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Johansson, J., Salami, A., Lundquist, A., Wahlin, A., Andersson, M. & Nyberg, L. (2020). Longitudinal evidence that reduced hemispheric encoding/retrieval asymmetry predicts episodic-memory impairment in aging. Neuropsychologia, 137, Article ID 107329.
Open this publication in new window or tab >>Longitudinal evidence that reduced hemispheric encoding/retrieval asymmetry predicts episodic-memory impairment in aging
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2020 (English)In: Neuropsychologia, ISSN 0028-3932, E-ISSN 1873-3514, Vol. 137, article id 107329Article in journal (Refereed) Published
Abstract [en]

The HERA (Hemispheric Encoding/Retrieval Asymmetry) model captures hemispheric lateralization of prefrontal cortex (PFC) brain activity during memory encoding and retrieval. Reduced HERA has been observed in cross-sectional aging studies, but there is no longitudinal evidence, to our knowledge, on age-related changes in HERA and whether maintained or reduced HERA relates to well-preserved memory functioning. In the present study we set out to explore HERA in a longitudinal neuroimaging sample from the Betula study [3 Waves over 10 years; Wave-1: n = 363, W2: n = 227, W3: n = 101]. We used fMRI data from a face-name paired-associates task to derive a HERA index. In support of the HERA model, the mean HERA index was positive across the three imaging waves. The longitudinal age-HERA relationship was highly significant (p < 10(-11)), with a HERA decline occurring after age 60. The age-related HERA decline was associated with episodic memory decline (p < 0.05). Taken together, the findings provide large-scale support for the HERA model, and suggest that reduced HERA in the PFC reflects pathological memory aging possibly related to impaired ability to bias mnemonic processing according to the appropriate encoding or retrieval state.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
Aging, Cognitive control, Episodic memory, Prefrontal cortex, Hemispheric asymmetry, Functional magnetic resonance imaging
National Category
Geriatrics
Identifiers
urn:nbn:se:umu:diva-168119 (URN)10.1016/j.neuropsychologia.2019.107329 (DOI)000509751200024 ()31887310 (PubMedID)
Available from: 2020-02-21 Created: 2020-02-21 Last updated: 2020-03-10Bibliographically approved
Boman, A., Brink, M., Lundquist, A., Hansson, M., Mathsson-Alm, L., Rönnelid, J., . . . Rantapää-Dahlqvist, S. (2019). Antibodies against citrullinated peptides are associated with clinical and radiological outcomes in patients with early rheumatoid arthritis: a prospective longitudinal inception cohort study. RMD Open, 5(2), Article ID e000946.
Open this publication in new window or tab >>Antibodies against citrullinated peptides are associated with clinical and radiological outcomes in patients with early rheumatoid arthritis: a prospective longitudinal inception cohort study
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2019 (English)In: RMD Open, E-ISSN 2056-5933, Vol. 5, no 2, article id e000946Article in journal (Refereed) Published
Abstract [en]

Introduction: Anticitrullinated peptide antibody (ACPA) responses for 22 citrullinated peptides in patients with early rheumatoid arthritis (RA) were analysed and related to radiological and clinical outcome during the first 2 years in a prospective inception cohort.

Methods: The ACPA reactivities were assessed in 1022 patients with early RA (symptoms <12 months) using the custom-made microarray chip (Thermo Fisher Scientific, Uppsala, Sweden) in a prospective longitudinal study of observational assessments of Disease Activity Score (DAS28 and its components) and radiology during the first 24 months, accounting for the treatment.

Results: Frequency of ACPA reactivities varied between 13.3% and 63.1%. Of the anticyclic citrullinated peptide-2 (anti-CCP2) antibody-negative patients, ACPA reactivities were positive in 32.6%. Smoking, human leucocyte antigen-shared epitope (HLA-SE), anti-CCP2/rheumatoid factor, protein tyrosine phosphatase non-receptor type 22 (1858C/T) and DAS28 were significantly associated with number of ACPA reactivities. The ACPA reactivities modified differently the development of DAS28 over 24 months (identified using trajectories). Anti-Filaggrin307-324, anti-hnRNP (Peptide)-Z1 and anti-F4-CIT-R antibodies anticipated lower DAS28 values (p<0.01–0.05), while positivity for anti-Fibrinogen(Fib)β62-78(74), and anti-Fibα563-583 predicted higher DAS28 (p<0.01 both). Interaction between anti-Fibß36-52, anti-Pept-5 and anti-Bla-26 antibodies, respectively, and DAS28 during 24 months decreased significantly the DAS28 values (p<0.01–0.05). Corticosteroids and biologicals were related to DAS28-area under the curve and Larsen score 24 months. Anti-vimentin2-17 antibodies remained significantly associated with Larsen score at baseline and 24 months, respectively, and radiological progression, besides biologicals at 24 months adjusted for sex and age.

Conclusions: Several ACPA reactivities modified significantly the DAS28 development during the first 24 months and were significantly associated with Larsen score at baseline, 24 months and radiological progression.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2019
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:umu:diva-165746 (URN)10.1136/rmdopen-2019-000946 (DOI)000496133800042 ()31565241 (PubMedID)
Funder
Swedish Research Council, K2013-52X-2030707-3Swedish Research Council, Dnr:2018-02551King Gustaf V Jubilee Fund
Available from: 2019-12-10 Created: 2019-12-10 Last updated: 2020-03-10Bibliographically approved
Nyberg, L., Andersson, M., Lundquist, A., Salami, A. & Wåhlin, A. (2019). Frontal Contribution to Hippocampal Hyperactivity During Memory Encoding in Aging. Frontiers in Molecular Neuroscience, 12, Article ID 229.
Open this publication in new window or tab >>Frontal Contribution to Hippocampal Hyperactivity During Memory Encoding in Aging
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2019 (English)In: Frontiers in Molecular Neuroscience, ISSN 1662-5099, Vol. 12, article id 229Article in journal (Refereed) Published
Abstract [en]

Hippocampal hypo- as well as hyper-activation have been reported during memory encoding in older individuals. Prefrontal cortex (PFC) provides top-down state signals to the hippocampus that bias its computation during memory encoding and retrieval, and disturbed top-down signals could contribute to hippocampal hyper-activation. Here, we used >500 cross-sectional and longitudinal observations from a face-name encoding-retrieval fMRI task to examine hippocampal hypo-and hyper-activation in aging. Age-related anterior hippocampal hypo-activation was observed during memory encoding. Next, older individuals who longitudinally dropped-out were compared with those who remained in the study. Older dropouts had lower memory performance and higher dementia risk, and hyper-activated right anterior and posterior hippocampus during memory encoding. During encoding, the dropouts also activated right prefrontal regions that instead were active during retrieval in younger and older remainers. Moreover, the dropouts showed altered frontal-hippocampal functional connectivity, notably elevated right PFC to anterior hippocampus (aHC) connectivity during encoding. In the context of a general pattern of age-related anterior hippocampal hypo-activation during encoding, these findings support a top-down contribution to paradoxically high anterior hippocampal activity in older dropouts who were at elevated risk of pathology.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2019
Keywords
hippocampus, pattern completion bias, aging, episodic memory, cognitive control
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-164045 (URN)10.3389/fnmol.2019.00229 (DOI)000487635300001 ()
Available from: 2019-10-15 Created: 2019-10-15 Last updated: 2019-10-15Bibliographically approved
Kissel, T., van Schie, K. A., Hafkenscheid, L., Lundquist, A., Kokkonen, H., Wuhrer, M., . . . Rantapää-Dahlqvist, S. (2019). On the presence of HLA-SE alleles and ACPA-IgG variable domain glycosylation in the phase preceding the development of rheumatoid arthritis. Annals of the Rheumatic Diseases, 78(12), 1616-1620
Open this publication in new window or tab >>On the presence of HLA-SE alleles and ACPA-IgG variable domain glycosylation in the phase preceding the development of rheumatoid arthritis
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2019 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 78, no 12, p. 1616-1620Article in journal (Refereed) Published
Abstract [en]

Objective: Anti-citrullinated protein antibodies (ACPA) in rheumatoid arthritis (RA) patients display a unique feature defined by the abundant presence of N-linked glycans within the variable domains (V-domains). Recently, we showed that N-glycosylation sites, which are required for the incorporation of V-domain glycans, are introduced following somatic hypermutation. However, it is currently unclear when V-domain glycosylation occurs. Further, it is unknown which factors might trigger the generation of V-domain glycans and whether such glycans are relevant for the transition towards RA. Here, we determined the presence of ACPA-IgG V-domain glycans in paired samples of pre-symptomatic individuals and RA patients.

Methods: ACPA-IgG V-domain glycosylation was analysed using ultra-high performance liquid chromatography (UHPLC) in paired samples of pre-symptomatic individuals (median interquartile range (IQR) pre-dating time: 5.8 (5.9) years; n=201; 139 ACPA-positive and 62 ACPA-negative) and RA patients (n=99; 94 ACPA-positive and 5 ACPA-negative).

Results: V-domain glycans on ACPA-IgG were already present up to 15 years before disease in pre-symptomatic individuals and their abundance increased closer to symptom onset. Noteworthy, human leucocyte antigen class II shared epitope (HLA-SE) alleles associated with the presence of V-domain glycans on ACPA-IgG.

Conclusion: Our observations indicate that somatic hypermutation of ACPA, which results in the incorporation of N-linked glycosylation sites and consequently V-domain glycans, occurs already years before symptom onset in individuals that will develop RA later in life. Moreover, our findings provide first evidence that HLA-SE alleles associate with ACPA-IgG V-domain glycosylation in the pre-disease phase and thereby further refine the connection between HLA-SE and the development of ACPA-positive RA.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2019
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:umu:diva-167073 (URN)10.1136/annrheumdis-2019-215698 (DOI)000500726200016 ()31471298 (PubMedID)
Available from: 2020-01-13 Created: 2020-01-13 Last updated: 2020-01-13Bibliographically approved
Brink, M., Lundquist, A., Alexeyenko, A., Lejon, K. & Rantapää-Dahlqvist, S. (2019). Protein profiling and network enrichment analysis in individuals before and after the onset of rheumatoid arthritis. Arthritis Research & Therapy, 21(1), Article ID 288.
Open this publication in new window or tab >>Protein profiling and network enrichment analysis in individuals before and after the onset of rheumatoid arthritis
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2019 (English)In: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 21, no 1, article id 288Article in journal (Refereed) Published
Abstract [en]

Background: Antibodies and upregulated cytokines and chemokines predate the onset of rheumatoid arthritis (RA) symptoms. We aimed to identify the pathways related to the early processes leading to RA development, as well as potential novel biomarkers, using multiple protein analyses.

Methods: A case-control study was conducted within the Biobank of northern Sweden. The plasma samples from 118 pre-symptomatic individuals (207 samples; median predating time 4.1 years), 79 early RA patients, and 74 matched controls were analyzed. The levels of 122 unique proteins with an acknowledged relationship to autoimmunity were analyzed using 153 antibodies and a bead-based multiplex system (FlexMap3D; Luminex Corp.). The data were analyzed using multifactorial linear regression model, random forest, and network enrichment analysis (NEA) based on the 10 most significantly differentially expressed proteins for each two-by-two group comparison, using the MSigDB collection of hallmarks.

Results: There was a high agreement between the different statistical methods to identify the most significant proteins. The adipogenesis and interferon alpha response hallmarks differentiated pre-symptomatic individuals from controls. These two hallmarks included proteins involved in innate immunity. Between pre-symptomatic individuals and RA patients, three hallmarks were identified as follows: apical junction, epithelial mesenchymal transition, and TGF-beta signaling, including proteins suggestive of cell interaction, remodulation, and fibrosis. The adipogenesis and heme metabolism hallmarks differentiated RA patients from controls.

Conclusions: We confirm the importance of interferon alpha signaling and lipids in the early phases of RA development. Network enrichment analysis provides a tool for a deeper understanding of molecules involved at different phases of the disease progression.

Place, publisher, year, edition, pages
BioMed Central, 2019
Keywords
Rheumatoid arthritis, Pre-symptomatic stage, Protein levels, Plasma biomarkers
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:umu:diva-168174 (URN)10.1186/s13075-019-2066-9 (DOI)000509121200002 ()31842970 (PubMedID)
Available from: 2020-03-17 Created: 2020-03-17 Last updated: 2020-03-17Bibliographically approved
Brink, M., Lundquist, A., Alexeyenko, A., Lejon, K. & Rantapää-Dahlqvist, S. (2019). Protein Profiling and Network Enrichment Analysis in Individuals Before and After the Onset of Rheumatoid Arthritis. Paper presented at 2019 ACR/ARP Annual Meeting, Atlanda, USA, November 8–13, 2019.. Arthritis & Rheumatology, 71
Open this publication in new window or tab >>Protein Profiling and Network Enrichment Analysis in Individuals Before and After the Onset of Rheumatoid Arthritis
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2019 (English)In: Arthritis & Rheumatology, ISSN 2326-5191, E-ISSN 2326-5205, Vol. 71Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
John Wiley & Sons, 2019
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:umu:diva-168156 (URN)000507466903349 ()
Conference
2019 ACR/ARP Annual Meeting, Atlanda, USA, November 8–13, 2019.
Note

Supplement: 10. Meeting Abstract: 2004.

Available from: 2020-03-18 Created: 2020-03-18 Last updated: 2020-03-18Bibliographically approved
Kissel, T., van Schie, K., Hafkenscheid, L., Lundquist, A., Scherer, H. U., Kokkonen, H., . . . Rantapää-Dahlqvist, S. (2019). Rising ACPA igg variable domain glycosylation pre-disease associates with an increase in autoantibody levels and the development of rheumatoid arthritis. Paper presented at Annual European Congress of Rheumatology (EULAR), Madrid, Spain, June 12-15, 2019. Annals of the Rheumatic Diseases, 78, 249-250
Open this publication in new window or tab >>Rising ACPA igg variable domain glycosylation pre-disease associates with an increase in autoantibody levels and the development of rheumatoid arthritis
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2019 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 78, p. 249-250Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Background: Anti-citrullinated protein antibodies (ACPA) are present in the majority of rheumatoid arthritis (RA) patients (60-70%) and play a pivotal role in disease development1. ACPA IgGs are unique in a way that they are abundantly N-glycosylated within their variable regions2. These variable domain (V-domain) glycans are found on over 90% of ACPAs present in sera from RA-patients3. To undergo N-linked glycosylation, a consensus sequence in the protein backbone is required (N-X-S/T, where X ≠ P)4. Recently, it was shown that the N-linked glycosylation sites in ACPA-IgG V-domains are introduced during somatic hypermutation and that the introduction of such sites likely conveys a selective advantage to ACPA expressing B-cells5. However, it is currently unknown, whether ACPA-expressing B-cells already introduced glycosylation-sites into their V-domains before disease onset or when ACPA-V-domain glycosylation occurs.

Objectives: Investigate the appearance of ACPA V-domain glycosylation in pre-symptomatic individuals and RA patients.

Methods In a case-control study, individuals (n=201) from the Medical Biobank, who were sampled before onset of symptoms (mean±SEM predating time; 5.8±0.3 years) (140 aCCP+ and 61 aCCP-), and after diagnosis of RA (n=99, 94 aCCP+ and 5 aCCP-) and randomly selected control samples (n=43, 3 aCCP+ and 40 aCCP-) were analyzed for their ACPA IgG V-domain glycosylation levels. ACPA IgGs were affinity purified, N-linked glycans released, and 2-AA labeled for further analysis using UHPLC6. Data calibration and integration was performed and a cut-off defined. Samples below the cut-off were determined as non-detectable and excluded from the analysis. The percentage V-domain glycosylation was calculated as described previously3. Statistical calculations were performed using SPSS.

Results: Our data indicated that ACPA IgG V-domain glycans are already present years before symptom onset, in pre-symptomatic individuals who subsequently will develop RA. Analysis of matched pairs showed a significant increase of ACPA V-domain glycosylation in RA patients compared to individuals pre-disease (p<0.001). The results showed that ACPA N-glycosylation was correlated with anti-CCP concentrations pre-disease (rs =0.504, p<0.001), while no such association can be found after RA onset. Further, V-domain glycosylation levels increase closer to symptom onset.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2019
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:umu:diva-161721 (URN)10.1136/annrheumdis-2019-eular.5341 (DOI)000472207100546 ()
Conference
Annual European Congress of Rheumatology (EULAR), Madrid, Spain, June 12-15, 2019
Note

 Supplement: 2

Meeting Abstract: OP0333

Available from: 2019-07-26 Created: 2019-07-26 Last updated: 2020-01-23Bibliographically approved
Davies, G., Lam, M., Harris, S. E., Trampush, J. W., Luciano, M., Hill, W. D., . . . Deary, I. J. (2018). Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function. Nature Communications, 9, Article ID 2098.
Open this publication in new window or tab >>Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function
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2018 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 9, article id 2098Article in journal (Refereed) Published
Abstract [en]

General cognitive function is a prominent and relatively stable human trait that is associated with many important life outcomes. We combine cognitive and genetic data from the CHARGE and COGENT consortia, and UK Biobank (total N = 300,486; age 16-102) and find 148 genome-wide significant independent loci (P < 5 x 10-8) associated with general cognitive function. Within the novel genetic loci are variants associated with neurodegenerative and neurodevelopmental disorders, physical and psychiatric illnesses, and brain structure. Gene-based analyses find 709 genes associated with general cognitive function. Expression levels across the cortex are associated with general cognitive function. Using polygenic scores, up to 4.3% of variance in general cognitive function is predicted in independent samples. We detect significant genetic overlap between general cognitive function, reaction time, and many health variables including eyesight, hypertension, and longevity. In conclusion we identify novel genetic loci and pathways contributing to the heritability of general cognitive function.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-149020 (URN)10.1038/s41467-018-04362-x (DOI)000433297900009 ()29844566 (PubMedID)2-s2.0-85048027481 (Scopus ID)
Note

Errata: Davies, G., Lam, M., Harris, S. E., Trampush, J. W., Luciano, M., Hill, W. D., … Deary, I. J. (2019). Author correction to Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function. [Nature Communications (2018), 9, Article number 2098]. Nature Communications, 10, Article number: 2068. DOI: 10.1038/s41467-019-10160-w

Available from: 2018-06-15 Created: 2018-06-15 Last updated: 2019-05-21Bibliographically approved
Jonasson, L., Nyberg, L., Kramer, A., Lundquist, A., Riklund, K. & Boraxbekk, C.-J. (2017). Aerobic Exercise Intervention, CognitivePerformance, and Brain Structure: results from the Physical Influences on Brain in Aging (PHIBRA) Study. Frontiers in Aging Neuroscience, 8, 1-15, Article ID 336.
Open this publication in new window or tab >>Aerobic Exercise Intervention, CognitivePerformance, and Brain Structure: results from the Physical Influences on Brain in Aging (PHIBRA) Study
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2017 (English)In: Frontiers in Aging Neuroscience, ISSN 1663-4365, E-ISSN 1663-4365, Vol. 8, p. 1-15, article id 336Article in journal (Refereed) Published
Abstract [en]

Studies have shown that aerobic exercise has the potential to improve cognition and reduce brain atrophy in older adults. However, the literature is equivocal with regards to the specificity or generality of these effects. To this end, we report results on cognitive function and brain structure from a 6-month training intervention with 60 sedentary adults (64–78 years) randomized to either aerobic training or stretching and toning control training. Cognitive functions were assessed with a neuropsychological test battery in which cognitive constructs were measured using several different tests. Freesurfer was used to estimate cortical thickness in frontal regions and hippocampus volume. Results showed that aerobic exercisers, compared to controls, exhibited a broad, rather than specific, improvement in cognition as indexed by a higher “Cognitive score,” a composite including episodic memory, processing speed, updating, and executive function tasks (p = 0.01). There were no group differences in cortical thickness, but additional analyses revealed that aerobic fitness at baseline was specifically related to larger thickness in dorsolateral prefrontal cortex (dlPFC), and hippocampus volume was positively associated with increased aerobic fitness over time. Moreover, “Cognitive score” was related to dlPFC thickness at baseline, but changes in “Cognitive score” and dlPFC thickness were associated over time in the aerobic group only. However, aerobic fitness did not predict dlPFC change, despite the improvement in “Cognitive score” in aerobic exercisers. Our interpretation of these observations is that potential exercise-induced changes in thickness are slow, and may be undetectable within 6-months, in contrast to change in hippocampus volume which in fact was predicted by the change in aerobic fitness. To conclude, our results add to a growing literature suggesting that aerobic exercise has a broad influence on cognitive functioning, which may aid in explaining why studies focusing on a narrower range of functions have sometimes reported mixed results.

Keywords
aerobic exercise, cognition, executive function, plasticity, hippocampus, prefrontal cortex, freesurfer, transfer
National Category
Neurosciences Sport and Fitness Sciences Psychology (excluding Applied Psychology)
Identifiers
urn:nbn:se:umu:diva-130526 (URN)10.3389/fnagi.2016.00336 (DOI)000392049000001 ()
Funder
Swedish Research Council, 2012- 00530
Available from: 2017-01-22 Created: 2017-01-22 Last updated: 2018-06-09Bibliographically approved
Gorbach, T., Pudas, S., Lundquist, A., Orädd, G., Josefsson, M., Salami, A., . . . Nyberg, L. (2017). Longitudinal association between hippocampus atrophy and episodic-memory decline. Neurobiology of Aging, 51, 167-176
Open this publication in new window or tab >>Longitudinal association between hippocampus atrophy and episodic-memory decline
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2017 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 51, p. 167-176Article in journal (Refereed) Published
Abstract [en]

There is marked variability in both onset and rate of episodic-memory decline in aging. Structural magnetic resonance imaging studies have revealed that the extent of age-related brain changes varies markedly across individuals. Past studies of whether regional atrophy accounts for episodic-memory decline in aging have yielded inconclusive findings. Here we related 15-year changes in episodic memory to 4-year changes in cortical and subcortical gray matter volume and in white-matter connectivity and lesions. In addition, changes in word fluency, fluid IQ (Block Design), and processing speed were estimated and related to structural brain changes. Significant negative change over time was observed for all cognitive and brain measures. A robust brain-cognition change-change association was observed for episodic-memory decline and atrophy in the hippocampus. This association was significant for older (65-80 years) but not middle-aged (55-60 years) participants and not sensitive to the assumption of ignorable attrition. Thus, these longitudinal findings highlight medial-temporal lobe system integrity as particularly crucial for maintaining episodic-memory functioning in older age. 

Keywords
Aging, cognitive decline, episodic memory, hippocampus, longitudinal changes, non-ignorable attrition
National Category
Probability Theory and Statistics Neurosciences
Identifiers
urn:nbn:se:umu:diva-128725 (URN)10.1016/j.neurobiolaging.2016.12.002 (DOI)000397168600018 ()28089351 (PubMedID)
Funder
Swedish Research CouncilKnut and Alice Wallenberg FoundationRagnar Söderbergs stiftelse
Available from: 2016-12-15 Created: 2016-12-13 Last updated: 2019-01-25Bibliographically approved
Projects
Methods for non-ignorable missingness in longitudinal brain imaging studies. [P16-0628:1_RJ]; Umeå University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-1524-0851

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