• Medientyp: E-Artikel
  • Titel: Hemodynamic and structural brain measures in high and low sedentary older adults
  • Beteiligte: Maasakkers, Carlijn M; Thijssen, Dick HJ; Knight, Silvin P; Newman, Louise; O'Connor, John D; Scarlett, Siobhan; Carey, Daniel; Buckley, Anne; McMorrow, Jason P; Leidhin, Caoilfhionn Ní; Feeney, Joanne; Melis, René JF; Kenny, Rose Anne; Claassen, Jurgen AHR; Looze, Céline De
  • Erschienen: SAGE Publications, 2021
  • Erschienen in: Journal of Cerebral Blood Flow & Metabolism, 41 (2021) 10, Seite 2607-2616
  • Sprache: Englisch
  • DOI: 10.1177/0271678x211009382
  • ISSN: 0271-678X; 1559-7016
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  • Beschreibung: Due to its cardiovascular effects sedentary behaviour might impact cerebrovascular function in the long term, affecting cerebrovascular regulatory mechanisms and perfusion levels. Consequently this could underly potential structural brain abnormalities associated with cognitive decline. We therefore assessed the association between sedentary behaviour and brain measures of cerebrovascular perfusion and structural abnormalities in community-dwelling older adults. Using accelerometery (GENEActiv) data from The Irish Longitudinal Study on Ageing (TILDA) we categorised individuals by low- and high-sedentary behaviour (≤8 vs >8 hours/day). We examined prefrontal haemoglobin oxygenation levels using Near-Infrared Spectroscopy during rest and after an orthostatic challenge in 718 individuals (66 ± 8 years, 52% female). Global grey matter cerebral blood flow, total grey and white matter volume, total and subfield hippocampal volumes, cortical thickness, and white matter hyperintensities were measured using arterial spin labelling, T1, and FLAIR MRI in 86 individuals (72 ± 6 years, 55% female). While no differences in prefrontal or global cerebral hemodynamics were found between groups, high-sedentary individuals showed lower hippocampal volumes and increased white matter hyperintensities compared to their low-sedentary counterparts. Since these structural cerebral abnormalities are associated with cognitive decline and Alzheimer’s disease, future work exploring the causal pathways underlying these differences is needed.
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