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Nordin Adolfsson, AnnelieORCID iD iconorcid.org/0000-0002-8114-7615
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Publications (10 of 41) 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
Schäfer Hackenhaar, F., Josefsson, M., Nordin Adolfsson, A., Landfors, M., Kauppi, K., Porter, T., . . . the Australian Imaging Biomarkers and Lifestyle Study, . (2023). Sixteen-year longitudinal evaluation of blood-based DNA methylation biomarkers for early prediction of Alzheimer’s disease. Journal of Alzheimer's Disease, 94(4), 1443-1464
Open this publication in new window or tab >>Sixteen-year longitudinal evaluation of blood-based DNA methylation biomarkers for early prediction of Alzheimer’s disease
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2023 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 94, no 4, p. 1443-1464Article in journal (Refereed) Published
Abstract [en]

Background: DNA methylation (DNAm), an epigenetic mark reflecting both inherited and environmental influences, hasshown promise for Alzheimer’s disease (AD) prediction.Objective: Testing long-term predictive ability (>15 years) of existing DNAm-based epigenetic age acceleration (EAA)measures and identifying novel early blood-based DNAm AD-prediction biomarkers.

Methods: EAA measures calculated from Illumina EPIC data from blood were tested with linear mixed-effects models(LMMs) in a longitudinal case-control sample (50 late-onset AD cases; 51 matched controls) with prospective data up to 16years before clinical onset, and post-onset follow-up. NovelDNAmbiomarkers were generated with epigenome-wide LMMs,and Sparse Partial Least Squares Discriminant Analysis applied at pre- (10–16 years), and post-AD-onset time-points.

Results: EAA did not differentiate cases from controls during the follow-up time (p > 0.05). Three new DNA biomarkersshowed in-sample predictive ability on average 8 years pre-onset, after adjustment for age, sex, and white blood cell proportions(p-values: 0.022-<0.00001). Our longitudinally-derived panel replicated nominally (p = 0.012) in an external cohort (n = 146cases, 324 controls). However, its effect size and discriminatory accuracy were limited compared to APOE 4-carriership(OR = 1.38 per 1 SD DNAmscore increase versus OR= 13.58 for 4-allele carriage; AUCs = 77.2% versus 87.0%). Literaturereview showed low overlap (n = 4) across 3275 AD-associated CpGs from 8 published studies, and no overlap with ouridentified CpGs.

Conclusion: The limited predictive value of EAA for AD extends prior findings by considering a longer follow-up time, andwith appropriate control for age, sex, APOE, and blood-cell proportions. Results also highlight challenges with replicatingdiscriminatory or predictive CpGs across studies.

Place, publisher, year, edition, pages
IOS Press, 2023
Keywords
Alzheimer’s disease, biomarkers, DNA methylation, epigenomics, longitudinal studies
National Category
Other Basic Medicine
Identifiers
urn:nbn:se:umu:diva-214007 (URN)10.3233/jad-230039 (DOI)37393498 (PubMedID)2-s2.0-85168428453 (Scopus ID)
Funder
Swedish Research Council, 2018-01729The Kempe Foundations, JCK-1922.1
Available from: 2023-09-02 Created: 2023-09-02 Last updated: 2024-04-08Bibliographically approved
Salami, A., Adolfsson, R., Andersson, M., Blennow, K., Lundquist, A., Nordin Adolfsson, A., . . . Nyberg, L. (2022). Association of APOE ɛ4 and Plasma p-tau181 with Preclinical Alzheimer's Disease and Longitudinal Change in Hippocampus Function. Journal of Alzheimer's Disease, 85(3), 1309-1320
Open this publication in new window or tab >>Association of APOE ɛ4 and Plasma p-tau181 with Preclinical Alzheimer's Disease and Longitudinal Change in Hippocampus Function
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2022 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 85, no 3, p. 1309-1320Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The Apolipoprotein E (APOE) ɛ4 allele has been linked to increased tau phosphorylation and tangle formation. APOE ɛ4 carriers with elevated tau might be at the higher risk for Alzheimer's disease (AD) progression. Previous studies showed that tau pathology begins early in areas of the medial temporal lobe. Similarly, APOE ɛ4 carriers showed altered hippocampal functional integrity. However, it remains unknown whether the influence of elevated tau accumulation on hippocampal functional changes would be more pronounced for APOE ɛ4 carriers.

OBJECTIVE: We related ɛ4 carriage to levels of plasma phosphorylated tau (p-tau181) up to 15 years prior to AD onset. Furthermore, elevated p-tau181 was explored in relation to longitudinal changes in hippocampal function and connectivity.

METHODS: Plasma p-tau181 was analyzed in 142 clinically defined AD cases and 126 matched controls. The longitudinal analysis involved 87 non-demented individuals (from population-based study) with two waves of plasma samples and three waves of functional magnetic resonance imaging during rest and memory encoding.

RESULTS: Increased p-tau181 was observed for both ɛ4 carriers and non-carriers close to AD onset, but exclusively for ɛ4 carriers in the early preclinical groups (7- and 13-years pre-AD). In ɛ4 carriers, longitudinal p-tau181 increase was paralleled by elevated local hippocampal connectivity at rest and subsequent reduction of hippocampus encoding-related activity.

CONCLUSION: Our findings support an association of APOE ɛ4 and p-tau181 with preclinical AD and hippocampus functioning.

Place, publisher, year, edition, pages
IOS Press, 2022
Keywords
Alzheimer’s disease, APOE, fMRI, hippocampus, longitudinal, magnetic resonance imaging, p-tau181, phosphorylated tau, population-based
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-192513 (URN)10.3233/JAD-210673 (DOI)000752449800030 ()34924376 (PubMedID)2-s2.0-85124174700 (Scopus ID)
Available from: 2022-02-22 Created: 2022-02-22 Last updated: 2024-04-08Bibliographically approved
Pudas, S., Josefsson, M., Nordin Adolfsson, A., Landfors, M., Kauppi, K., Veng-Taasti, L. M., . . . Degerman, S. (2021). Short leukocyte telomeres, but not telomere attrition rates, predict memory decline in the 20-year longitudinal Betula study. The journals of gerontology. Series A, Biological sciences and medical sciences, 76(6), 955-963
Open this publication in new window or tab >>Short leukocyte telomeres, but not telomere attrition rates, predict memory decline in the 20-year longitudinal Betula study
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2021 (English)In: The journals of gerontology. Series A, Biological sciences and medical sciences, ISSN 1079-5006, E-ISSN 1758-535X, Vol. 76, no 6, p. 955-963Article in journal (Refereed) Published
Abstract [en]

Leukocyte telomere length (LTL) is a proposed biomarker for aging-related disorders, including cognitive decline and dementia. Long-term longitudinal studies measuring intra-individual changes in both LTL and cognitive outcomes are scarce, precluding strong conclusions about a potential aging-related relationship between LTL shortening and cognitive decline. This study investigated associations between baseline levels and longitudinal changes in LTL and memory performance across an up to 20-year follow-up in 880 dementia-free participants from a population-based study (mean baseline age: 56.8 years, range: 40–80; 52% female). Shorter baseline LTL significantly predicted subsequent memory decline (r = .34, 95% confidence interval: 0.06, 0.82), controlling for age, sex, and other relevant covariates. No significant associations were however observed between intra-individual changes in LTL and memory, neither concurrently nor with a 5-year time-lag between LTL shortening and memory decline. These results support the notion of short LTL as a predictive factor for aging-related memory decline, but suggest that LTL dynamics in adulthood and older age may be less informative of cognitive outcomes in aging. Furthermore, the results highlight the importance of long-term longitudinal evaluation of outcomes in biomarker research.

Place, publisher, year, edition, pages
Oxford University Press, 2021
Keywords
Cognitive aging, Leukocyte telomere length, Longitudinal, Memory, Population-based
National Category
Gerontology, specialising in Medical and Health Sciences Geriatrics Neurosciences
Research subject
medical behavioral science; Geriatrics; Psychology
Identifiers
urn:nbn:se:umu:diva-181484 (URN)10.1093/gerona/glaa322 (DOI)000659456700002 ()33367599 (PubMedID)2-s2.0-85107088699 (Scopus ID)
Funder
Swedish Research Council, 2018-01729Region Västerbotten, RV-735451, RV-453141, RV-225461
Available from: 2021-03-13 Created: 2021-03-13 Last updated: 2024-04-08Bibliographically approved
Schäfer Hackenhaar, F., Josefsson, M., Nordin Adolfsson, A., Landfors, M., Kauppi, K., Hultdin, M., . . . Pudas, S. (2021). Short leukocyte telomeres predict 25-year Alzheimer's disease incidence in non-APOE ε4-carriers. Alzheimer's Research & Therapy, 13, Article ID 130.
Open this publication in new window or tab >>Short leukocyte telomeres predict 25-year Alzheimer's disease incidence in non-APOE ε4-carriers
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2021 (English)In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 13, article id 130Article in journal (Refereed) Published
Abstract [en]

Background: Leukocyte telomere length (LTL) has been shown to predict Alzheimer’s disease (AD), albeit inconsistently. Failing to account for the competing risks between AD, other dementia types, and mortality, can be an explanation for the inconsistent findings in previous time-to-event analyses. Furthermore, previous studies indicate that the association between LTL and AD is non-linear and may differ depending on apolipoprotein E (APOE) ε4 allele carriage, the strongest genetic AD predictor.

Methods: We analyzed whether baseline LTL in interaction with APOE ε4 predicts AD, by following 1306 initially non-demented subjects for 25 years. Gender- and age-residualized LTL (rLTL) was categorized into tertiles of short, medium, and long rLTLs. Two complementary time-to-event models that account for competing risks were used; the Fine-Gray model to estimate the association between the rLTL tertiles and the cumulative incidence of AD, and the cause-specific hazard model to assess whether the cause-specific risk of AD differed between the rLTL groups. Vascular dementia and death were considered competing risk events. Models were adjusted for baseline lifestyle-related risk factors, gender, age, and non-proportional hazards.

Results: After follow-up, 149 were diagnosed with AD, 96 were diagnosed with vascular dementia, 465 died without dementia, and 596 remained healthy. Baseline rLTL and other covariates were assessed on average 8 years before AD onset (range 1–24). APOE ε4-carriers had significantly increased incidence of AD, as well as increased cause-specific AD risk. A significant rLTL-APOE interaction indicated that short rLTL at baseline was significantly associated with an increased incidence of AD among non-APOE ε4-carriers (subdistribution hazard ratio = 3.24, CI 1.404–7.462, P = 0.005), as well as borderline associated with increased cause-specific risk of AD (cause-specific hazard ratio = 1.67, CI 0.947–2.964, P = 0.07). Among APOE ε4-carriers, short or long rLTLs were not significantly associated with AD incidence, nor with the cause-specific risk of AD.

Conclusions: Our findings from two complementary competing risk time-to-event models indicate that short rLTL may be a valuable predictor of the AD incidence in non-APOE ε4-carriers, on average 8 years before AD onset. More generally, the findings highlight the importance of accounting for competing risks, as well as the APOE status of participants in AD biomarker research.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2021
Keywords
Leukocyte telomere length, Dementia, Risk factors, Time-to-event analysis, Competing risks, Vascular dementia, Death
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-186769 (URN)10.1186/s13195-021-00871-y (DOI)000673978800001 ()34266503 (PubMedID)2-s2.0-85110170246 (Scopus ID)
Note

Correction: Hackenhaar, F.S., Josefsson, M., Adolfsson, A.N. et al. Correction: Short leukocyte telomeres predict 25-year Alzheimer’s disease incidence in non-APOE ε4-carriers. Alz Res Therapy 16, 39 (2024). DOI: 10.1186/s13195-024-01388-w

Available from: 2021-08-20 Created: 2021-08-20 Last updated: 2024-04-08Bibliographically 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
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
Kauppi, K., Rönnlund, M., Nordin Adolfsson, A., Pudas, S. & Adolfsson, R. (2020). Effects of polygenic risk for Alzheimer's disease on rate of cognitive decline in normal aging. Translational Psychiatry, 10(1), Article ID 250.
Open this publication in new window or tab >>Effects of polygenic risk for Alzheimer's disease on rate of cognitive decline in normal aging
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2020 (English)In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 10, no 1, article id 250Article in journal (Refereed) Published
Abstract [en]

Most people's cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. Although APOE 4 and genetic scores for late-onset Alzheimer's disease (LOAD) have been related to cognitive decline during preclinical stages of dementia, there is limited knowledge concerning genetic factors implied in normal cognitive aging. In the present study, we examined three potential genetic predictors of age-related cognitive decline as follows: (1) the APOE 4 allele, (2) a polygenic score for general cognitive ability (PGS-cog), and (3) a polygenic risk score for late-onset AD (PRS-LOAD). We examined up to six time points of cognitive measurements in the longitudinal population-based Betula study, covering a 25-year follow-up period. Only participants that remained alive and non-demented until the most recent dementia screening (1-3 years after the last test occasion) were included (n=1087). Individual differences in rate of cognitive change (composite score) were predicted by the PRS-LOAD and APOE 4, but not by PGS-cog. To control for the possibility that the results reflected a preclinical state of Alzheimer's disease in some participants, we re-ran the analyses excluding cognitive data from the last test occasion to model cognitive change up-until a minimum of 6 years before potential onset of clinical Alzheimers. Strikingly, the association of PRS-LOAD, but not APOE 4, with cognitive change remained. The results indicate that PRS-LOAD predicts individual difference in rate of cognitive decline in normal aging, but it remains to be determined to what extent this reflects preclinical Alzheimer's disease brain pathophysiology and subsequent risk to develop the disease.

Place, publisher, year, edition, pages
Nature Publishing Group, 2020
National Category
Psychiatry Neurosciences
Identifiers
urn:nbn:se:umu:diva-174322 (URN)10.1038/s41398-020-00934-y (DOI)000555898200001 ()32709845 (PubMedID)2-s2.0-85088532332 (Scopus ID)
Available from: 2020-08-24 Created: 2020-08-24 Last updated: 2024-04-08Bibliographically approved
Nyberg, L., Lundquist, A., Nordin Adolfsson, A., Andersson, M., Zetterberg, H., Blennow, K. & Adolfsson, R. (2020). Elevated plasma neurofilament light in aging reflects brain white-matter alterations but does not predict cognitive decline or Alzheimer's disease. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring (DADM), 12(1), Article ID e12050.
Open this publication in new window or tab >>Elevated plasma neurofilament light in aging reflects brain white-matter alterations but does not predict cognitive decline or Alzheimer's disease
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2020 (English)In: Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring (DADM), ISSN 2352-8729, Vol. 12, no 1, article id e12050Article in journal (Refereed) Published
Abstract [en]

Introduction: We investigated neurofilament light (NFL) accumulation in normal aging as well as in preclinical and clinical Alzheimer's disease (AD) and assessed individual differences in NFL load in relation to cognition and brain white-matter integrity.

Methods: We analyzed longitudinal data covering 30 years (1988-2017). Cognitive testing was done up to six times. Plasma NFL was quantified for controls and 142 cases who developed AD over time, and longitudinal changes in NFL were quantified for 100 individuals with three brain-imaging sessions.

Results: Longitudinal analyses revealed age-related NFL increases with marked variability. AD cases had elevated NFL levels, while no significant group differences were seen in the preclinical phase. Variability in NFL levels showed non-significant correlations with cognition but was associated with brain white matter.

Discussion: Our findings suggest that elevated blood NFL, likely reflecting brain white-matter alterations, characterizes clinical AD, while NFL levels do not predict age-related cognitive impairment or impending AD.

Place, publisher, year, edition, pages
John Wiley & Sons, 2020
Keywords
Alzheimer's disease, biomarker, brain white matter, cognition, early prediction, longitudinal, neurofilament light
National Category
Neurosciences
Research subject
Physiology
Identifiers
urn:nbn:se:umu:diva-182787 (URN)10.1002/dad2.12050 (DOI)000707203600049 ()32587884 (PubMedID)2-s2.0-85092715551 (Scopus ID)
Funder
Knut and Alice Wallenberg FoundationRegion VästerbottenTorsten Söderbergs stiftelseSwedish Research Council, #2017-00915Alzheimerfonden, AF-742881The Swedish Brain Foundation, FO2017-0243Region Västerbotten, ALFGBG715986
Available from: 2021-05-04 Created: 2021-05-04 Last updated: 2024-04-08Bibliographically 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
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-8114-7615

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