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Frailty and the risk of dementia: is the association explained by shared environmental and genetic factors?
Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17165 Stockholm, Sweden..
Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17165 Stockholm, Sweden..
Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17165 Stockholm, Sweden..
Karolinska Inst, Dept Med Epidemiol & Biostat, Nobels Vag 12A, S-17165 Stockholm, Sweden..
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2021 (Engelska)Ingår i: BMC Medicine, E-ISSN 1741-7015, Vol. 19, nr 1, artikel-id 248Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background Frailty has been identified as a risk factor for cognitive impairment and dementia. However, it is not known whether familial factors, such as genetics and shared environmental factors, underlie this association. We analyzed the association between frailty and the risk of dementia in a large twin cohort and examined the role of familial factors in the association. Methods The Rockwood frailty index (FI) based on 44 health deficits was used to assess frailty. The population-level association between FI and the risk of all-cause dementia was analyzed in 41,550 participants of the Screening Across the Lifespan Twin (SALT) study (full sample, aged 41-97 years at baseline), using Cox and competing risk models. A subsample of 10,487 SALT participants aged 65 and older who received a cognitive assessment (cognitive sample) was used in a sensitivity analysis to assess the effect of baseline cognitive level on the FI-dementia association. To analyze the influence of familial effects on the FI-dementia association, a within-pair analysis was performed. The within-pair model was also used to assess whether the risk conferred by frailty varies by age at FI assessment. Results A total of 3183 individuals were diagnosed with dementia during the 19-year follow-up. A 10% increase in FI was associated with an increased risk of dementia (hazard ratio [HR] 1.17 (95% confidence interval [CI] 1.07, 1.18)) in the full sample adjusted for age, sex, education, and tobacco use. A significant association was likewise found in the cognitive sample, with an HR of 1.13 (95% CI 1.09, 1.20), adjusted for age, sex, and cognitive level at baseline. The associations were not attenuated when adjusted for APOE e4 carrier status or considering the competing risk of death. After adjusting for familial effects, we found no evidence for statistically significant attenuation of the effect. The risk conferred by higher FI on dementia was constant after age 50 until very old age. Conclusions A higher level of frailty predicts the risk of dementia and the association appears independent of familial factors. Targeting frailty might thus contribute to preventing or delaying dementia.

Ort, förlag, år, upplaga, sidor
BioMed Central, 2021. Vol. 19, nr 1, artikel-id 248
Nyckelord [en]
Frailty, Dementia, Twin design, Cohort study, Genetic factors
Nationell ämneskategori
Gerontologi, medicinsk/hälsovetenskaplig inriktning
Identifikatorer
URN: urn:nbn:se:hj:diva-54969DOI: 10.1186/s12916-021-02104-3ISI: 000707918000001PubMedID: 34657626Scopus ID: 2-s2.0-85117281747Lokalt ID: GOA;intsam;773795OAI: oai:DiVA.org:hj-54969DiVA, id: diva2:1606854
Forskningsfinansiär
Magnus Bergvalls StiftelseNIH (National Institute of Health), R01 AG060470, R01 AG08724Vetenskapsrådet, 2015-03255, 2017-00641, 2018-02077Forte, Forskningsrådet för hälsa, arbetsliv och välfärd, 2013-2292Tillgänglig från: 2021-10-28 Skapad: 2021-10-28 Senast uppdaterad: 2022-10-31Bibliografiskt granskad

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Karlsson, Ida K.Jylhava, Juulia
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HHJ, Institutet för gerontologiHHJ. ARN-J (Aging Research Network - Jönköping)
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BMC Medicine
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