Evidence on the role of early-life adversity in later-life memory decline is conflicting. We investigated the relationships between adverse childhood experiences (ACEs) and memory performance and rate of decline over a 10-year follow-up among middle-aged and older adults in England. Data were from biennial interviews with 5,223 participants aged 54 years or older in the population-representative English Longitudinal Study of Ageing from 2006/2007 to 2016/2017. We examined self-reports of 9 ACEs prior to age 16 years that related to abuse, household dysfunction, and separation from family. Memory was assessed at each time point as immediate and delayed recall of 10 words. Using linear mixed-effects models with person-specific random intercepts and slopes and adjusted for baseline age, participants' baseline age squared, sex, ethnicity, and childhood socioeconomic factors, we observed that most individual and cumulative ACE exposures had null to weakly negative associations with memory function and rate of decline over the 10-year follow-up. Having lived in residential or foster care was associated with lower baseline memory (adjusted β = -0.124 standard deviation units; 95% confidence interval: -0.273, -0.025) but not memory decline. Our findings suggest potential long-term impacts of residential or foster care on memory and highlight the need for accurate and detailed exposure measures when studying ACEs in relation to later-life cognitive outcomes.
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http://dx.doi.org/10.1093/aje/kwab019 | DOI Listing |
Alzheimers Res Ther
January 2025
Department of Bioengineering, University of California, San Diego, La Jolla, CA, 92093, USA.
Background: PSEN1, PSEN2, and APP mutations cause Alzheimer's disease (AD) with an early age at onset (AAO) and progressive cognitive decline. PSEN1 mutations are more common and generally have an earlier AAO; however, certain PSEN1 mutations cause a later AAO, similar to those observed in PSEN2 and APP.
Methods: We examined whether common disease endotypes exist across these mutations with a later AAO (~ 55 years) using hiPSC-derived neurons from familial Alzheimer's disease (FAD) patients harboring mutations in PSEN1, PSEN2, and APP and mechanistically characterized by integrating RNA-seq and ATAC-seq.
Immun Ageing
January 2025
Institute for Behavioral Medicine Research, Ohio State University, 460 Medical Center Drive, Columbus, OH, 43210, USA.
Background: Obesity and metabolic syndrome are major public health concerns linked to cognitive decline with aging. Prior work from our lab has demonstrated that short-term high fat diet (HFD) rapidly impairs memory function via a neuroinflammatory mechanism. However, the degree to which these rapid inflammatory changes are unique to the brain is unknown.
View Article and Find Full Text PDFBackground: Population aging and the increase in memory-related diseases have motivated the search for accessible cognitive screening instruments. To develop a digital memory and learning test (DMLT) based on Rey's Auditory Verbal Learning Test (RAVLT) principles to assess cognition in the elderly and identify early cognitive decline.
Methods: The research was divided into two phases: developing the digital test and the experimental phase of comparison with a reference test.
Neurobiol Aging
December 2024
Vanderbilt Memory and Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, USA; Pharmacology Department, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, USA; Epidemiology Doctoral Program, School of Medicine, Vanderbilt University, Nashville, TN, USA; Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address:
We have identified FLT1 as a protein that changes during Alzheimer's disease (AD) whereby higher brain protein levels are associated with more amyloid, more tau, and faster longitudinal cognitive decline. Given FLT1's role in angiogenesis and immune activation, we hypothesized that FLT1 is upregulated in response to amyloid pathology, driving a vascular-immune cascade resulting in neurodegeneration and cognitive decline. We sought to determine (1) if in vivo FLT1 levels (CSF and plasma) associate with biomarkers of AD neuropathology or differ between diagnostic staging in an aged cohort enriched for early disease, and (2) whether FLT1 expression interacts with amyloid on downstream outcomes, such as phosphorylated tau levels and cognitive performance.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The Second Affiliated Hospital of Chongqing Medical University, Chongqing, Chong Qing, China.
Background: Alzheimer's disease (AD) frequently coexists with cerebral small vessel disease (CSVD) is common in the aging population, yet the underlying mechanisms are not yet fully understood. Both long-term blood pressure variability (BPV) and plasma neurofilament light (PNFL) were identified as potential biomarkers for AD and CSVD. This study aims to understand the mechanisms of comorbidity between AD and CSVD by investigating the associations among BPV, PNFL, and comorbidity.
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