Aims: To investigate the association between parity and the risk of incident dementia in women.
Methods: We pooled baseline and follow-up data for community-dwelling women aged 60 or older from six population-based, prospective cohort studies from four European and two Asian countries. We investigated the association between parity and incident dementia using Cox proportional hazards regression models adjusted for age, educational level, hypertension, diabetes mellitus and cohort, with additional analysis by dementia subtype (Alzheimer dementia (AD) and non-Alzheimer dementia (NAD)).
Results: Of 9756 women dementia-free at baseline, 7010 completed one or more follow-up assessments. The mean follow-up duration was 5.4 ± 3.1 years and dementia developed in 550 participants. The number of parities was associated with the risk of incident dementia (hazard ratio (HR) = 1.07, 95% confidence interval (CI) = 1.02-1.13). Grand multiparity (five or more parities) increased the risk of dementia by 30% compared to 1-4 parities (HR = 1.30, 95% CI = 1.02-1.67). The risk of NAD increased by 12% for every parity (HR = 1.12, 95% CI = 1.02-1.23) and by 60% for grand multiparity (HR = 1.60, 95% CI = 1.00-2.55), but the risk of AD was not significantly associated with parity.
Conclusions: Grand multiparity is a significant risk factor for dementia in women. This may have particularly important implications for women in low and middle-income countries where the fertility rate and prevalence of grand multiparity are high.
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http://dx.doi.org/10.1017/S2045796020000876 | DOI Listing |
JAMA Netw Open
January 2025
Department of Health Policy and Management, Yale School of Public Health, New Haven, Connecticut.
Importance: Disparities in cognition, including dementia occurrence, persist between non-Hispanic Black (hereinafter, Black) and non-Hispanic White (hereinafter, White) older adults, and are possibly influenced by early educational differences stemming from structural racism. However, the association between school racial segregation and later-life cognition remains underexplored.
Objective: To investigate the association between childhood contextual exposure to school racial segregation and cognitive outcomes in later life.
Alzheimers Dement
December 2024
University of Pennsylvania, Philadelphia, PA, USA.
Background: Alzheimer's disease (AD), characterized by significant brain volume reduction, is influenced by genetic predispositions related to brain volumetric phenotypes. While genome-wide association studies (GWASs) have linked brain imaging-derived phenotypes (IDPs) with AD, existing polygenic risk scores (PRSs) based models inadequately capture this relationship. We develop BrainNetScore, a network-based model enhancing AD risk prediction by integrating genetic associations between multiple brain IDPs and AD incidence.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
German Center for Neurodegenerative Diseases (DZNE), Bonn, North Rhine-Westphalia, Germany.
Background: MicroRNAs have been linked to dementia. However, understanding their relation to cognition in the general population is required to determine their potential use for the detection and prevention of age-associated cognitive decline and preclinical dementia. Therefore, we examined the association of circulating microRNAs with cognitive performance in a population-based cohort and the possible underlying mechanisms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The University of Arizona - Tucson, Tucson, AZ, USA.
Background: Host commensal gut microbes are shown to be crucial for microglial maturation, and functions that involve innate immune responses to maintain brain homeostasis. Sex has a crucial role in the incidence of neurological diseases with females showing higher progression of AD compared with males. Transcriptomics has been a powerful tool for the characterization of microglial phenotypes however, there is a large gap in relating to their functional protein abundances.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Weill Cornell Medicine, New York, NY, USA.
Background: The strongest genetic risk factors for AD include the e4 allele of APOE and the R47H point mutation in the TREM2 receptor. TREM2 is required for the induction of a disease-associated microglia (DAM) signature and microglial neurodegenerative phenotype (MGnD) in response to disease pathology, signatures which both include APOE upregulation. There is currently limited information regarding how the TREM2-APOE pathway ultimately contributes to AD risk, and downstream mechanisms of this pathway are unknown.
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