Cognitive change before old age (11 to 70) predicts cognitive change after old age (70 to 82)

2021 ◽  
Author(s):  
Federica Conte ◽  
Judith Okely ◽  
Olivia Hamilton ◽  
Janie Corley ◽  
Danielle Page ◽  
...  

Identifying predictors of cognitive decline within older age helps to understand its mechanisms and to identify those at greater risk. Here we examine how cognitive change from 11 to 70 years is associated with cognitive change within older age (70 to 82 years) in the Lothian Birth Cohort 1936 longitudinal study (N=1091 at recruitment). Using latent growth curve models, we estimate rates of change from age 70 to 82 in general cognitive ability (g) and in three cognitive domains: visuospatial, memory and processing speed. g accounted for 71.3% of interindividual change variance. Greater 11-70 cognitive gain predicted slower decline in g over 12 subsequent years (β = .163, p = .001), independently of cognitive level at age 70, and domain-specific change beyond g. These results contribute toward identifying people at higher risk of age-related cognitive decline. Age-related cognitive decline is a significant threat to the quality of life in older age. Its economic and social impact on society will increase together with the steadily rising life expectancy. How can we preserve cognitive health in older age? Researchers have made significant advances in identifying protective and risk factors. However, most studies focus on a limited age range, and cognitive change mechanisms are not yet completely understood. This work takes advantage of almost life-spanning longitudinal data to test if cognitive trajectory across childhood and adulthood can predict cognitive trajectories in older age. Our findings show that earlier change is associated with later change. Some factors related to individual differences in cognitive change might thus operate over much of the adult life course, and certainly before older age. This knowledge can help identify individuals at higher risk of decline and understand the mechanisms and factors responsible.

2021 ◽  
Author(s):  
Tyler S Saunders ◽  
Amanda Heslegrave ◽  
Declan King ◽  
Sarah Harris ◽  
Craig W Ritchie ◽  
...  

INTRODUCTION: Plasma phospho-tau 181 (p-tau181) is a promising blood biomarker for Alzheimer's disease. However, its predictive validity for age-related cognitive decline without dementia remains unclear. Several forms of p-tau have been shown to contribute to synapse degeneration, but it is unknown whether p-tau181 is present in synapses. Here, we tested whether plasma p-tau181predicts cognitive decline and whether it is present in synapses in human brain. METHODS: General cognitive ability and plasma p-tau181 concentration were measured in 195 participants at ages 72 and 82. Levels of p-tau181 in total homogenate and synaptic fractions were compared with western blot (n=10-12 per group), and synaptic localisation was examined using array tomography. RESULTS: Elevated baseline plasma p-tau181 and increasing p-tau181 over time predicted steeper general cognitive decline. We observe p-tau181 in neurites, presynapses, and post-synapses in the brain. DISCUSSION: Baseline and subsequent change in plasma p-tau181 may represent rare biomarkers of differences in cognitive ageing across the 8th decade of life and may play a role in synaptic function in the brain.


2021 ◽  
Author(s):  
Raihaan Patel ◽  
Clare E. Mackay ◽  
Michelle G. Jansen ◽  
Gabriel A. Devenyi ◽  
M. Clare O’Donoghue ◽  
...  

AbstractWhile all individuals are susceptible to age-related cognitive decline, significant inter- and intra-individual variability exists. However, the sources of this variation remain poorly understood. Here, we examined the association between 30-year trajectories of cognitive decline and multimodal indices of brain microstructure and morphology in older age. We used the Whitehall II Study, an extensively characterised cohort using 3T brain magnetic resonance images acquired at older age (mean age = 69.52 ± 4.9) and 5 repeated cognitive performance assessments between mid-life (mean age = 53.2 ± 4.9 years) and late-life (mean age = 67.7 ± 4.9). Using non-negative matrix factorization, we identified 10 brain microstructural components that integrate measures of cortical thickness, surface area, fractional anisotropy, and mean and radial diffusivities. We observed two modes of variance that describe the association between cognition and brain microstructure. The first describes variations in 5 microstructural components associated with low mid-life performance across multiple cognitive domains, decline in reasoning abilities, but a relative maintenance of lexical and semantic fluency from mid-to-late life. The second describes variations in 5 microstructural components that are associated with low mid-life performance in lexical fluency, semantic fluency and short-term memory performance, but a retention of abilities in multiple domains from mid-to-late life. The extent to which a subject loads onto a latent variables predicts their future cognitive performance 3.2 years later (mean age = 70.87 ± 4.9). This data-driven approach highlights a complex pattern of brain-behavior relationships, wherein the same individuals express both decline and maintenance in function across cognitive domains and in brain structural features.Significance StatementAlthough declines in cognitive performance are an established aspect of aging, inter- and intra-individual variation exists. Nevertheless, the sources of this variation remain unclear. We analyse a unique sample to examine associations between 30-year trajectories of cognitive decline and multimodal indices of brain anatomy in older age. Using data-driven techniques, we find that age-related cognitive decline is not uniform. Instead, each individual expresses a mixture of maintenance and decline across cognitive domains, that are associated with a mixture of preservation and degeneration of brain structure. Further, we find the primary determinants of late-life cognitive performance are mid-life performance and higher brain surface area. These results suggest that early and mid-life preventative measures may be needed to reduce age-related cognitive decline.


2011 ◽  
Vol 17 (3) ◽  
pp. 315-324 ◽  
Author(s):  
O J G Schiepers ◽  
S E Harris ◽  
A J Gow ◽  
A Pattie ◽  
C E Brett ◽  
...  

1997 ◽  
Vol 171 (5) ◽  
pp. 449-451 ◽  
Author(s):  
Friedel M. Reischies ◽  
Bernhard Geiselmann

BackgroundCurrently the Mini Mental State Examination (MMSE) is widely used as a screening instrument for dementia syndrome. Diagnostic validity may be lowered in old age by normal age-related cognitive decline. Furthermore, visual impairment, occurring frequently in old age, leads to missing values which prevent an interpretation of the test result.MethodIn the Berlin Ageing Study (n=516, age range 70–103 years) MMSE and clinical dementia diagnosis, made by a psychiatrist investigating all subjects by the Geriatric Mental State–A and History and Aetiology Schedule interviews, were investigated independently. The MMblind was analysed, an MMSE version for vision impairment in which all items requiring image processing are omitted. The study sample is population-based; dementia cases (DSM–III–R) were excluded on the basis of the clinical diagnosis.ResultsNorms are reported for very old age regarding MMSE as well as MMblind. There is a considerable age effect on MMSE scores. In contrast to MMSE, sensitivity and specificity of the shorter MMblind version are not reduced.ConclusionsThe considerable age effect requires the adaptation of cut-off values for old age. The blind version of the MMSE seems to be a valid instrument improving the applicability of the MMSE in old age.


2016 ◽  
Vol 3 (1) ◽  
pp. e125 ◽  
Author(s):  
Towfique Raj ◽  
Lori B. Chibnik ◽  
Cristin McCabe ◽  
Andus Wong ◽  
Joseph M. Replogle ◽  
...  

Objective:To identify genetic risk factors associated with susceptibility to age-related cognitive decline in African Americans (AAs).Methods:We performed a genome-wide association study (GWAS) and an admixture-mapping scan in 3,964 older AAs from 5 longitudinal cohorts; for each participant, we calculated a slope of an individual's global cognitive change from neuropsychological evaluations. We also performed a pathway-based analysis of the age-related cognitive decline GWAS.Results:We found no evidence to support the existence of a genomic region which has a strongly different contribution to age-related cognitive decline in African and European genomes. Known Alzheimer disease (AD) susceptibility variants in the ABCA7 and MS4A loci do influence this trait in AAs. Of interest, our pathway-based analyses returned statistically significant results highlighting a shared risk from lipid/metabolism and protein tyrosine signaling pathways between cognitive decline and AD, but the role of inflammatory pathways is polarized, being limited to AD susceptibility.Conclusions:The genetic architecture of aging-related cognitive in AA individuals is largely similar to that of individuals of European descent. In both populations, we note a surprising lack of enrichment for immune pathways in the genetic risk for cognitive decline, despite strong enrichment of these pathways among genetic risk factors for AD.


2019 ◽  
Vol 54 (4) ◽  
pp. 446-454 ◽  
Author(s):  
Marie Grønkjær ◽  
Trine Flensborg-Madsen ◽  
Merete Osler ◽  
Holger J Sørensen ◽  
Ulrik Becker ◽  
...  

Abstract Aims Alcohol consumption is a modifiable and plausible risk factor for age-related cognitive decline but more longitudinal studies investigating the association are needed. Our aims were to estimate associations of adult-life alcohol consumption and consumption patterns with age-related cognitive decline. Methods We investigated the associations of self-reported adult-life weekly alcohol consumption and weekly extreme binge drinking (≥10 units on the same occasion) with changes in test scores on an identical validated test of intelligence completed in early adulthood and late midlife in 2498 Danish men from the Lifestyle and Cognition Follow-up study 2015. Analyses were adjusted for year of birth, retest interval, baseline IQ, education and smoking. Results Men with adult-life alcohol consumption of more than 28 units/week had a larger decline in IQ scores from early adulthood to late midlife than men consuming 1–14 units/week (B29–35units/week = −3.6; P < 0.001). Likewise, a 1-year increase in weekly extreme binge drinking was associated with a 0.12-point decline in IQ scores (P < 0.001). Weekly extreme binge drinking explained more variance in IQ changes than average weekly consumption. In analyses including mutual adjustment of weekly extreme binge drinking and average weekly alcohol consumption, the estimated IQ decline associated with extreme binge drinking was largely unaffected, whereas the association with weekly alcohol consumption became non-significant. Conclusions Adult-life heavy alcohol consumption and extreme binge drinking appear to be associated with larger cognitive decline in men. Moreover, extreme binge drinking may be more important than weekly alcohol consumption in relation to cognitive decline.


Author(s):  
Yvonne Rogalski ◽  
Muriel Quintana

The population of older adults is rapidly increasing, as is the number and type of products and interventions proposed to prevent or reduce the risk of age-related cognitive decline. Advocacy and prevention are part of the American Speech-Language-Hearing Association’s (ASHA’s) scope of practice documents, and speech-language pathologists must have basic awareness of the evidence contributing to healthy cognitive aging. In this article, we provide a brief overview outlining the evidence on activity engagement and its effects on cognition in older adults. We explore the current evidence around the activities of eating and drinking with a discussion on the potential benefits of omega-3 fatty acids, polyphenols, alcohol, and coffee. We investigate the evidence on the hypothesized neuroprotective effects of social activity, the evidence on computerized cognitive training, and the emerging behavioral and neuroimaging evidence on physical activity. We conclude that actively aging using a combination of several strategies may be our best line of defense against cognitive decline.


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