Aging, and Dementia index (CAIDE), LIfestyle for BRAin health index (LIBRA), Australian National University Alzheimer’s Disease Risk Index (ANU-ADRI), and risks selected by the Lancet Commission on Dementia. The Dunedin benchmark was comprised of 48 separate indicators of risk organized into 10 conceptually distinct risk domains. Midlife antecedents of ADRD treated as outcome measures included age-45 measures of brain structural integrity [magnetic resonance imaging-assessed: (i) machine-learning-algorithm-estimated brain age, (ii) log-transformed volume of white matter hyperintensities, and (iii) mean grey matter volume of the hippocampus] and measures of brain functional integrity [(i) objective cognitive function assessed via the Wechsler Adult Intelligence Scale-IV, (ii) subjective problems in everyday cognitive function, and (iii) objective cognitive decline measured as residualized change in cognitive scores from childhood to midlife on matched Weschler Intelligence scales]. All indexes were quantitatively distributed and proved informative about midlife antecedents of ADRD, including algorithm-estimated brain age (β's from 0.16 to 0.22), white matter hyperintensities volume (β's from 0.16 to 0.19), hippocampal volume (β's from −0.08 to −0.11), tested cognitive deficits (β's from −0.36 to −0.49), everyday cognitive problems (β's from 0.14 to 0.38), and longitudinal cognitive decline (β's from −0.18 to −0.26). Existing indexes compared favourably to the comprehensive benchmark in their association with the brain structural integrity measures but were outperformed in their association with the functional integrity measures, particularly subjective cognitive problems and tested cognitive decline. Results indicated that existing indexes could be improved with targeted additions, particularly of measures assessing socioeconomic status, physical and sensory function, epigenetic aging, and subjective overall health. Existing premorbid ADRD risk indexes perform well in identifying linear gradients of risk among members of the general population at midlife, even when they include only a small subset of potential risk factors. They could be improved, however, with targeted additions to more holistically capture the different facets of risk for this multiply determined, age-related disease.

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Section: What Is the Population Distribution Of Risk As Measured By P...mentioning

confidence: 99%

Improving risk indexes for Alzheimer’s disease and related dementias for use in midlife

Reuben

Moffitt

Abraham

et al. 2022

Brain Communications

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“…Baseline data collection has been described in detail previously (17). Information on demographics and lifestyle of the participants including age, sex, education, smoking, and alcohol drinking were collected via an interviewer-administered questionnaire.…”

Section: Baseline Data Collectionmentioning

confidence: 99%

Is Olfactory Impairment Associated With 10-year Mortality Mediating by Neurodegenerative Diseases in Older Adults? The Four-Way Decomposition Analysis

Cao

Xiao

et al. 2021

Front. Public Health

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Background: Literature shows that olfactory impairment (OI) is associated not only with neurodegenerative diseases (NDDs), but also with increased mortality. In this study, we analyzed data collected from the prospective phase of the 10-year follow-up of the Shanghai Aging Study (SAS) to explore the mediation effect of NDDs on the OI-mortality relationship.Methods: We analyzed data collected from the prospective phase of the 10-year follow-up of the SAS. We included 1,811 participants aged 60 years or older who completed both an olfactory identification test and a cognitive assessment at baseline (2010–2011). Survival status of the participants from baseline to December 31, 2019 was obtained from the local mortality surveillance system. We used the four-way decomposition method to attribute effects to interaction and mediation and to explore the mediation effect of NDDs on the OI-mortality relationship.Results: The four-way decomposition method revealed a statistically significant association of OI with death. Overall, 43% higher risk for death was associated with OI [excess relative risk (ERR) = 0.43, 95% CI: 0.06–0.80, p = 0.023]. Excluding the mediation from NDDs and interaction between OI and NDDs, the controlled direct effect of OI on death was even higher in NDDs participants, with an ERR of 77% (95% CI: 0.00–1.55, p = 0.050). Statistically significant association was found for failure to identify coffee (ERR = 0.77, 95% CI: 0.18–1.36, p = 0.010) and marginally significant associations were found for failure to identify cinnamon (ERR = 0.33, 95% CI: −0.02–0.68, p = 0.068) and rose (ERR = 0.33, 95% CI: −0.01–0.67, p = 0.054) with death.Conclusion: OI was associated with the long-term mortality in older adults and the association was even stronger in those with NDDs. Failure to identify coffee or rose was associated with a higher mortality risk, and the association was mediated by NDDs.

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Impact of In Utero Folate Exposure on DNA Methylation and Its Potential Relevance for Later‐Life Health—Evidence from Mouse Models Translated to Human Cohorts

Kok

Richmond²,

Adriaens

et al. 2021

Molecular Nutrition Food Res

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Scope: Persistent DNA methylation changes may mediate effects of early-life exposures on later-life health. Human lifespan is challenging for prospective studies, therefore data from longitudinal studies are limited. Projecting data from mouse models of early-life exposure to human studies offers a tool to address this challenge. Methods and Results: C57BL/6J mice were fed low/normal folate diets before and during pregnancy and lactation. Genome-wide promoter methylation was measured in male offspring livers at 17.5 days gestation and 28 weeks. Eight promoters were concurrently hypermethylated by folate depletion in fetuses and adults (>1.10 fold-change; p < 0.05). Processes/pathways potentially influenced by global changes, and function of these eight genes, suggest neurocognitive effects. Human observational and randomized controlled trial data were interrogated for translation. Methylation at birth was inversely associated with maternal plasma folate in six genes (−1.15% to −0.16% per nmol L −1 ; p < 0.05), while maternal folic acid supplementation was associated with differential methylation of four genes in adulthood. Three CpGs were persistently hypermethylated with lower maternal folate (p = 0.04). Conclusion: Some persistent folate-induced methylation changes in mice are mirrored in humans. This demonstrates utility of mouse data in identifying human loci for interrogation as biomarkers of later-life health.

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Predictive Value of Odor Identification for Incident Dementia: The Shanghai Aging Study

Cited by 5 publications

References 62 publications

Improving risk indexes for Alzheimer’s disease and related dementias for use in midlife

Improving risk indexes for Alzheimer’s disease and related dementias for use in midlife

Is Olfactory Impairment Associated With 10-year Mortality Mediating by Neurodegenerative Diseases in Older Adults? The Four-Way Decomposition Analysis

Impact of In Utero Folate Exposure on DNA Methylation and Its Potential Relevance for Later‐Life Health—Evidence from Mouse Models Translated to Human Cohorts

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