James Michael Roe

• Roe, James Michael; Vidal-Piñeiro, Didac; Sørensen, Øystein; Mowinckel, Athanasia Monika; Walhovd, Kristine B; Fjell, Anders Martin & Westerhausen, Rene (2021). Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer’s Disease. Nature Communications.  ISSN 2041-1723. . doi: https://doi.org/10.1101/2020.06.18.158980 Show summary

  Normal aging and Alzheimer’s Disease (AD) are accompanied by large-scale alterations in brain organization that undermine brain function. Although hemispheric asymmetry is a global organizing feature of cortex thought to promote brain efficiency, current descriptions of cortical thinning in aging and AD have largely overlooked cortical asymmetry. Consequently, the foundational question of whether and where the cerebral hemispheres change at different rates in aging and AD remains open. First, applying vertex-wise data-driven clustering in a longitudinal discovery sample (aged 20-89; 2577 observations; 1851 longitudinal) we identified cortical regions exhibiting similar age-trajectories of asymmetry across the adult lifespan. Next, we sought replication in 4 independent longitudinal aging cohorts. We show that higher-order regions of cortex that exhibit pronounced asymmetry at age ~20 also show asymmetry change in aging. Results revealed that both leftward and rightward asymmetry is progressively lost on a similar time-scale across adult life. Hence, faster thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This simple organizational principle showed high consistency across multiple aging cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics of asymmetry-loss were markedly similar across replicating samples. Finally, we show that regions exhibiting gradual asymmetry-loss over healthy adult life exhibit faster asymmetry-change in AD. 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.06.18.158980; this version posted June 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Overall, our results suggest a system-wide breakdown in the adaptive asymmetric organization of cortex across adult life which is further accelerated in AD, and may implicate thickness asymmetry as a viable marker for declining hemispheric specialization in aging and AD.

• Fjell, Anders Martin; Sørensen, Øystein; Amlien, Inge Kasbohm; Mowinckel, Athanasia Monika; Vidal-Piñeiro, Didac; Westerhausen, Rene; Walhovd, Kristine B; Bartrés-Faz, David; Brandmaier, Andreas M.; Buchmann, Nikolaus; Demuth, Ilja; Drevon, Christian A; Düzel, Sandra; Ebmeier, Klaus; Ghisletta, Paolo; Idland, Ane-Victoria; Kietzmann, Tim C; Kievit, Rogier A.; Kühn, Simone; Lindenberger, Ulman; Magnussen, Fredrik; Macià Bros, Didac; Nyberg, Lars Erik; Sexton, Claire E; Sole-Padulles, Cristina; Pudas, Sara; Roe, James Michael; Sederevicius, Donatas; Suri, Sana; Wagner, Gerd; Watne, Leiv Otto & Zsoldos, Eniko (2020). Poor Self-Reported Sleep is Related to Regional Cortical Thinning in Aging but not Memory Decline-Results From the Lifebrain Consortium. Cerebral Cortex.  ISSN 1047-3211. . doi: 10.1093/cercor/bhaa332 Show summary

  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.

• Vidal-Piñeiro, Didac; Sneve, Markus Handal; Amlien, Inge Kasbohm; Grydeland, Håkon; Mowinckel, Athanasia Monika; Roe, James Michael; Sørensen, Øystein; Nyberg, Lars; Walhovd, Kristine B & Fjell, Anders Martin (2020). The Functional Foundations of Episodic Memory Remain Stable Throughout the Lifespan. Cerebral Cortex.  ISSN 1047-3211.
• Roe, James Michael; Vidal-Piñeiro, Didac; Sneve, Markus Handal; Kompus, Kristiina; Greve, Douglas N.; Walhovd, Kristine B; Fjell, Anders Martin & Westerhausen, René (2019). Age-Related Differences in Functional AsymmetryDuring Memory Retrieval Revisited: No Evidence forContralateral Overactivation or Compensation. Cerebral Cortex.  ISSN 1047-3211.  0(0), s 1- 19 . doi: 10.1093/cercor/bhz153 Full text in Research Archive.
• Vidal-Piñeiro, Didac; Sneve, Markus Handal; Storsve, Andreas Berg; Roe, James Michael; Walhovd, Kristine B & Fjell, Anders Martin (2017). Neural correlates of durable memories across the adult lifespan: brain activity at encoding and retrieval. Neurobiology of Aging.  ISSN 0197-4580.  60, s 20- 33 . doi: 10.1016/j.neurobiolaging.2017.08.017 Full text in Research Archive.
• Roe, James; Nesheim, Mathias; Mathiesen, Nina Chung; Moberget, Torgeir; Alnæs, Dag & Sneve, Markus Handal (2016). The effects of tDCS upon sustained visual attention are dependent on cognitive load. Neuropsychologia.  ISSN 0028-3932.  80, s 1- 8 . doi: 10.1016/j.neuropsychologia.2015.11.005

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