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5. Individual differences in brain aging: heterogeneity in cortico-hippocampal but not caudate atrophy rates.

Author

Nyberg, L., Andersson, M., Lundquist, A., Baaré, W.F.C., Bartrés-Faz, D., Bertram, L., Boraxbekk, C.J., Brandmaier, A.M., Demnitz, N., Drevon, C.A., Duezel, S., Ebmeier, K.P., Ghisletta, P., Henson, R., Jensen, D.E.A., Kievit, R.A., Knights, E., Kühn, S., Lindenberger, U., Plachti, A., Pudas, S., Roe, J.M., Madsen, K.S., Solé-Padullés, C., Sommerer, Y., Suri, S., Zsoldos, E., Fjell, A.M., Walhovd, K.B., Nyberg, L., Andersson, M., Lundquist, A., Baaré, W.F.C., Bartrés-Faz, D., Bertram, L., Boraxbekk, C.J., Brandmaier, A.M., Demnitz, N., Drevon, C.A., Duezel, S., Ebmeier, K.P., Ghisletta, P., Henson, R., Jensen, D.E.A., Kievit, R.A., Knights, E., Kühn, S., Lindenberger, U., Plachti, A., Pudas, S., Roe, J.M., Madsen, K.S., Solé-Padullés, C., Sommerer, Y., Suri, S., Zsoldos, E., Fjell, A.M., and Walhovd, K.B.

Abstract

Item does not contain fulltext, It is well documented that some brain regions, such as association cortices, caudate, and hippocampus, are particularly prone to age-related atrophy, but it has been hypothesized that there are individual differences in atrophy profiles. Here, we document heterogeneity in regional-atrophy patterns using latent-profile analysis of 1,482 longitudinal magnetic resonance imaging observations. The results supported a 2-group solution reflecting differences in atrophy rates in cortical regions and hippocampus along with comparable caudate atrophy. The higher-atrophy group had the most marked atrophy in hippocampus and also lower episodic memory, and their normal caudate atrophy rate was accompanied by larger baseline volumes. Our findings support and refine models of heterogeneity in brain aging and suggest distinct mechanisms of atrophy in striatal versus hippocampal-cortical systems.

Published
2023

7. Lifestyle-related risk factors and their cumulative associations with hippocampal and total grey matter volume across the adult lifespan: a pooled analysis in the European Lifebrain consortium

Author

Binnewies, J, Nawijn, L, Brandmaier, AM, Baaré, WFC, Boraxbekk, C-J, Demnitz, N, Drevon, CA, Fjell, AM, Lindenberger, U, Madsen, KS, Nyberg, L, Topiwala, A, Walhovd, KB, Ebmeier, KP, and Penninx, BWJH

Abstract

Background: Lifestyle-related risk factors, such as obesity, physical inactivity, short sleep, smoking and alcohol use, have been associated with low hippocampal and total grey matter volumes (GMV). However, these risk factors have mostly been assessed as separate factors, leaving it unknown if variance explained by these factors is overlapping or additive. We investigated associations of five lifestyle-related factors separately and cumulatively with hippocampal and total GMV, pooled across eight European cohorts. Methods: We included 3838 participants aged 18-90 years from eight cohorts of the European Lifebrain consortium. Using individual person data, we performed cross-sectional meta-analyses on associations of presence of lifestyle-related risk factors separately (overweight/obesity, physical inactivity, short sleep, smoking, high alcohol use) as well as a cumulative unhealthy lifestyle score (counting the number of present lifestyle-related risk factors) with FreeSurfer-derived hippocampal volume and total GMV. Lifestyle-related risk factors were defined according to public health guidelines. Results: High alcohol use was associated with lower hippocampal volume (r=-0.10, p=0.021), and overweight/obesity with lower total GMV (r=-0.09, p=0.001). Other lifestyle-related risk factors were not significantly associated with hippocampal volume or GMV. The cumulative unhealthy lifestyle score was negatively associated with total GMV (r=-0.08, p=0.001), but not hippocampal volume (r=-0.01, p=0.625). Conclusions: This large pooled study confirmed the negative association of some lifestyle- related risk factors with hippocampal volume and GMV, although with small effect sizes. Lifestyle factors should not be seen in isolation as there is evidence that having multiple unhealthy lifestyle factors is associated with a linear reduction in overall brain volume.

Published
2023

8. Lifestyle-related risk factors and their cumulative associations with hippocampal and total grey matter volume across the adult lifespan : a pooled analysis in the European Lifebrain consortium

Author

Binnewies, J., Nawijn, L., Brandmaier, A., https://orcid.org/0000-0001-8765-6982, Baaré, W., Boraxbekk, C., Demnitz, N., Drevon, C., Fjell, A., Lindenberger, U., https://orcid.org/0000-0001-8428-6453, Skak Madsen, K., Nyberg, L., Topiwala, A., Walhovd, K., Ebmeier, K., and Penninx, B.

Subjects
Physical activity, Smoking, Brain structure, Neurosciences, Obesity, Alcohol, Sleep, Neurovetenskaper
Abstract

Background: Lifestyle-related risk factors, such as obesity, physical inactivity, short sleep, smoking and alcohol use, have been associated with low hippocampal and total grey matter volumes (GMV). However, these risk factors have mostly been assessed as separate factors, leaving it unknown if variance explained by these factors is overlapping or additive. We investigated associations of five lifestyle-related factors separately and cumulatively with hippocampal and total GMV, pooled across eight European cohorts. Methods: We included 3838 participants aged 18–90 years from eight cohorts of the European Lifebrain consortium. Using individual person data, we performed cross-sectional meta-analyses on associations of presence of lifestyle-related risk factors separately (overweight/obesity, physical inactivity, short sleep, smoking, high alcohol use) as well as a cumulative unhealthy lifestyle score (counting the number of present lifestyle-related risk factors) with FreeSurfer-derived hippocampal volume and total GMV. Lifestyle-related risk factors were defined according to public health guidelines. Results: High alcohol use was associated with lower hippocampal volume (r = −0.10, p = 0.021), and overweight/obesity with lower total GMV (r = −0.09, p = 0.001). Other lifestyle-related risk factors were not significantly associated with hippocampal volume or GMV. The cumulative unhealthy lifestyle score was negatively associated with total GMV (r = −0.08, p = 0.001), but not hippocampal volume (r = −0.01, p = 0.625). Conclusions: This large pooled study confirmed the negative association of some lifestyle-related risk factors with hippocampal volume and GMV, although with small effect sizes. Lifestyle factors should not be seen in isolation as there is evidence that having multiple unhealthy lifestyle factors is associated with a linear reduction in overall brain volume.

Published
2023

9. Education and Income Show Heterogeneous Relationships to Lifespan Brain and Cognitive Differences Across European and US Cohorts

Author

Walhovd, K.B., Fjell, A.M., Wang, Y., Amlien, I.K., Mowinckel, A.M., Lindenberger, U., Düzel, S., Bartrés-Faz, D., Ebmeier, K.P., Drevon, C.A., Baaré, W.F.C., Ghisletta, P., Johansen, L.B., Kievit, R.A., Henson, R.N.A., Madsen, K.S., Nyberg, L., Harris, J.R., Solé-Padullés, C., Pudas, S., Sørensen, Ø., Westerhausen, R., Zsoldos, E., Nawijn, L., Lyngstad, T.H., Suri, S., Penninx, B., Rogeberg, O.J., Brandmaier, A.M., Walhovd, K.B., Fjell, A.M., Wang, Y., Amlien, I.K., Mowinckel, A.M., Lindenberger, U., Düzel, S., Bartrés-Faz, D., Ebmeier, K.P., Drevon, C.A., Baaré, W.F.C., Ghisletta, P., Johansen, L.B., Kievit, R.A., Henson, R.N.A., Madsen, K.S., Nyberg, L., Harris, J.R., Solé-Padullés, C., Pudas, S., Sørensen, Ø., Westerhausen, R., Zsoldos, E., Nawijn, L., Lyngstad, T.H., Suri, S., Penninx, B., Rogeberg, O.J., and Brandmaier, A.M.

Abstract

Item does not contain fulltext, Higher socio-economic status (SES) has been proposed to have facilitating and protective effects on brain and cognition. We ask whether relationships between SES, brain volumes and cognitive ability differ across cohorts, by age and national origin. European and US cohorts covering the lifespan were studied (4-97 years, N = 500 000; 54 000 w/brain imaging). There was substantial heterogeneity across cohorts for all associations. Education was positively related to intracranial (ICV) and total gray matter (GM) volume. Income was related to ICV, but not GM. We did not observe reliable differences in associations as a function of age. SES was more strongly related to brain and cognition in US than European cohorts. Sample representativity varies, and this study cannot identify mechanisms underlying differences in associations across cohorts. Differences in neuroanatomical volumes partially explained SES-cognition relationships. SES was more strongly related to ICV than to GM, implying that SES-cognition relations in adulthood are less likely grounded in neuroprotective effects on GM volume in aging. The relatively stronger SES-ICV associations rather are compatible with SES-brain volume relationships being established early in life, as ICV stabilizes in childhood. The findings underscore that SES has no uniform association with, or impact on, brain and cognition.

Published
2022

10. Author Correction: Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer’s disease (Nature Communications, (2021), 12, 1, (721), 10.1038/s41467-021-21057-y)

Author

Roe, JM, Vidal-Piñeiro, D, Sørensen, Ø, Brandmaier, AM, Düzel, S, Gonzalez, HA, Kievit, RA, Knights, E, Kühn, S, Lindenberger, U, Mowinckel, AM, Nyberg, L, Park, DC, Pudas, S, Rundle, MM, Walhovd, KB, Fjell, AM, Westerhausen, R, Masters, CL, Bush, AI, Fowler, C, Darby, D, Pertile, K, Restrepo, C, Roberts, B, Robertson, J, Rumble, R, Ryan, T, Collins, S, Thai, C, Trounson, B, Lennon, K, Li, QX, Ugarte, FY, Volitakis, I, Vovos, M, Williams, R, Baker, J, Russell, A, Peretti, M, Milicic, L, Lim, L, Rodrigues, M, Taddei, K, Taddei, T, Hone, E, Lim, F, Fernandez, S, Rainey-Smith, S, Pedrini, S, Martins, R, Doecke, J, Bourgeat, P, Fripp, J, Gibson, S, Leroux, H, Hanson, D, Dore, V, Zhang, P, Burnham, S, Rowe, CC, Villemagne, VL, Yates, P, Pejoska, SB, Jones, G, Ames, D, Cyarto, E, Lautenschlager, N, Barnham, K, Cheng, L, Hill, A, Killeen, N, Maruff, P, Silbert, B, Brown, B, Sohrabi, H, Savage, G, Vacher, M, Roe, JM, Vidal-Piñeiro, D, Sørensen, Ø, Brandmaier, AM, Düzel, S, Gonzalez, HA, Kievit, RA, Knights, E, Kühn, S, Lindenberger, U, Mowinckel, AM, Nyberg, L, Park, DC, Pudas, S, Rundle, MM, Walhovd, KB, Fjell, AM, Westerhausen, R, Masters, CL, Bush, AI, Fowler, C, Darby, D, Pertile, K, Restrepo, C, Roberts, B, Robertson, J, Rumble, R, Ryan, T, Collins, S, Thai, C, Trounson, B, Lennon, K, Li, QX, Ugarte, FY, Volitakis, I, Vovos, M, Williams, R, Baker, J, Russell, A, Peretti, M, Milicic, L, Lim, L, Rodrigues, M, Taddei, K, Taddei, T, Hone, E, Lim, F, Fernandez, S, Rainey-Smith, S, Pedrini, S, Martins, R, Doecke, J, Bourgeat, P, Fripp, J, Gibson, S, Leroux, H, Hanson, D, Dore, V, Zhang, P, Burnham, S, Rowe, CC, Villemagne, VL, Yates, P, Pejoska, SB, Jones, G, Ames, D, Cyarto, E, Lautenschlager, N, Barnham, K, Cheng, L, Hill, A, Killeen, N, Maruff, P, Silbert, B, Brown, B, Sohrabi, H, Savage, G, and Vacher, M

Abstract

In this article the affiliation details for Ulman Lindenberger were incorrectly given as ‘Department of Psychiatry and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany’ but should have been ‘Center for Lifespan Psychology, Max Planck Institute for Human Development, Berlin, Germany’, ‘Max Planck UCL Centre for Computational Psychiatry and Ageing Research, Berlin, Germany’. The original article has been corrected.

Published
2022

11. Associations of depression and regional brain structure across the adult lifespan: Pooled analyses of six population-based and two clinical cohort studies in the European Lifebrain consortium

Author

Binnewies, J, Nawijn, L, Brandmaier, AM, Baare, WFC, Bartres-Faz, D, Drevon, CA, Duezel, S, Fjell, AM, Han, LKM, Knights, E, Lindenberger, U, Milaneschi, Y, Mowinckel, AM, Nyberg, L, Plachti, A, Madsen, KS, Sole-Padulles, C, Suri, S, Walhovd, KB, Zsoldos, E, Ebmeier, KP, Penninx, BWJH, Binnewies, J, Nawijn, L, Brandmaier, AM, Baare, WFC, Bartres-Faz, D, Drevon, CA, Duezel, S, Fjell, AM, Han, LKM, Knights, E, Lindenberger, U, Milaneschi, Y, Mowinckel, AM, Nyberg, L, Plachti, A, Madsen, KS, Sole-Padulles, C, Suri, S, Walhovd, KB, Zsoldos, E, Ebmeier, KP, and Penninx, BWJH

Abstract

OBJECTIVE: Major depressive disorder has been associated with lower prefrontal thickness and hippocampal volume, but it is unknown whether this association also holds for depressive symptoms in the general population. We investigated associations of depressive symptoms and depression status with brain structures across population-based and patient-control cohorts, and explored whether these associations are similar over the lifespan and across sexes. METHODS: We included 3,447 participants aged 18-89 years from six population-based and two clinical patient-control cohorts of the European Lifebrain consortium. Cross-sectional meta-analyses using individual person data were performed for associations of depressive symptoms and depression status with FreeSurfer-derived thickness of bilateral rostral anterior cingulate cortex (rACC) and medial orbitofrontal cortex (mOFC), and hippocampal and total grey matter volume (GMV), separately for population-based and clinical cohorts. RESULTS: Across patient-control cohorts, depressive symptoms and presence of mild-to-severe depression were associated with lower mOFC thickness (rsymptoms = -0.15/ rstatus = -0.22), rACC thickness (rsymptoms = -0.20/ rstatus = -0.25), hippocampal volume (rsymptoms = -0.13/ rstatus = 0.13) and total GMV (rsymptoms = -0.21/ rstatus = -0.25). Effect sizes were slightly larger for presence of moderate-to-severe depression. Associations were similar across age groups and sex. Across population-based cohorts, no associations between depression and brain structures were observed. CONCLUSIONS: Fitting with previous meta-analyses, depressive symptoms and depression status were associated with lower mOFC, rACC thickness, and hippocampal and total grey matter volume in clinical patient-control cohorts, although effect sizes were small. The absence of consistent associations in population-based cohorts with mostly mild depressive symptoms, suggests that significantly lower thickness and volume of the studied

Published
2022

14. Genetic contributions to variation in general cognitive function: a meta-analysis of genome-wide association studies in the CHARGE consortium (N=53 949)

Author

Davies, G, Armstrong, N, Bis, J C, Bressler, J, Chouraki, V, Giddaluru, S, Hofer, E, Ibrahim-Verbaas, C A, Kirin, M, Lahti, J, van der Lee, S J, Le Hellard, S, Liu, T, Marioni, R E, Oldmeadow, C, Postmus, I, Smith, A V, Smith, J A, Thalamuthu, A, Thomson, R, Vitart, V, Wang, J, Yu, L, Zgaga, L, Zhao, W, Boxall, R, Harris, S E, Hill, W D, Liewald, D C, Luciano, M, Adams, H, Ames, D, Amin, N, Amouyel, P, Assareh, A A, Au, R, Becker, J T, Beiser, A, Berr, C, Bertram, L, Boerwinkle, E, Buckley, B M, Campbell, H, Corley, J, De Jager, P L, Dufouil, C, Eriksson, J G, Espeseth, T, Faul, J D, Ford, I, Scotland, Generation, Gottesman, R F, Griswold, M E, Gudnason, V, Harris, T B, Heiss, G, Hofman, A, Holliday, E G, Huffman, J, Kardia, S L R, Kochan, N, Knopman, D S, Kwok, J B, Lambert, J-C, Lee, T, Li, G, Li, S-C, Loitfelder, M, Lopez, O L, Lundervold, A J, Lundqvist, A, Mather, K A, Mirza, S S, Nyberg, L, Oostra, B A, Palotie, A, Papenberg, G, Pattie, A, Petrovic, K, Polasek, O, Psaty, B M, Redmond, P, Reppermund, S, Rotter, J I, Schmidt, H, Schuur, M, Schofield, P W, Scott, R J, Steen, V M, Stott, D J, van Swieten, J C, Taylor, K D, Trollor, J, Trompet, S, Uitterlinden, A G, Weinstein, G, Widen, E, Windham, B G, Jukema, J W, Wright, A F, Wright, M J, Yang, Q, Amieva, H, Attia, J R, Bennett, D A, Brodaty, H, de Craen, A J M, Hayward, C, Ikram, M A, Lindenberger, U, Nilsson, L-G, Porteous, D J, Räikkönen, K, Reinvang, I, Rudan, I, Sachdev, P S, Schmidt, R, Schofield, P R, Srikanth, V, Starr, J M, Turner, S T, Weir, D R, Wilson, J F, van Duijn, C, Launer, L, Fitzpatrick, A L, Seshadri, S, Mosley, Jr, T H, and Deary, I J

Published
2015
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17. Genetic contributions to variation in general cognitive function: a meta-analysis of genome-wide association studies in the CHARGE consortium (N = 53 949)

Author

Davies, G, Armstrong, N, Bis, J C, Bressler, J, Chouraki, V, Giddaluru, S, Hofer, E, Ibrahim-Verbaas, C A, Kirin, M, Lahti, J, van der Lee, S J, Le Hellard, S, Liu, T, Marioni, R E, Oldmeadow, C, Postmus, I, Smith, A V, Smith, J A, Thalamuthu, A, Thomson, R, Vitart, V, Wang, J, Yu, L, Zgaga, L, Zhao, W, Boxall, R, Harris, S E, Hill, W D, Liewald, D C, Luciano, M, Adams, H, Ames, D, Amin, N, Amouyel, P, Assareh, A A, Au, R, Becker, J T, Beiser, A, Berr, C, Bertram, L, Boerwinkle, E, Buckley, B M, Campbell, H, Corley, J, De Jager, P L, Dufouil, C, Eriksson, J G, Espeseth, T, Faul, J D, Ford, I, Scotland, Generation, Gottesman, R F, Griswold, M E, Gudnason, V, Harris, T B, Heiss, G, Hofman, A, Holliday, E G, Huffman, J, Kardia, S LR, Kochan, N, Knopman, D S, Kwok, J B, Lambert, J-C, Lee, T, Li, G, Li, S-C, Loitfelder, M, Lopez, O L, Lundervold, A J, Lundqvist, A, Mather, K A, Mirza, S S, Nyberg, L, Oostra, B A, Palotie, A, Papenberg, G, Pattie, A, Petrovic, K, Polasek, O, Psaty, B M, Redmond, P, Reppermund, S, Rotter, J I, Schmidt, H, Schuur, M, Schofield, P W, Scott, R J, Steen, V M, Stott, D J, van Swieten, J C, Taylor, K D, Trollor, J, Trompet, S, Uitterlinden, A G, Weinstein, G, Widen, E, Windham, B G, Jukema, J W, Wright, A F, Wright, M J, Yang, Q, Amieva, H, Attia, J R, Bennett, D A, Brodaty, H, de Craen, A JM, Hayward, C, Ikram, M A, Lindenberger, U, Nilsson, L-G, Porteous, D J, Räikkönen, K, Reinvang, I, Rudan, I, Sachdev, P S, Schmidt, R, Schofield, P R, Srikanth, V, Starr, J M, Turner, S T, Weir, D R, Wilson, J F, van Duijn, C, Launer, L, Fitzpatrick, A L, Seshadri, S, Mosley, TH, Jr, and Deary, I J

Published
2015
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18. The genetic organization of longitudinal subcortical volumetric change is stable throughout the lifespan

Author

Fjell, A.M., Grydeland, H., Wang, Y., Amlien, I.K., Bartrés-Faz, D., Brandmaier, A.M., Düzel, S., Elman, J., Franz, C.E., Haberg, A.K., Kietzmann, T.C., Kievit, R., Kremen, W.S., Krogsrud, S.K., Kühn, S., Lindenberger, U., Macià, D., Mowinckel, A.M., Nyberg, L., Panizzon, M.S., Solé-Padullés, C., Sorensen, O., Westerhausen, R., Walhovd, K.B., Fjell, A.M., Grydeland, H., Wang, Y., Amlien, I.K., Bartrés-Faz, D., Brandmaier, A.M., Düzel, S., Elman, J., Franz, C.E., Haberg, A.K., Kietzmann, T.C., Kievit, R., Kremen, W.S., Krogsrud, S.K., Kühn, S., Lindenberger, U., Macià, D., Mowinckel, A.M., Nyberg, L., Panizzon, M.S., Solé-Padullés, C., Sorensen, O., Westerhausen, R., and Walhovd, K.B.

Abstract

Contains fulltext : 235500.pdf (Publisher’s version ) (Open Access), Development and aging of the cerebral cortex show similar topographic organization and are governed by the same genes. It is unclear whether the same is true for subcortical regions, which follow fundamentally different ontogenetic and phylogenetic principles. We tested the hypothesis that genetically governed neurodevelopmental processes can be traced throughout life by assessing to which degree brain regions that develop together continue to change together through life. Analyzing over 6000 longitudinal MRIs of the brain, we used graph theory to identify five clusters of coordinated development, indexed as patterns of correlated volumetric change in brain structures. The clusters tended to follow placement along the cranial axis in embryonic brain development, suggesting continuity from prenatal stages, and correlated with cognition. Across independent longitudinal datasets, we demonstrated that developmental clusters were conserved through life. Twin-based genetic correlations revealed distinct sets of genes governing change in each cluster. Single-nucleotide polymorphisms-based analyses of 38,127 cross-sectional MRIs showed a similar pattern of genetic volume-volume correlations. In conclusion, coordination of subcortical change adheres to fundamental principles of lifespan continuity and genetic organization.

Published
2021

19. Educational attainment does not influence brain aging

Author

Nyberg, L., Magnussen, F., Lundquist, A., Baaré, W., Bartrés-Faz, D., Bertram, L., Boraxbekk, C.J., Brandmaier, A.M., Drevon, C.A., Ebmeier, K., Ghisletta, P., Henson, R.N., Junqué, C., Kievit, R., Kleemeyer, M., Knights, E., Kühn, S., Lindenberger, U., Penninx, B., Pudas, S., Sørensen, Ø., Vaqué-Alcázar, L., Walhovd, K.B., Fjell, A.M., Nyberg, L., Magnussen, F., Lundquist, A., Baaré, W., Bartrés-Faz, D., Bertram, L., Boraxbekk, C.J., Brandmaier, A.M., Drevon, C.A., Ebmeier, K., Ghisletta, P., Henson, R.N., Junqué, C., Kievit, R., Kleemeyer, M., Knights, E., Kühn, S., Lindenberger, U., Penninx, B., Pudas, S., Sørensen, Ø., Vaqué-Alcázar, L., Walhovd, K.B., and Fjell, A.M.

Abstract

Item does not contain fulltext, Education has been related to various advantageous lifetime outcomes. Here, using longitudinal structural MRI data (4,422 observations), we tested the influential hypothesis that higher education translates into slower rates of brain aging. Cross-sectionally, education was modestly associated with regional cortical volume. However, despite marked mean atrophy in the cortex and hippocampus, education did not influence rates of change. The results were replicated across two independent samples. Our findings challenge the view that higher education slows brain aging.

Published
2021

20. Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer’s disease

Author

Roe, J.M., Vidal-Piñeiro, D., Sørensen, Ø., Brandmaier, A.M., Düzel, S., Gonzalez, H.A., Kievit, R.A., Knights, E., Kühn, S., Lindenberger, U., Mowinckel, A.M., Nyberg, L., Park, D.C., Pudas, S., Rundle, M.M., Walhovd, K.B., Fjell, A.M., Westerhausen, R., Brown, B., Roe, J.M., Vidal-Piñeiro, D., Sørensen, Ø., Brandmaier, A.M., Düzel, S., Gonzalez, H.A., Kievit, R.A., Knights, E., Kühn, S., Lindenberger, U., Mowinckel, A.M., Nyberg, L., Park, D.C., Pudas, S., Rundle, M.M., Walhovd, K.B., Fjell, A.M., Westerhausen, R., and Brown, B.

Abstract

Aging and Alzheimer’s disease (AD) are associated with progressive brain disorganization. Although structural asymmetry is an organizing feature of the cerebral cortex it is unknown whether continuous age- and AD-related cortical degradation alters cortical asymmetry. Here, in multiple longitudinal adult lifespan cohorts we show that higher-order cortical regions exhibiting pronounced asymmetry at age ~20 also show progressive asymmetry-loss across the adult lifespan. Hence, accelerated thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This organizational principle showed high consistency across cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics of asymmetry-loss were markedly similar across replicating samples. Asymmetry-change was further accelerated in AD. Results suggest a system-wide dedifferentiation of the adaptive asymmetric organization of heteromodal cortex in aging and AD.

Published
2021

21. Poor self-reported sleep is related to regional cortical thinning in aging but not memory decline: Results from the Lifebrain Consortium

Author

Fjell, A.M., Sorensen, O., Amlien, I.K., Bartrés-Faz, D., Brandmaier, A.M., Buchmann, N., Demuth, I., Drevon, C.A., Düzel, S., Ebmeier, K.P., Ghisletta, P., Idland, A.V., Kietzmann, T.C., Kievit, R., Kühn, S., Lindenberger, U., Magnussen, F., Macià, D., Mowinckel, A.M., Nyberg, L., Sexton, C.E., Solé-Padullés, C., Pudas, S., Roe, J.M., Sederevicius, D., Suri, S., Vidal-Piñeiro, D., Wagner, G., Watne, L.O., Westerhausen, R., Zsoldos, E., Walhovd, K.B., Fjell, A.M., Sorensen, O., Amlien, I.K., Bartrés-Faz, D., Brandmaier, A.M., Buchmann, N., Demuth, I., Drevon, C.A., Düzel, S., Ebmeier, K.P., Ghisletta, P., Idland, A.V., Kietzmann, T.C., Kievit, R., Kühn, S., Lindenberger, U., Magnussen, F., Macià, D., Mowinckel, A.M., Nyberg, L., Sexton, C.E., Solé-Padullés, C., Pudas, S., Roe, J.M., Sederevicius, D., Suri, S., Vidal-Piñeiro, D., Wagner, G., Watne, L.O., Westerhausen, R., Zsoldos, E., and Walhovd, K.B.

Abstract

Contains fulltext : 228447.pdf (Publisher’s version ) (Open Access), We examined whether sleep quality and quantity are associated with cortical and memory changes in cognitively healthy participants across the adult lifespan. Associations between self-reported sleep parameters (Pittsburgh Sleep Quality Index, PSQI) and longitudinal cortical change were tested using five samples from the Lifebrain consortium (n = 2205, 4363 MRIs, 18-92 years). In additional analyses, we tested coherence with cell-specific gene expression maps from the Allen Human Brain Atlas, and relations to changes in memory performance. "PSQI # 1 Subjective sleep quality" and "PSQI #5 Sleep disturbances" were related to thinning of the right lateral temporal cortex, with lower quality and more disturbances being associated with faster thinning. The association with "PSQI #5 Sleep disturbances" emerged after 60 years, especially in regions with high expression of genes related to oligodendrocytes and S1 pyramidal neurons. None of the sleep scales were related to a longitudinal change in episodic memory function, suggesting that sleep-related cortical changes were independent of cognitive decline. The relationship to cortical brain change suggests that self-reported sleep parameters are relevant in lifespan studies, but small effect sizes indicate that self-reported sleep is not a good biomarker of general cortical degeneration in healthy older adults.

Published
2021

22. Individual variations in 'brain age' relate to early-life factors more than to longitudinal brain change

Author

Vidal-Pineiro, D, Wang, Y, Krogsrud, SK, Amlien, IK, Baare, WF, Bartres-Faz, D, Bertram, L, Brandmaier, AM, Drevon, CA, Duezel, S, Ebmeier, K, Henson, RN, Junque, C, Kievit, RA, Kuehn, S, Leonardsen, E, Lindenberger, U, Madsen, KS, Magnussen, F, Mowinckel, AM, Nyberg, L, Roe, JM, Segura, B, Smith, SM, Sorensen, O, Suri, S, Westerhausen, R, Zalesky, A, Zsoldos, E, Walhovd, KB, Fjell, A, Vidal-Pineiro, D, Wang, Y, Krogsrud, SK, Amlien, IK, Baare, WF, Bartres-Faz, D, Bertram, L, Brandmaier, AM, Drevon, CA, Duezel, S, Ebmeier, K, Henson, RN, Junque, C, Kievit, RA, Kuehn, S, Leonardsen, E, Lindenberger, U, Madsen, KS, Magnussen, F, Mowinckel, AM, Nyberg, L, Roe, JM, Segura, B, Smith, SM, Sorensen, O, Suri, S, Westerhausen, R, Zalesky, A, Zsoldos, E, Walhovd, KB, and Fjell, A

Abstract

Brain age is a widely used index for quantifying individuals' brain health as deviation from a normative brain aging trajectory. Higher-than-expected brain age is thought partially to reflect above-average rate of brain aging. Here, we explicitly tested this assumption in two independent large test datasets (UK Biobank [main] and Lifebrain [replication]; longitudinal observations ≈ 2750 and 4200) by assessing the relationship between cross-sectional and longitudinal estimates of brain age. Brain age models were estimated in two different training datasets (n ≈ 38,000 [main] and 1800 individuals [replication]) based on brain structural features. The results showed no association between cross-sectional brain age and the rate of brain change measured longitudinally. Rather, brain age in adulthood was associated with the congenital factors of birth weight and polygenic scores of brain age, assumed to reflect a constant, lifelong influence on brain structure from early life. The results call for nuanced interpretations of cross-sectional indices of the aging brain and question their validity as markers of ongoing within-person changes of the aging brain. Longitudinal imaging data should be preferred whenever the goal is to understand individual change trajectories of brain and cognition in aging.

Published
2021

23. Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer's disease

Author

Roe, JM, Vidal-Pineiro, D, Sorensen, O, Brandmaier, AM, Duzel, S, Gonzalez, HA, Kievit, RA, Knights, E, Kuhn, S, Lindenberger, U, Mowinckel, AM, Nyberg, L, Park, DC, Pudas, S, Rundle, MM, Walhovd, KB, Fjell, AM, Westerhausen, R, Roe, JM, Vidal-Pineiro, D, Sorensen, O, Brandmaier, AM, Duzel, S, Gonzalez, HA, Kievit, RA, Knights, E, Kuhn, S, Lindenberger, U, Mowinckel, AM, Nyberg, L, Park, DC, Pudas, S, Rundle, MM, Walhovd, KB, Fjell, AM, and Westerhausen, R

Abstract

Aging and Alzheimer's disease (AD) are associated with progressive brain disorganization. Although structural asymmetry is an organizing feature of the cerebral cortex it is unknown whether continuous age- and AD-related cortical degradation alters cortical asymmetry. Here, in multiple longitudinal adult lifespan cohorts we show that higher-order cortical regions exhibiting pronounced asymmetry at age ~20 also show progressive asymmetry-loss across the adult lifespan. Hence, accelerated thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This organizational principle showed high consistency across cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics of asymmetry-loss were markedly similar across replicating samples. Asymmetry-change was further accelerated in AD. Results suggest a system-wide dedifferentiation of the adaptive asymmetric organization of heteromodal cortex in aging and AD.

Published
2021

24. Self-reported sleep relates to microstructural hippocampal decline in β-amyloid positive adults beyond genetic risk

Author

Grydeland, H, Sederevičius, D, Wang, Y, Bartrés-Faz, D, Bertram, L, Dobricic, V, Düzel, S, Ebmeier, KP, Idland, I-V, Kietzmann, TC, Kievit, R, Kühn, S, Lindenberger, U, Mowinckel, AM, Nyberg, L, Price, D, Sexton, CE, Solé-Padullés, C, Sørensen, Ø, Walhovd, KB, and Fjell, AM

Subjects
Neurologi, hippocampus, Hippocampus, Disease, Neuropsychological Tests, Audiology, Hippocampal formation, Pittsburgh Sleep Quality Index, memory, 0302 clinical medicine, β amyloid, Genetic risk, Aged, 80 and over, 0303 health sciences, AcademicSubjects/SCI01870, β-amyloid, beta-amyloid, Brain, Middle Aged, Alzheimer's disease, Sleep in non-human animals, Diffusion Tensor Imaging, Neurology, mean diffusivity, Alzheimer’s disease, lifespan, Neurovetenskaper, AcademicSubjects/MED00370, Adult, medicine.medical_specialty, longitudinal, Neurological Disorders, Young Adult, 03 medical and health sciences, Alzheimer Disease, Physiology (medical), medicine, Humans, AcademicSubjects/MED00385, sleep, Aged, 030304 developmental biology, Amyloid beta-Peptides, Sleep quality, business.industry, aging, Neurosciences, Positron-Emission Tomography, Self Report, Neurology (clinical), business, 030217 neurology & neurosurgery
Abstract

Study Objectives A critical role linking sleep with memory decay and β-amyloid (Aβ) accumulation, two markers of Alzheimer’s disease (AD) pathology, may be played by hippocampal integrity. We tested the hypotheses that worse self-reported sleep relates to decline in memory and intra-hippocampal microstructure, including in the presence of Aβ. Methods Two-hundred and forty-three cognitively healthy participants, aged 19–81 years, completed the Pittsburgh Sleep Quality Index once, and two diffusion tensor imaging sessions, on average 3 years apart, allowing measures of decline in intra-hippocampal microstructure as indexed by increased mean diffusivity. We measured memory decay at each imaging session using verbal delayed recall. One session of positron emission tomography, in 108 participants above 44 years of age, yielded 23 Aβ positive. Genotyping enabled control for APOE ε4 status, and polygenic scores for sleep and AD, respectively. Results Worse global sleep quality and sleep efficiency related to more rapid reduction of hippocampal microstructure over time. Focusing on efficiency (the percentage of time in bed at night spent asleep), the relation was stronger in presence of Aβ accumulation, and hippocampal integrity decline mediated the relation with memory decay. The results were not explained by genetic risk for sleep efficiency or AD. Conclusions Worse sleep efficiency related to decline in hippocampal microstructure, especially in the presence of Aβ accumulation, and Aβ might link poor sleep and memory decay. As genetic risk did not account for the associations, poor sleep efficiency might constitute a risk marker for AD, although the driving causal mechanisms remain unknown.

Published
2021

28. Menschen überschätzen Risiko einer Covid-19-Erkrankung, berücksichtigen aber individuelle Risikofaktoren

Author

Hertwig, R., Liebig, S., Lindenberger, U., and Wagner, G.

Subjects
ddc:330
Abstract

Um mit der Corona-Pandemie möglichst angemessen umgehen zu können, ist es wichtig, dass die Menschen hierzulande eine realistische Vorstellung davon haben, wie hoch ihr individuelles Risiko einer Erkrankung ist. Wie aktuelle Analysen der SOEP-CoV-Studie nun zeigen, sind sich die meisten Menschen in Deutschland durchaus bewusst, dass Faktoren wie das Lebensalter, Vorerkrankungen und der Beruf einen starken Einfluss auf ihr individuelles Risiko haben, lebensbedrohlich an Covid-19 zu erkranken. Gleichzeitig wird das durchschnittliche Risiko dafür deutlich überschätzt. Dies könnte durchaus dazu beitragen, dass die Bevölkerung die derzeitigen Schutzmaßnahmen wie das Abstandhalten und das Tragen von Masken auch bei geringen Neuinfektionszahlen beibehält. Nichtsdestoweniger ist die Politik gefordert, den Informationsstand und die Risikomündigkeit der Bevölkerung weiter zu stärken.

Published
2020

30. Wie gefährlich ist COVID-19? Die subjektive Risikoeinschätzung einer lebensbedrohlichen COVID-19-Erkrankung im Frühjahr und Frühsommer 2020 in Deutschland

Author

Hertwig, R., Liebig, S., Lindenberger, U., and Wagner, G.

Subjects
D83, D84, I12, ddc:330, SOEP-CoV, COVID-19, Corona, Z18, subjective risk
Abstract

Um die Corona-Krise und die Wahrnehmung ihrer Risiken zu untersuchen, wird für die vorliegenden Ausführungen auf Informationen aus der Längsschnittstudie Sozio-oekonomisches Panel (SOEP) und der darin eingebetteten SOEP-CoV-Studie zurückgegriffen, bei der im Zeitraum vom 1. April bis 5. Juli 2020 wurde unter anderem die Frage gestellt wurde: "Für wie groß halten Sie die Wahrscheinlichkeit, dass das neue Corona-Virus bei Ihnen im Laufe der nächsten 12 Monate eine lebensbedrohliche Erkrankung auslöst?". Als Antwort konnten die Befragten Prozentangaben von null bis hundert machen. Die Angaben von 5.783 Befragten zeigen, dass sich die Befragten von dieser durchaus nicht einfach zu beantwortenden Frage nicht überfordert fühlen. Der Anteil derer, die keine Angabe machen, beträgt nur 2,3 Prozent. Die durchschnittliche subjektive Wahrscheinlichkeit für eine lebensbedrohliche COVID-19-Infektion wird mit 25,9 Prozent angegeben (gewichtetes Ergebnis). Diese subjektive Einschätzung steigt sowohl mit dem Alter wie auch mit einer - im Jahr 2019 selbst berichteten - Vorerkrankung an. Auch wer selbst getestet wurde oder in seinem Haushalt einen Test erlebt hat, gibt ein höheres Risiko für eine lebensbedrohende Erkrankung durch das neue Coronavirus. To investigate the coronavirus crisis and perceptions of risks associated with the virus, we analyzed data from the longitudinal Socio-Economic Panel (SOEP) study and the SOEP-CoV study, which is embedded in the SOEP. In the period from April 1 to July 5, 2020, the CoV-questionnaire included the item: "How likely do you think it is that the novel coronavirus will cause you to become critically ill in the next 12 months?" Respondents responded by estimating the likelihood on a scale from 0 to 100 percent. The apparent difficulty of this question did not pose an obstacle for most of the 5,783 respondents: Only 2.3 percent of all respondents gave no answer. The average subjective probability of a life-threatening COVID-19 infection amounted to 25.9 percent (weighted average). This subjective estimate increases both with age and with preexisting medical conditions (self-reported in 2019). Those who had been tested themselves or who lived in the same household as someone who had been tested estimated a higher risk of becoming critically ill as a result of the novel coronavirus.

Published
2020

34. Perception

Author

Nagel, I.E., primary, Werkle-Bergner, M., additional, Li, S.-C., additional, and Lindenberger, U., additional

Published
2007
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36. Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function (vol 9, 2098, 2018)

Author

Davies, G., Lam, M., Harris, S.E., Trampush, J.W., Luciano, M., Hill, W.D., Hagenaars, S.P., Ritchie, S.J., Marioni, R.E., Fawns-Ritchie, C., Liewald, D.C.M., Okely, J.A., Ahola-Olli, A.V., Barnes, C.L.K., Bertram, L., Bis, J.C., Burdick, K.E., Christoforou, A., DeRosse, P., Djurovic, S., Espeseth, T., Giakoumaki, S., Giddaluru, S., Gustavson, D.E., Hayward, C., Hofer, E., Ikram, M.A., Karlsson, R., Knowles, E., Lahti, J., Leber, M., Li, S., Mather, K.A., Melle, I., Morris, D., Oldmeadow, C., Palviainen, T., Payton, A., Pazoki, R., Petrovic, K., Reynolds, C.A., Sargurupremraj, M., Scholz, M., Smith, J.A., Smith, A.V., Terzikhan, N., Thalamuthu, A., Trompet, S., Lee, S.J. van der, Ware, E.B., Windham, B.G., Wright, M.J., Yang, J.Y., Yu, J., Ames, D., Amin, N., Amouyel, P., Andreassen, O.A., Armstrong, N.J., Assareh, A.A., Attia, J.R., Attix, D., Avramopoulos, D., Bennett, D.A., Bohmer, A.C., Boyle, P.A., Brodaty, H., Campbell, H., Cannon, T.D., Cirulli, E.T., Congdon, E., Conley, E.D., Corley, J., Cox, S.R., Dale, A.M., Dehghan, A., Dick, D., Dickinson, D., Eriksson, J.G., Evangelou, E., Faul, J.D., Ford, I., Freimer, N.A., Gao, H., Giegling, I., Gillespie, N.A., Gordon, S.D., Gottesman, R.F., Griswold, M.E., Gudnason, V., Harris, T.B., Hartmann, A.M., Hatzimanolis, A., Heiss, G., Holliday, E.G., Joshi, P.K., Kahonen, M., Kardia, S.L.R., Karlsson, I., Kleineidam, L., Knopman, D.S., Kochan, N.A., Konte, B., Kwok, J.B., Hellard, S. le, Lee, T., Lehtimaki, T., Li, S.C., Lill, C.M., Liu, T., Koini, M., London, E., Longstreth, W.T., Lopez, O.L., Loukola, A., Luck, T., Lundervold, A.J., Lundquist, A., Lyytikainen, L.P., Martin, N.G., Montgomery, G.W., Murray, A.D., Need, A.C., Noordam, R., Nyberg, L., Ollier, W., Papenberg, G., Pattie, A., Polasek, O., Poldrack, R.A., Psaty, B.M., Reppermund, S., Riedel-Heller, S.G., Rose, R.J., Rotter, J.I., Roussos, P., Rovio, S.P., Saba, Y., Sabb, F.W., Sachdev, P.S., Satizabal, C.L., Schmid, M., Scott, R.J., Scult, M.A., Simino, J., Slagboom, P.E., Smyrnis, N., Soumare, A., Stefanis, N.C., Stott, D.J., Straub, R.E., Sundet, K., Taylor, A.M., Taylor, K.D., Tzoulaki, I., Tzourio, C., Uitterlinden, A., Vitart, V., Voineskos, A.N., Kaprio, J., Wagner, M., Wagner, H., Weinhold, L., Wen, K.H., Widen, E., Yang, Q., Zhao, W., Adams, H.H.H., Arking, D.E., Bilder, R.M., Bitsios, P., Boerwinkle, E., Chiba-Falek, O., Corvin, A., Jager, P.L. de, Debette, S., Donohoe, G., Elliott, P., Fitzpatrick, A.L., Gill, M., Glahn, D.C., Hagg, S., Hansell, N.K., Hariri, A.R., Ikram, M.K., Jukema, J.W., Vuoksimaa, E., Keller, M.C., Kremen, W.S., Launer, L., Lindenberger, U., Palotie, A., Pedersen, N.L., Pendleton, N., Porteous, D.J., Raikkonen, K., Raitakari, O.T., Ramirez, A., Reinvang, I., Rudan, I., Rujescu, D., Schmidt, R., Schmidt, H., Schofield, P.W., Schofield, P.R., Starr, J.M., Steen, V.M., Trollor, J.N., Turner, S.T., Duijn, C.M. van, Villringer, A., Weinberger, D.R., Weir, D.R., Wilson, J.F., Malhotra, A., McIntosh, A.M., Gale, C.R., Seshadri, S., Mosley, T.H., Bressler, J., Lencz, T., and Deary, I.J.

Published
2019

37. Author Correction: Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function

Author

Davies, G., Lam, M., Harris, S. E., TRAMPUSH, J. W., LUCIANO, M., HILL, W. D., HAGENAARS, S. P., RITCHIE, S. J., MARIONI, R. E., FAWNS-RITCHIE, C., LIEWALD, D. C. M., OKELY, J. A., AHOLA-OLLI, A. V., BARNES, C. L. K., Bertram, L., BIS, J. C., BURDICK, K. E., CHRISTOFOROU, A., DEROSSE, P., Djurovic, S., ESPESETH, T., GIAKOUMAKI, S., GIDDALURU, S., GUSTAVSON, D. E., Hayward, C., Hofer, E., KARLSSON, R., KNOWLES, E., Lahti, J., Leber, M., MATHER, K. A., Melle, I., Morris, D., OLDMEADOW, C., PALVIAINEN, T., PAYTON, A., PAZOKI, R., PETROVIC, K., Reynolds, C. A., SARGURUPREMRAJ, M., Scholz, M., Smith, J. A., SMITH, A. V., TERZIKHAN, N., THALAMUTHU, A., TROMPET, S., VAN DER LEE, S. J., WARE, E. B., WINDHAM, B. G., WRIGHT, M. J., Yang, J., Yu, J., Ames, D., Amin, N., Amouyel, P., ANDREASSEN, O. A., ARMSTRONG, N. J., ASSAREH, A. A., ATTIA, J. R., ATTIX, D., AVRAMOPOULOS, D., BENNETT, D. A., BOHMER, A. C., BOYLE, P. A., BRODATY, H., Campbell, H., CANNON, T. D., CIRULLI, E. T., CONGDON, E., CONLEY, E. D., CORLEY, J., COX, S. R., DALE, A. M., DEHGHAN, A., Dick, D., Dickinson, D., ERIKSSON, J. G., EVANGELOU, E., FAUL, J. D., Ford, I., FREIMER, N. A., Gao, H., Giegling, I., GILLESPIE, N. A., GORDON, S. D., GOTTESMAN, R. F., GRISWOLD, M. E., GUDNASON, V., HARRIS, T. B., HARTMANN, A. M., Hatzimanolis, A., Heiss, G., HOLLIDAY, E. G., Joshi, P. K., KAHONEN, M., KARDIA, S. L. R., KARLSSON, I., KLEINEIDAM, L., KNOPMAN, D. S., KOCHAN, N. A., Konte, B., KWOK, J. B., LE HELLARD, S., Lee, T., LEHTIMAKI, T., Li, S. C., Lill, C. M., Liu, T., KOINI, M., London, E., LONGSTRETH, W. T., Jr., LOPEZ, O. L., LOUKOLA, A., LUCK, T., LUNDERVOLD, A. J., LUNDQUIST, A., LYYTIKAINEN, L. P., Martin, N. G., MONTGOMERY, G. W., MURRAY, A. D., NEED, A. C., NOORDAM, R., Nyberg, L., OLLIER, W., PAPENBERG, G., PATTIE, A., POLASEK, O., POLDRACK, R. A., PSATY, B. M., REPPERMUND, S., RIEDEL-HELLER, S. G., ROSE, R. J., ROTTER, J. I., ROUSSOS, P., ROVIO, S. P., SABA, Y., SABB, F. W., SACHDEV, P. S., SATIZABAL, C. L., Schmid, M., Scott, R. J., SCULT, M. A., SIMINO, J., SLAGBOOM, P. E., SMYRNIS, N., Soumare, A., Stefanis, N. C., STOTT, D. J., STRAUB, R. E., SUNDET, K., Taylor, A. M., TAYLOR, K. D., TZOULAKI, I., Tzourio, C., Uitterlinden, A., Vitart, V., VOINESKOS, A. N., Kaprio, J., Wagner, M., Wagner, H., WEINHOLD, L., WEN, K. H., WIDEN, E., Yang, Q., Zhao, W., ADAMS, H. H. H., ARKING, D. E., Bilder, R. M., BITSIOS, P., BOERWINKLE, E., CHIBA-FALEK, O., Corvin, A., DE JAGER, P. L., Debette, S., Donohoe, G., Elliott, P., FITZPATRICK, A. L., Gill, M., GLAHN, D. C., HAGG, S., HANSELL, N. K., HARIRI, A. R., Ikram, M. A., JUKEMA, J. W., VUOKSIMAA, E., KELLER, M. C., KREMEN, W. S., LAUNER, L., LINDENBERGER, U., Palotie, A., PEDERSEN, N. L., PENDLETON, N., PORTEOUS, D. J., RAIKKONEN, K., RAITAKARI, O. T., Ramirez, A., REINVANG, I., RUDAN, I., DAN, Rujescu, Schmidt, R., Schmidt, H., SCHOFIELD, P. W., STARR, J. M., STEEN, V. M., TROLLOR, J. N., TURNER, S. T., VAN DUIJN, C. M., VILLRINGER, A., WEINBERGER, D. R., WEIR, D. R., WILSON, J. F., Malhotra, A., MCINTOSH, A. M., GALE, C. R., SESHADRI, S., MOSLEY, T. H., Jr., BRESSLER, J., Lencz, T., DEARY, I. J., Bordeaux population health (BPH), and Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
VINTAGE, ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, HEALTHY, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries)
Abstract

Christina M. Lill, who contributed to analysis of data, was inadvertently omitted from the author list in the originally published version of this article. This has now been corrected in both the PDF and HTML versions of the article.

Published
2019

39. Progress update from the hippocampal subfields group: [Brain Imaging Working Group Summaries for the European Joint Programming for Neurodegenerative Research (JPND)]

Author

Olsen, R., Carr, V., Daugherty, A., La Joie, R., Amaral, R., Amunts, K., Augustinack, J., Bakker, A., Bender, A., Berron, D., Boccardi, M., Bocchetta, M., Burggren, A., Chakravarty, M., Chételat, G., de Flores, R., DeKraker, J., Ding, S., Geerlings, M., Huang, Y., Insausti, R., Johnson, E., Kanel, P., Kedo, O., Kennedy, K., Keresztes, A., Lee, J., Lindenberger, U., https://orcid.org/0000-0001-8428-6453, Mueller, S., Mulligan, E., Ofen, N., Palombo, D., Pasquini, L., Pluta, J., Raz, N., https://orcid.org/0000-0002-5080-2138, Rodrigue, K., Schlichting, M., Shing, Y., Stark, C., Steve, T., Suthana, N., Wang, L., Werkle-Bergner, M., https://orcid.org/0000-0002-6399-9996, Yushkevich, P., Yu, Q., Wisse, L., and Hippocampal Subfields Group

Published
2019

41. Author Correction: Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function (Nature Communications, (2018), 9, 1, (2098), 10.1038/s41467-018-04362-x)

Author

Davies, G. Lam, M. Harris, S.E. Trampush, J.W. Luciano, M. Hill, W.D. Hagenaars, S.P. Ritchie, S.J. Marioni, R.E. Fawns-Ritchie, C. Liewald, D.C.M. Okely, J.A. Ahola-Olli, A.V. Barnes, C.L.K. Bertram, L. Bis, J.C. Burdick, K.E. Christoforou, A. DeRosse, P. Djurovic, S. Espeseth, T. Giakoumaki, S. Giddaluru, S. Gustavson, D.E. Hayward, C. Hofer, E. Ikram, M.A. Karlsson, R. Knowles, E. Lahti, J. Leber, M. Li, S. Mather, K.A. Melle, I. Morris, D. Oldmeadow, C. Palviainen, T. Payton, A. Pazoki, R. Petrovic, K. Reynolds, C.A. Sargurupremraj, M. Scholz, M. Smith, J.A. Smith, A.V. Terzikhan, N. Thalamuthu, A. Trompet, S. van der Lee, S.J. Ware, E.B. Windham, B.G. Wright, M.J. Yang, J. Yu, J. Ames, D. Amin, N. Amouyel, P. Andreassen, O.A. Armstrong, N.J. Assareh, A.A. Attia, J.R. Attix, D. Avramopoulos, D. Bennett, D.A. Böhmer, A.C. Boyle, P.A. Brodaty, H. Campbell, H. Cannon, T.D. Cirulli, E.T. Congdon, E. Conley, E.D. Corley, J. Cox, S.R. Dale, A.M. Dehghan, A. Dick, D. Dickinson, D. Eriksson, J.G. Evangelou, E. Faul, J.D. Ford, I. Freimer, N.A. Gao, H. Giegling, I. Gillespie, N.A. Gordon, S.D. Gottesman, R.F. Griswold, M.E. Gudnason, V. Harris, T.B. Hartmann, A.M. Hatzimanolis, A. Heiss, G. Holliday, E.G. Joshi, P.K. Kähönen, M. Kardia, S.L.R. Karlsson, I. Kleineidam, L. Knopman, D.S. Kochan, N.A. Konte, B. Kwok, J.B. Le Hellard, S. Lee, T. Lehtimäki, T. Li, S.-C. Lill, C.M. Liu, T. Koini, M. London, E. Longstreth, W.T., Jr. Lopez, O.L. Loukola, A. Luck, T. Lundervold, A.J. Lundquist, A. Lyytikäinen, L.-P. Martin, N.G. Montgomery, G.W. Murray, A.D. Need, A.C. Noordam, R. Nyberg, L. Ollier, W. Papenberg, G. Pattie, A. Polasek, O. Poldrack, R.A. Psaty, B.M. Reppermund, S. Riedel-Heller, S.G. Rose, R.J. Rotter, J.I. Roussos, P. Rovio, S.P. Saba, Y. Sabb, F.W. Sachdev, P.S. Satizabal, C.L. Schmid, M. Scott, R.J. Scult, M.A. Simino, J. Slagboom, P.E. Smyrnis, N. Soumaré, A. Stefanis, N.C. Stott, D.J. Straub, R.E. Sundet, K. Taylor, A.M. Taylor, K.D. Tzoulaki, I. Tzourio, C. Uitterlinden, A. Vitart, V. Voineskos, A.N. Kaprio, J. Wagner, M. Wagner, H. Weinhold, L. Wen, K.H. Widen, E. Yang, Q. Zhao, W. Adams, H.H.H. Arking, D.E. Bilder, R.M. Bitsios, P. Boerwinkle, E. Chiba-Falek, O. Corvin, A. De Jager, P.L. Debette, S. Donohoe, G. Elliott, P. Fitzpatrick, A.L. Gill, M. Glahn, D.C. Hägg, S. Hansell, N.K. Hariri, A.R. Ikram, M.K. Jukema, J.W. Vuoksimaa, E. Keller, M.C. Kremen, W.S. Launer, L. Lindenberger, U. Palotie, A. Pedersen, N.L. Pendleton, N. Porteous, D.J. Räikkönen, K. Raitakari, O.T. Ramirez, A. Reinvang, I. Rudan, I. Dan Rujescu Schmidt, R. Schmidt, H. Schofield, P.W. Schofield, P.R. Starr, J.M. Steen, V.M. Trollor, J.N. Turner, S.T. Van Duijn, C.M. Villringer, A. Weinberger, D.R. Weir, D.R. Wilson, J.F. Malhotra, A. McIntosh, A.M. Gale, C.R. Seshadri, S. Mosley, T.H., Jr. Bressler, J. Lencz, T. Deary, I.J.

Subjects
ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries)
Abstract

Christina M. Lill, who contributed to analysis of data, was inadvertently omitted from the author list in the originally published version of this article. This has now been corrected in both the PDF and HTML versions of the article. © 2019, The Author(s).

Published
2019

44. Sensory Systems in Old Age

Author

Marsiske, M., primary, Delius, J., additional, Maas, I., additional, Lindenberger, U., additional, Scherer, H., additional, and Tesch-Römer, C., additional

Published
1998
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47. Höheres Erwachsenenalter

Author

Lindenberger, U., https://orcid.org/0000-0001-8428-6453, and Staudinger, U.

Published
2018

48. Complex networks emerging during choir singing

Author

Müller, V., Delius, J., Lindenberger, U., and https://orcid.org/0000-0001-8428-6453

Subjects
Phase synchronization, Oscillations, Task, Graph-theoretic approach, Cross-frequency coupling, Singers, Heart-rate, Hippocampus, Benefits, Heart rate variability, Social networks, Frequency couplings, Music
Abstract

First published: 29 July 2018 Choir singing is positively associated with well-being and quality of life, and requires the coordination of physiological systems within and across individuals. Informed by models of interpersonal action coordination, we delineate the network topography of choir singing by analyzing cross-frequency couplings and within-frequency couplings (WFCs) of respiratory, cardiac, vocalizing, and motor subsystems. We find that respiratory and cardiac subsystems synchronize with one another during singing and are coupled to oscillatory vocalizing patterns, and to the hand-movement oscillations of the choir's conductor. The choir's cross-frequency connections are particularly strong when singing a canon in parts, apparently supporting the interaction and coordination of the different canon entries. In contrast, WFCs are more pronounced when singing the same canon in unison. We conclude that the temporal coordination dynamics of the observed subsystems form part of the functional substrate for choir singing. During singing, the choir functions as a superordinate system, or superorganism, that imposes boundary conditions on the dynamic features of the individual singers.

Published
2018

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