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Publications (10 of 44) Show all publications
Josefsson, M., Sundström, A., Pudas, S., Nordin Adolfsson, A., Nyberg, L. & Adolfsson, R. (2023). Memory profiles predict dementia over 23–28 years in normal but not successful aging. International psychogeriatrics, 35(7), 351-359
Open this publication in new window or tab >>Memory profiles predict dementia over 23–28 years in normal but not successful aging
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2023 (English)In: International psychogeriatrics, ISSN 1041-6102, E-ISSN 1741-203X, Vol. 35, no 7, p. 351-359Article in journal (Refereed) Published
Abstract [en]

Objectives: Prospective studies suggest that memory deficits are detectable decades before clinical symptoms of dementia emerge. However, individual differences in long-term memory trajectories prior to diagnosis need to be further elucidated. The aim of the current study was to investigate long-term dementia and mortality risk for individuals with different memory trajectory profiles in a well-characterized population-based sample.

Methods: 1062 adults (aged 45–80 years) who were non-demented at baseline were followed over 23–28 years. Dementia and mortality risk were studied for three previously classified episodic memory trajectory groups: maintained high performance (Maintainers; 26%), average decline (Averages; 64%), and accelerated decline (Decliners; 12%), using multistate modeling to characterize individuals’ transitions from an initial non-demented state, possibly to a state of dementia and/or death.

Results: The memory groups showed considerable intergroup variability in memory profiles, starting 10–15 years prior to dementia diagnosis, and prior to death. A strong relationship between memory trajectory group and dementia risk was found. Specifically, Decliners had more than a fourfold risk of developing dementia compared to Averages. In contrast, Maintainers had a 2.6 times decreased dementia risk compared to Averages, and in addition showed no detectable memory decline prior to dementia diagnosis. A similar pattern of association was found for the memory groups and mortality risk, although only among non-demented.

Conclusion: There was a strong relationship between accelerated memory decline and dementia, further supporting the prognostic value of memory decline. The intergroup differences, however, suggest that mechanisms involved in successful memory aging may delay symptom onset.

Place, publisher, year, edition, pages
Cambridge University Press, 2023
Keywords
memory decline, episodic memory, death, competing risk, multistate model
National Category
Psychology (excluding Applied Psychology)
Identifiers
urn:nbn:se:umu:diva-165499 (URN)10.1017/S1041610219001844 (DOI)31762427 (PubMedID)2-s2.0-85163913454 (Scopus ID)
Available from: 2019-11-25 Created: 2019-11-25 Last updated: 2024-04-08Bibliographically approved
Andersson, J., Sundström, A., Nordin, M., Segersson, D., Forsberg, B., Adolfsson, R. & Oudin, A. (2023). Pm2.5 and dementia in a low exposure setting: the influence of odor identification ability and APOE. Journal of Alzheimer's Disease, 92(2), 679-689
Open this publication in new window or tab >>Pm2.5 and dementia in a low exposure setting: the influence of odor identification ability and APOE
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2023 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 92, no 2, p. 679-689Article in journal (Refereed) Published
Abstract [en]

Background: Growing evidence show that long term exposure to air pollution increases the risk of dementia.

Objective: The aim of this study was to investigate associations between PM2.5 exposure and dementia in a low exposure area, and to investigate the role of olfaction and the APOE ε4 allele in these associations.

Methods: Data were drawn from the Betula project, a longitudinal study on aging, memory, and dementia in Sweden. Odor identification ability was assessed using the Scandinavian Odor Identification Test (SOIT). Annual mean PM2.5 concentrations were obtained from a dispersion-model and matched at the participants’ residential address. Proportional hazard regression was used to calculate hazard ratios.

Results: Of 1,846 participants, 348 developed dementia during the 21-year follow-up period. The average annual mean PM2.5 exposure at baseline was 6.77 µg/m3, which is 1.77 µg/m3 above the WHO definition of clean air. In a fully adjusted model (adjusted for age, sex, APOE, SOIT, cardiovascular diseases and risk factors, and education) each 1 µg/m3 difference in annual mean PM2.5-concentration was associated with a hazard ratio of 1.23 for dementia (95% CI: 1.01–1.50). Analyses stratified by APOE status (ε4 carriers versus non-carriers), and odor identification ability (high versus low), showed associations only for ε4 carriers, and for low performance on odor identification ability.

Conclusion: PM2.5 was associated with an increased risk of dementia in this low pollution setting. The associations between PM2.5 and dementia seemed stronger in APOE carriers and those with below average odor identification ability.

Place, publisher, year, edition, pages
IOS Press, 2023
Keywords
Alzheimer’s disease, Apolipoprotein E, olfaction, particulate matter, vascular dementia
National Category
Occupational Health and Environmental Health
Research subject
Psychology; Occupational and Environmental Medicine
Identifiers
urn:nbn:se:umu:diva-205123 (URN)10.3233/jad-220469 (DOI)000952023800024 ()36776047 (PubMedID)2-s2.0-85151044242 (Scopus ID)
Funder
EU, Horizon 2020, 814978-2Swedish Research Council Formas, 942-2015-1099
Available from: 2023-02-23 Created: 2023-02-23 Last updated: 2024-04-08Bibliographically approved
Eriksson Sörman, D., Stenling, A., Sundström, A., Rönnlund, M., Vega-Mendoza, M., Hansson, P. & Ljungberg, J. K. (2021). Occupational cognitive complexity and episodic memory in old age. Intelligence, 89, Article ID 101598.
Open this publication in new window or tab >>Occupational cognitive complexity and episodic memory in old age
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2021 (English)In: Intelligence, ISSN 0160-2896, E-ISSN 1873-7935, Vol. 89, article id 101598Article in journal (Refereed) Published
Abstract [en]

The aim of this study was to investigate occupational cognitive complexity of main lifetime occupation in relation to level and 15-year change in episodic memory recall in a sample of older adults (≥ 65 years, n = 780). We used latent growth curve modelling with occupational cognitive complexity (O*NET indicators) as independent variable. Subgroup analyses in a sample of middle-aged (mean: 49.9 years) men (n = 260) were additionally performed to investigate if a general cognitive ability (g) factor at age 18 was predictive of future occupational cognitive complexity and cognitive performance in midlife. For the older sample, a higher level of occupational cognitive complexity was related to a higher level of episodic recall (β = 0.15, p < .001), but the association with rate of change (β = 0.03, p = .64) was not statistically significant. In the middle-aged sample, g at age 18 was both directly (β = 0.19, p = .01) and indirectly (via years of education after age 18, ab = 0.19) predictive of midlife levels of occupational cognitive complexity. Cognitive ability at age 18 was also a direct predictor of midlife episodic recall (β = 0.60, p ≤ 0.001). Critically, entry of the early adult g factor attenuated the association between occupational complexity and cognitive level (from β = 0.21, p = .01 to β = 0.12, p = .14). Overall, our results support a pattern of preserved differentiation from early to late adulthood for individuals with different histories of occupational complexity.

Place, publisher, year, edition, pages
Elsevier, 2021
Keywords
Cognitive reserve, Episodic memory, Intelligence, Occupational cognitive complexity, Preserved differentiation
National Category
Psychology (excluding Applied Psychology)
Identifiers
urn:nbn:se:umu:diva-189589 (URN)10.1016/j.intell.2021.101598 (DOI)000720544800001 ()2-s2.0-85118684966 (Scopus ID)
Funder
Knut and Alice Wallenberg Foundation, 2014.0205Swedish Research Council, K2010-61X-21446-01, 2017-00273, 2007–2653Forte, Swedish Research Council for Health, Working Life and Welfare, 2013–2056
Available from: 2021-11-16 Created: 2021-11-16 Last updated: 2024-04-25Bibliographically approved
Oudin, A., Andersson, J., Sundström, A., Nordin Adolfsson, A., Oudin Åström, D., Adolfsson, R., . . . Nordin, M. (2021). Traffic-Related air pollution as a risk factor for dementia: no clear modifying effects of apoe ɛ4 in the betula cohort. In: Lilian Calderón-Garcidueñas (Ed.), Alzheimer's disease and air pollution: the development and progression of a fatal disease from childhood and the opportunities for early prevention (pp. 357-364). Amsterdam: IOS Press
Open this publication in new window or tab >>Traffic-Related air pollution as a risk factor for dementia: no clear modifying effects of apoe ɛ4 in the betula cohort
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2021 (English)In: Alzheimer's disease and air pollution: the development and progression of a fatal disease from childhood and the opportunities for early prevention / [ed] Lilian Calderón-Garcidueñas, Amsterdam: IOS Press, 2021, p. 357-364Chapter in book (Refereed)
Abstract [en]

It is widely known that the apolipoprotein E (APOE) ε4 allele imposes a higher risk for Alzheimer's disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOE ε4 carriers than in non-carriers. Air pollution and interaction with APOE ε4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOE ε4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOE ε4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOE ε4 carriers than in the total population.

Place, publisher, year, edition, pages
Amsterdam: IOS Press, 2021
Series
Advances in Alzheimer's Disease, ISSN 2210-5727, E-ISSN 2210-5735 ; 8
Keywords
Air pollution, Alzheimer's disease, Apolipoprotein E, Dementia
National Category
Occupational Health and Environmental Health Neurology
Identifiers
urn:nbn:se:umu:diva-186440 (URN)10.3233/AIAD210029 (DOI)2-s2.0-85110853331 (Scopus ID)9781643681597 (ISBN)9781643681580 (ISBN)
Available from: 2021-08-02 Created: 2021-08-02 Last updated: 2024-04-08Bibliographically approved
Sundström, A., Rönnlund, M. & Josefsson, M. (2020). A Nationwide Swedish Study of Age at Retirement and Dementia Risk. International Journal of Geriatric Psychiatry, 35(10), 1234-1249
Open this publication in new window or tab >>A Nationwide Swedish Study of Age at Retirement and Dementia Risk
2020 (English)In: International Journal of Geriatric Psychiatry, ISSN 0885-6230, E-ISSN 1099-1166, Vol. 35, no 10, p. 1234-1249Article in journal (Refereed) Published
Abstract [en]

Objectives: The aim of this nationwide study was to examine the association between age at retirement and dementia risk, with a follow-up period of up to 24 years.

Methods/design: This cohort study comprised Swedish citizens born in 1930 who were alive in the year 1990 (n=63,505). The cohort was followed for incidents of dementia through data provided by the Swedish National Patient Register and the Cause of Death Register. Age at retirement and socioeconomic variables were retrieved from Statistics Sweden.

Results: During the follow-up, 5,181 individuals received a dementia diagnosis. Competing risk regression models, adjusted for sex, education, marital status, occupation, and previous history of cardiovascular diseases, showed that later-than-average retirement age was associated with decreased dementia risk.

Conclusions: The present results supports the idea that individuals who retired at an older age has a decrease risk of dementia. However, as this was an observation study, unmeasured factors, such as premorbid cognitive level and genetic predisposition, may have influenced our findings and remains to be elucidated in future studies.

Place, publisher, year, edition, pages
John Wiley & Sons, 2020
Keywords
age at retirement, aging, cognitive aging, cognitive decline, dementia, retirement
National Category
Psychology Geriatrics
Research subject
Psychology
Identifiers
urn:nbn:se:umu:diva-172957 (URN)10.1002/gps.5363 (DOI)000571331000020 ()32557831 (PubMedID)2-s2.0-85087426926 (Scopus ID)
Available from: 2020-06-25 Created: 2020-06-25 Last updated: 2023-03-24Bibliographically approved
Nyberg, L., Boraxbekk, C.-J., Eriksson Sörman, D., Hansson, P., Herlitz, A., Kauppi, K., . . . Adolfsson, R. (2020). Biological and environmental predictors of heterogeneity in neurocognitive ageing: Evidence from Betula and other longitudinal studies. Ageing Research Reviews, 64, Article ID 101184.
Open this publication in new window or tab >>Biological and environmental predictors of heterogeneity in neurocognitive ageing: Evidence from Betula and other longitudinal studies
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2020 (English)In: Ageing Research Reviews, ISSN 1568-1637, E-ISSN 1872-9649, Vol. 64, article id 101184Article in journal (Refereed) Published
Abstract [en]

Individual differences in cognitive performance increase with advancing age, reflecting marked cognitive changes in some individuals along with little or no change in others. Genetic and lifestyle factors are assumed to influence cognitive performance in ageing by affecting the magnitude and extent of age-related brain changes (i.e., brain maintenance or atrophy), as well as the ability to recruit compensatory processes. The purpose of this review is to present findings from the Betula study and other longitudinal studies, with a focus on clarifying the role of key biological and environmental factors assumed to underlie individual differences in brain and cognitive ageing. We discuss the vital importance of sampling, analytic methods, consideration of non-ignorable dropout, and related issues for valid conclusions on factors that influence healthy neurocognitive ageing.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
ageing, memory, longitudinal, brain, genetics, lifestyle, brain maintenance, cognitive reserve
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-176224 (URN)10.1016/j.arr.2020.101184 (DOI)000595935300003 ()32992046 (PubMedID)2-s2.0-85092710312 (Scopus ID)
Funder
Knut and Alice Wallenberg Foundation, KAW-scholarEU, Horizon 2020, 732592EU, Horizon 2020, H2020-SC1-2016-2017EU, Horizon 2020, H2020-SC1-2016-RTDSwedish Research Council, 2017- 00639Region VästerbottenThe Dementia Association - The National Association for the Rights of the DementedKnut and Alice Wallenberg Foundation, KAW 2014.0205Swedish Research Council, 2015–02199Swedish Research Council, 2017- 03011Swedish Research Council, (2018-01729Swedish Research Council Formas, 942–2015-1099
Available from: 2020-10-22 Created: 2020-10-22 Last updated: 2024-04-25Bibliographically approved
Sundström, A., Nordin Adolfsson, A., Nordin, M. & Adolfsson, R. (2020). Loneliness increases the risk of all-cause dementia and Alzheimer's disease. The journals of gerontology. Series B, Psychological sciences and social sciences, 75(5), 919-926
Open this publication in new window or tab >>Loneliness increases the risk of all-cause dementia and Alzheimer's disease
2020 (English)In: The journals of gerontology. Series B, Psychological sciences and social sciences, ISSN 1079-5014, E-ISSN 1758-5368, Vol. 75, no 5, p. 919-926Article in journal (Refereed) Published
Abstract [en]

Objectives: To examine the effect of perceived loneliness on the development of dementia (all-cause), Alzheimer's disease (AD), and vascular dementia (VaD).

Method: The study comprised 1,905 nondemented participants at baseline, drawn from the longitudinal Betula study in Sweden, with a follow-up time of up to 20 years (mean 11.1 years). Loneliness was measured with a single question: "Do you often feel lonely?".

Results: During the follow-up, 428 developed dementia; 221 had AD, 157 had VaD, and 50 had dementia of other subtypes. The entire dementia group is denoted "all-cause dementia". Cox regression models, adjusted for age, gender, and a baseline report of perceived loneliness, showed increased risk of all-cause dementia (hazard ratio [HR] = 1.46, 95% confidence interval [CI] 1.14–1.89), and AD (HR = 1.69, 95% CI 1.20–2.37), but not VaD (HR = 1.34, 95% CI 0.87–2.08). After adjusting for a range of potential confounders, and excluding participants with dementia onset within the first 5 years of baseline (to consider the possibility of reverse causality), the increased risk for the development of all-cause dementia and AD still remained significant (HR = 1.51, 95% CI 1.01–2.25 for all-cause dementia; HR = 2.50, 95% CI 1.44–4.36 for AD).

Discussion: The results suggest that perceived loneliness is an important risk factor for all-cause dementia and especially for AD, but not for VaD. These results underscore the importance of paying attention to subjective reports of loneliness among the elderly adults and identifying potential intervention strategies that can reduce loneliness.

Place, publisher, year, edition, pages
Oxford University Press, 2020
Keywords
Living alone, Longitudinal, Risk factors, Social isolation, Social relationship
National Category
Psychology
Research subject
Psychology
Identifiers
urn:nbn:se:umu:diva-165205 (URN)10.1093/geronb/gbz139 (DOI)000535916300004 ()2-s2.0-85083623378 (Scopus ID)
Available from: 2019-11-14 Created: 2019-11-14 Last updated: 2024-04-08Bibliographically approved
Sundström, A., Eriksson Sörman, D., Hansson, P., Körning-Ljungberg, J. & Adolfsson, R. (2020). Mental demands at work and risk of dementia. Journal of Alzheimer's Disease, 74(3), 735-740
Open this publication in new window or tab >>Mental demands at work and risk of dementia
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2020 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 74, no 3, p. 735-740Article in journal (Refereed) Published
Abstract [en]

High mental demands at work was examined as a possible protective factor to reduce the risk of dementia in 1,277 initially dementia-free participants, aged 60 years and older. The cohort was followed for a mean of 13.6 years. During follow-up, 376 participants developed all-cause dementia (Alzheimer’s disease = 199; vascular dementia = 145). The association between mental demands at work and dementia was analyzed with Cox hazard models, adjusted for a range of covariates. The results revealed no significant association between mental demands at work and incidence of dementia. Based on the measures used in this study, it was concluded that high mental demands at work may not reduce the risk of dementia later on in life.

Place, publisher, year, edition, pages
IOS Press, 2020
Keywords
aging, Alzheimer’s disease, cognitive occupation complexity, cognitive reserve, dementia, mental demands at work, vascular dementia
National Category
Neurology
Research subject
Psychology
Identifiers
urn:nbn:se:umu:diva-169514 (URN)10.3233/JAD-190920 (DOI)000526816100002 ()32083580 (PubMedID)2-s2.0-85083293840 (Scopus ID)
Available from: 2020-04-02 Created: 2020-04-02 Last updated: 2024-05-03Bibliographically approved
Oudin, A., Andersson, J., Sundström, A., Nordin Adolfsson, A., Oudin Åström, D., Adolfsson, R., . . . Nordin, M. (2019). Traffic-Related Air Pollution as a Risk Factor for Dementia: No Clear Modifying Effects of APOEɛ4 in the Betula Cohort. Journal of Alzheimer's Disease, 71(3), 733-740
Open this publication in new window or tab >>Traffic-Related Air Pollution as a Risk Factor for Dementia: No Clear Modifying Effects of APOEɛ4 in the Betula Cohort
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2019 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 71, no 3, p. 733-740Article in journal (Refereed) Published
Abstract [en]

It is widely known that the apolipoprotein E (APOE) ɛ4 allele imposes a higher risk for Alzheimer’s disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOE ɛ4 carriers than in non-carriers. Air pollution and interaction with APOE ɛ4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOE ɛ4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOE ɛ4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOE ɛ4 carriers than in the total population.

Place, publisher, year, edition, pages
IOS Press, 2019
Keywords
Air pollution, Alzheimer’s disease, apolipoprotein E, dementia
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-163266 (URN)10.3233/JAD-181037 (DOI)000488819100002 ()31450491 (PubMedID)2-s2.0-85073082152 (Scopus ID)
Available from: 2019-09-12 Created: 2019-09-12 Last updated: 2024-04-08Bibliographically approved
Lebedeva, A., Sundström, A., Lindgren, L., Stomby, A., Aarsland, D., Westman, E., . . . Nyberg, L. (2018). Longitudinal relationships among depressive symptoms, cortisol, and brain atrophy in the neocortex and the hippocampus. Acta Psychiatrica Scandinavica, 167(6), 491-502
Open this publication in new window or tab >>Longitudinal relationships among depressive symptoms, cortisol, and brain atrophy in the neocortex and the hippocampus
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2018 (English)In: Acta Psychiatrica Scandinavica, ISSN 0001-690X, E-ISSN 1600-0447, Vol. 167, no 6, p. 491-502Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: Depression is associated with accelerated aging and age-related diseases. However, mechanisms underlying this relationship remain unclear. The aim of this study was to longitudinally assess the link between depressive symptoms, brain atrophy, and cortisol levels.

METHOD: Participants from the Betula prospective cohort study (mean age = 59 years, SD = 13.4 years) underwent clinical, neuropsychological and brain 3T MRI assessments at baseline and a 4-year follow-up. Cortisol levels were measured at baseline in four saliva samples. Cortical and hippocampal atrophy rates were estimated and compared between participants with and without depressive symptoms (n = 81) and correlated with cortisol levels (n = 49).

RESULTS: Atrophy in the left superior frontal gyrus and right lingual gyrus developed in parallel with depressive symptoms, and in the left temporal pole, superior temporal cortex, and supramarginal cortex after the onset of depressive symptom. Depression-related atrophy was significantly associated with elevated cortisol levels. Elevated cortisol levels were also associated with widespread prefrontal, parietal, lateral, and medial temporal atrophy.

CONCLUSION: Depressive symptoms and elevated cortisol levels are associated with atrophy of the prefrontal and limbic areas of the brain.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018
Keywords
depressive symptomatology, neuroimaging, superior temporal gyrus, superior frontal gyrus, MRI
National Category
Nursing Psychiatry
Identifiers
urn:nbn:se:umu:diva-146479 (URN)10.1111/acps.12860 (DOI)000433560700006 ()29457245 (PubMedID)2-s2.0-85042120842 (Scopus ID)
Available from: 2018-04-10 Created: 2018-04-10 Last updated: 2023-03-24Bibliographically approved
Projects
Lifestyle and socioeconomic risk factors for cognitive decline and dementia [P11-0876:1_RJ]; Umeå University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-3606-3057

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