Pub Date : 2024-06-01DOI: 10.1016/S2666-7568(24)00061-8
Prof Blossom C M Stephan PhD , Louie Cochrane MSc , Aysegul Humeyra Kafadar MSc , Jacob Brain MSc , Elissa Burton PhD , Prof Bronwyn Myers PhD , Prof Carol Brayne MD , Aliya Naheed PhD , Prof Kaarin J Anstey PhD , Ammar W Ashor PhD , Prof Mario Siervo PhD
Background
More than 57 million people have dementia worldwide. Evidence indicates a change in dementia prevalence and incidence in high-income countries, which is likely to be due to improved life-course population health. Identifying key modifiable risk factors for dementia is essential for informing risk reduction and prevention strategies. We therefore aimed to estimate the population attributable fraction (PAF) for dementia associated with modifiable risk factors.
Methods
In this systematic review and meta-analysis, we searched Embase, MEDLINE, and PsycINFO, via Ovid, from database inception up to June 29, 2023, for population-derived or community-based studies and reviews reporting a PAF value for one or more modifiable risk factor for later-life dementia (prevalent or incident dementia in people aged ≥60 years), with no restrictions on dementia subtype, the sex or baseline age of participants, or the period of study. Articles were independently screened for inclusion by four authors, with disagreements resolved through consensus. Data including unweighted and weighted PAF values (weighted to account for communality or overlap in risk) were independently extracted into a predefined template by two authors and checked by two other authors. When five or more unique studies investigated a given risk factor or combination of the same factors, random-effects meta-analyses were used to calculate a pooled PAF percentage estimate for the factor or combination of factors. The review protocol was registered on PROSPERO, CRD42022323429.
Findings
4024 articles were identified, and 74 were included in our narrative synthesis. Overall, PAFs were reported for 61 modifiable risk factors, with sufficient data available for meta-analysis of 12 factors (n=48 studies). In meta-analyses, the highest pooled unweighted PAF values were estimated for low education (17·2% [95% CI 14·4–20·0], p<0·0001), hypertension (15·8% [14·7–17·1], p<0·0001), hearing loss (15·6% [10·3–20·9], p<0·0001), physical inactivity (15·2% [12·8–17·7], p<0·0001), and obesity (9·4% [7·3–11·7], p<0·0001). According to weighted PAF values, low education (9·3% [6·9–11·7], p<0·0001), physical inactivity (7·3% [3·9–11·2], p=0·0021), hearing loss (7·2% [5·2–9·7], p<0·0001), hypertension (7·1% [5·4–8·8], p<0·0001), and obesity (5·3% [3·2–7·4], p=0·0001) had the highest pooled estimates. When low education, midlife hypertension, midlife obesity, smoking, physical inactivity, depression, and diabetes were combined (Barnes and Yaffe seven-factor model; n=9 studies), the pooled unweighted and weighted PAF values were 55·0% (46·5–63·5; p<0·0001) and 32·0% (26·6–37·5; p<0·0001), respectively. The pooled PAF values for most individual risk factors were higher in low-income and middle-income countries (LMICs) versus high-income countries.
{"title":"Population attributable fractions of modifiable risk factors for dementia: a systematic review and meta-analysis","authors":"Prof Blossom C M Stephan PhD , Louie Cochrane MSc , Aysegul Humeyra Kafadar MSc , Jacob Brain MSc , Elissa Burton PhD , Prof Bronwyn Myers PhD , Prof Carol Brayne MD , Aliya Naheed PhD , Prof Kaarin J Anstey PhD , Ammar W Ashor PhD , Prof Mario Siervo PhD","doi":"10.1016/S2666-7568(24)00061-8","DOIUrl":"10.1016/S2666-7568(24)00061-8","url":null,"abstract":"<div><h3>Background</h3><p>More than 57 million people have dementia worldwide. Evidence indicates a change in dementia prevalence and incidence in high-income countries, which is likely to be due to improved life-course population health. Identifying key modifiable risk factors for dementia is essential for informing risk reduction and prevention strategies. We therefore aimed to estimate the population attributable fraction (PAF) for dementia associated with modifiable risk factors.</p></div><div><h3>Methods</h3><p>In this systematic review and meta-analysis, we searched Embase, MEDLINE, and PsycINFO, via Ovid, from database inception up to June 29, 2023, for population-derived or community-based studies and reviews reporting a PAF value for one or more modifiable risk factor for later-life dementia (prevalent or incident dementia in people aged ≥60 years), with no restrictions on dementia subtype, the sex or baseline age of participants, or the period of study. Articles were independently screened for inclusion by four authors, with disagreements resolved through consensus. Data including unweighted and weighted PAF values (weighted to account for communality or overlap in risk) were independently extracted into a predefined template by two authors and checked by two other authors. When five or more unique studies investigated a given risk factor or combination of the same factors, random-effects meta-analyses were used to calculate a pooled PAF percentage estimate for the factor or combination of factors. The review protocol was registered on PROSPERO, CRD42022323429.</p></div><div><h3>Findings</h3><p>4024 articles were identified, and 74 were included in our narrative synthesis. Overall, PAFs were reported for 61 modifiable risk factors, with sufficient data available for meta-analysis of 12 factors (n=48 studies). In meta-analyses, the highest pooled unweighted PAF values were estimated for low education (17·2% [95% CI 14·4–20·0], p<0·0001), hypertension (15·8% [14·7–17·1], p<0·0001), hearing loss (15·6% [10·3–20·9], p<0·0001), physical inactivity (15·2% [12·8–17·7], p<0·0001), and obesity (9·4% [7·3–11·7], p<0·0001). According to weighted PAF values, low education (9·3% [6·9–11·7], p<0·0001), physical inactivity (7·3% [3·9–11·2], p=0·0021), hearing loss (7·2% [5·2–9·7], p<0·0001), hypertension (7·1% [5·4–8·8], p<0·0001), and obesity (5·3% [3·2–7·4], p=0·0001) had the highest pooled estimates. When low education, midlife hypertension, midlife obesity, smoking, physical inactivity, depression, and diabetes were combined (Barnes and Yaffe seven-factor model; n=9 studies), the pooled unweighted and weighted PAF values were 55·0% (46·5–63·5; p<0·0001) and 32·0% (26·6–37·5; p<0·0001), respectively. The pooled PAF values for most individual risk factors were higher in low-income and middle-income countries (LMICs) versus high-income countries.</p></div><div><h3>Interpretation</h3><p>Governments need to invest in a li","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":null,"pages":null},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000618/pdfft?md5=cb707008c5477ab286a5261b3c99539f&pid=1-s2.0-S2666756824000618-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-01DOI: 10.1016/S2666-7568(24)00072-2
Constantinos Christopoulos
{"title":"Polypharmacy research: in need of a new conceptual framework","authors":"Constantinos Christopoulos","doi":"10.1016/S2666-7568(24)00072-2","DOIUrl":"10.1016/S2666-7568(24)00072-2","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":null,"pages":null},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000722/pdfft?md5=5ea13d3fc28ceaf01ae04528180f6b9e&pid=1-s2.0-S2666756824000722-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-01DOI: 10.1016/S2666-7568(24)00071-0
Jason R Smith , Jennifer A Deal
{"title":"The need for a more holistic approach to dementia prevention","authors":"Jason R Smith , Jennifer A Deal","doi":"10.1016/S2666-7568(24)00071-0","DOIUrl":"10.1016/S2666-7568(24)00071-0","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":null,"pages":null},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000710/pdfft?md5=d34ed927a82584c80c8c85556652372b&pid=1-s2.0-S2666756824000710-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The ε4 allele of the apolipoprotein E gene (APOE4) plays a role in neurodegeneration and in cardiovascular disease, but findings on its association with mortality are inconsistent. We aimed to examine the association between APOE4 and mortality, and the role of dementia in this association.
Methods
In this pooled analysis, data on White participants aged 45–90 years who underwent APOE genotyping were drawn from two population-based cohorts: the Whitehall II study (UK), which began in 1985 and is ongoing, and the Three-City study (France), initiated in 1999 and ended in 2012. In the Three-City study, vital status was ascertained through linkage to the national registry of death Institut National de la Statistique des Études économiques, and dementia was ascertained via a neuropsychological evaluation and validation of diagnoses by an independent committee of neurologists and geriatricians. In the Whitehall II study, vital status was ascertained through linkage to the UK national mortality register, and dementia cases were ascertained by linkage to three national registers. Participants with prevalent dementia at baseline and participants missing an APOE genotype were excluded from analyses. Cox regression proportional hazard models were used to examine the association of APOE4 with all-cause, cardiovascular, and cancer mortality. The role of dementia in the association between APOE4 status and mortality was examined by excluding participants who developed dementia during follow-up from the analyses. An illness-death model was then used to examine the role of incident dementia in these associations.
Findings
14 091 participants (8492 from the Three-City study and 5599 from the Whitehall II study; 6668 [47%] of participants were women and 7423 [53%] were men), with a median follow-up of 15·4 years (IQR 10·6–21·2), were included in the analyses. Of these participants, APOE4 carriers (3264 [23%] of the cohort carried at least one ε4 allele) had a higher risk of all-cause mortality compared with non-carriers, with hazard ratios (HR) of 1·16 (95% CI 1·07–1·26) for heterozygotes and 1·59 (1·24–2·06) for homozygotes. Compared with APOE3 homozygotes, higher cardiovascular mortality was observed in APOE4 carriers, with a HR of 1·23 (1·01–1·50) for heterozygotes, and no association was found between APOE4 and cancer mortality. Excluding cases of incident dementia over the follow-up resulted in attenuated associations with mortality in homozygotes but not in heterozygotes. The illness-death model indicated that the higher mortality risk in APOE4 carriers was not solely attributable to dementia.
Interpretation
We found a robust association between APOE4 and all-cause and cardiovascular mortality but not cancer mortality. Dementia explained a sig
{"title":"The role of dementia in the association between APOE4 and all-cause mortality: pooled analyses of two population-based cohort studies","authors":"Mélina Régy PhD , Aline Dugravot PhD , Séverine Sabia PhD , Catherine Helmer PhD , Prof Christophe Tzourio PhD , Prof Bernard Hanseeuw PhD , Prof Archana Singh-Manoux PhD , Prof Julien Dumurgier PhD","doi":"10.1016/S2666-7568(24)00066-7","DOIUrl":"10.1016/S2666-7568(24)00066-7","url":null,"abstract":"<div><h3>Background</h3><p>The ε4 allele of the apolipoprotein E gene (<em>APOE4</em>) plays a role in neurodegeneration and in cardiovascular disease, but findings on its association with mortality are inconsistent. We aimed to examine the association between <em>APOE4</em> and mortality, and the role of dementia in this association.</p></div><div><h3>Methods</h3><p>In this pooled analysis, data on White participants aged 45–90 years who underwent <em>APOE</em> genotyping were drawn from two population-based cohorts: the Whitehall II study (UK), which began in 1985 and is ongoing, and the Three-City study (France), initiated in 1999 and ended in 2012. In the Three-City study, vital status was ascertained through linkage to the national registry of death Institut National de la Statistique des Études économiques, and dementia was ascertained via a neuropsychological evaluation and validation of diagnoses by an independent committee of neurologists and geriatricians. In the Whitehall II study, vital status was ascertained through linkage to the UK national mortality register, and dementia cases were ascertained by linkage to three national registers. Participants with prevalent dementia at baseline and participants missing an <em>APOE</em> genotype were excluded from <em>analyses</em>. Cox regression proportional hazard models were used to examine the association of <em>APOE4</em> with all-cause, cardiovascular, and cancer mortality. The role of dementia in the association between <em>APOE4</em> status and mortality was examined by excluding participants who developed dementia during follow-up from the analyses. An illness-death model was then used to examine the role of incident dementia in these associations.</p></div><div><h3>Findings</h3><p>14 091 participants (8492 from the Three-City study and 5599 from the Whitehall II study; 6668 [47%] of participants were women and 7423 [53%] were men), with a median follow-up of 15·4 years (IQR 10·6–21·2), were included in the analyses. Of these participants, <em>APOE4</em> carriers (3264 [23%] of the cohort carried at least one ε4 allele) had a higher risk of all-cause mortality compared with non-carriers, with hazard ratios (HR) of 1·16 (95% CI 1·07–1·26) for heterozygotes and 1·59 (1·24–2·06) for homozygotes. Compared with <em>APOE3</em> homozygotes, higher cardiovascular mortality was observed in <em>APOE4</em> carriers, with a HR of 1·23 (1·01–1·50) for heterozygotes, and no association was found between <em>APOE4</em> and cancer mortality. Excluding cases of incident dementia over the follow-up resulted in attenuated associations with mortality in homozygotes but not in heterozygotes. The illness-death model indicated that the higher mortality risk in <em>APOE4</em> carriers was not solely attributable to dementia.</p></div><div><h3>Interpretation</h3><p>We found a robust association between <em>APOE4</em> and all-cause and cardiovascular mortality but not cancer mortality. Dementia explained a sig","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":null,"pages":null},"PeriodicalIF":13.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000667/pdfft?md5=f558e5586e63a8f953114a471aedc44b&pid=1-s2.0-S2666756824000667-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1016/S2666-7568(24)00045-X
Wanyang Li , Wei Chen
{"title":"10-h time-restricted eating: are there broad health benefits?","authors":"Wanyang Li , Wei Chen","doi":"10.1016/S2666-7568(24)00045-X","DOIUrl":"https://doi.org/10.1016/S2666-7568(24)00045-X","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":null,"pages":null},"PeriodicalIF":13.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266675682400045X/pdfft?md5=b61f07f903018eb2edeeb00eb8632054&pid=1-s2.0-S266675682400045X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140824641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1016/S2666-7568(24)00029-1
Caroline Hartwell Garred MD , Morten Malmborg PhD , Mariam Elmegaard Malik MD , Deewa Zahir MD , Daniel Mølager Christensen PhD , Anojhaan Arulmurugananthavadivel MD , Prof Emil L Fosbøl PhD , Prof Gunnar Gislason PhD , Prof John J V McMurray MD , Prof Mark C Petrie MD , Charlotte Andersson PhD , Prof Lars Køber DMSc , Prof Morten Schou PhD
Background
Despite advances in heart failure care reducing mortality in clinical trials, it remains unclear whether real-life cohorts have had similar improvements in life expectancy across the age spectrum. We aimed to investigate how mortality trends changed in patients with heart failure over the past 25 years, stratified by age groups.
Methods
Using Danish nationwide registries, we identified patients with new-onset heart failure aged 18–95 years. The 5-year all-cause mortality risk and the absolute risk difference of mortality between patients with heart failure and age-matched and sex-matched heart failure-free controls were assessed using Kaplan–Meier estimates and multivariable Cox regression models. Mortality trends were analysed across five calendar periods (1996–2000, 2001–05, 2006–10, 2011–15, and 2016–20) and three age groups (<65 years, 65–79 years, and ≥80 years).
Findings
194 997 patients with heart failure were included. Mortality significantly decreased from 1996–2000 (66% [95% CI 65·5–66·4]) to 2016–20 (43% [42·1–43·4]), with similar results shown in all age groups (<65 years: 35% [33·9–36·1] to 15% [14·6–16·3]; 65–79 years: 64% [63·1–64·5] to 39% [37·6–39·6]; and ≥80 years: 84% [83·1–84·3] to 73% [71·7–73·9]). Adjusted mortality rates supported these associations. The absolute risk difference declined notably in younger age groups (<65 years: 29·9% [28·8–31·0] to 12·7% [12·0–13·4] and 65–79 years: 41·1% [40·3–41·9] to 25·1% [24·4–25·8]), remaining relatively stable in those aged 80 years or older (30·6% [29·9–31·3] to 28% [27·2–28·8]).
Interpretation
Over 25 years, there has been a consistent decrease in mortality among patients with heart failure across age groups, albeit less prominently in patients aged 80 years or older. Further insight is needed to identify effective strategies for improving disease burden in older patients with heart failure.
Funding
None.
Translation
For the Danish translation of the abstract see Supplementary Materials section.
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Pub Date : 2024-05-01DOI: 10.1016/S2666-7568(24)00033-3
Shahram Oveisgharan MD , Tianhao Wang PhD , Lisa L Barnes PhD , Julie A Schneider MD , David A Bennett MD , Aron S Buchman MD
Background
Many studies have reported that impaired gait precedes cognitive impairment in older people. We aimed to characterise the time course of cognitive and motor decline in older individuals and the association of these declines with the pathologies of Alzheimer's disease and related dementias.
Methods
This multicohort study used data from three community-based cohort studies (Religious Orders Study, Rush Memory and Aging Project, and Minority Aging Research Study, all in the USA). The inclusion criteria for all three cohorts were no clinical dementia at the time of enrolment and consent to annual clinical assessments. Eligible participants consented to post-mortem brain donation and had post-mortem pathological assessments and three or more repeated annual measures of cognition and motor functions. Clinical and post-mortem data were analysed using functional mixed-effects models. Global cognition was based on 19 neuropsychological tests, a hand strength score was based on grip and pinch strength, and a gait score was based on the number of steps and time to walk 8 feet and turn 360°. Brain pathologies of Alzheimer's disease and related dementias were assessed at autopsy.
Findings
From 1994 to 2022, there were 1570 eligible cohort participants aged 65 years or older, 1303 of whom had cognitive and motor measurements and were included in the analysis. Mean age at death was 90·3 years (SD 6·3), 905 (69%) participants were female, and 398 (31%) were male. Median follow-up time was 9 years (IQR 5–11). On average, cognition was stable from 25 to 15 years before death, when cognition began to decline. By contrast, gait function and hand strength declined during the entire study. The combinations of pathologies of Alzheimer's disease and related dementias associated with cognitive and motor decline and their onsets of associations varied; only tau tangles, Parkinson's disease pathology, and macroinfarcts were associated with decline of all three phenotypes. Tau tangles were significantly associated with cognitive decline, gait function decline, and hand function decline (p<0·0001 for each); however, the association with cognitive decline persisted for more than 11 years before death, but the association with hand strength only began 3·57 years before death and the association with gait began 3·49 years before death. By contrast, the association of macroinfarcts with declining gait function began 9·25 years before death (p<0·0001) compared with 6·65 years before death (p=0·0005) for cognitive decline and 2·66 years before death (p=0·024) for decline in hand strength.
Interpretation
Our findings suggest that average motor decline in older adults precedes cognitive decline. Macroinfarcts but not tau tangles are associated with declining gait function that precedes cognitive decline. This suggests the need for further studies to test if gait impairment is
{"title":"The time course of motor and cognitive decline in older adults and their associations with brain pathologies: a multicohort study","authors":"Shahram Oveisgharan MD , Tianhao Wang PhD , Lisa L Barnes PhD , Julie A Schneider MD , David A Bennett MD , Aron S Buchman MD","doi":"10.1016/S2666-7568(24)00033-3","DOIUrl":"https://doi.org/10.1016/S2666-7568(24)00033-3","url":null,"abstract":"<div><h3>Background</h3><p>Many studies have reported that impaired gait precedes cognitive impairment in older people. We aimed to characterise the time course of cognitive and motor decline in older individuals and the association of these declines with the pathologies of Alzheimer's disease and related dementias.</p></div><div><h3>Methods</h3><p>This multicohort study used data from three community-based cohort studies (Religious Orders Study, Rush Memory and Aging Project, and Minority Aging Research Study, all in the USA). The inclusion criteria for all three cohorts were no clinical dementia at the time of enrolment and consent to annual clinical assessments. Eligible participants consented to post-mortem brain donation and had post-mortem pathological assessments and three or more repeated annual measures of cognition and motor functions. Clinical and post-mortem data were analysed using functional mixed-effects models. Global cognition was based on 19 neuropsychological tests, a hand strength score was based on grip and pinch strength, and a gait score was based on the number of steps and time to walk 8 feet and turn 360°. Brain pathologies of Alzheimer's disease and related dementias were assessed at autopsy.</p></div><div><h3>Findings</h3><p>From 1994 to 2022, there were 1570 eligible cohort participants aged 65 years or older, 1303 of whom had cognitive and motor measurements and were included in the analysis. Mean age at death was 90·3 years (SD 6·3), 905 (69%) participants were female, and 398 (31%) were male. Median follow-up time was 9 years (IQR 5–11). On average, cognition was stable from 25 to 15 years before death, when cognition began to decline. By contrast, gait function and hand strength declined during the entire study. The combinations of pathologies of Alzheimer's disease and related dementias associated with cognitive and motor decline and their onsets of associations varied; only tau tangles, Parkinson's disease pathology, and macroinfarcts were associated with decline of all three phenotypes. Tau tangles were significantly associated with cognitive decline, gait function decline, and hand function decline (p<0·0001 for each); however, the association with cognitive decline persisted for more than 11 years before death, but the association with hand strength only began 3·57 years before death and the association with gait began 3·49 years before death. By contrast, the association of macroinfarcts with declining gait function began 9·25 years before death (p<0·0001) compared with 6·65 years before death (p=0·0005) for cognitive decline and 2·66 years before death (p=0·024) for decline in hand strength.</p></div><div><h3>Interpretation</h3><p>Our findings suggest that average motor decline in older adults precedes cognitive decline. Macroinfarcts but not tau tangles are associated with declining gait function that precedes cognitive decline. This suggests the need for further studies to test if gait impairment is ","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":null,"pages":null},"PeriodicalIF":13.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000333/pdfft?md5=e34bd8bbc108b19f2ab62d243ea22f5d&pid=1-s2.0-S2666756824000333-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140824571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1016/S2666-7568(24)00065-5
Shian Ming Tan, Iris Rawtaer
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