ArticleFrontiers in aging neuroscience2025
Protocol of a randomized, single-blind, controlled trial of an 18-month, home-based, high-intensity, exercise intervention in older, cognitively unimpaired
Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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25 authors.
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Abstract
Background: The World Health Organization highlighted the potential protective role of exercise against cognitive decline, all-cause dementia, Alzheimer's disease (AD), and vascular dementia in healthy individuals. We have previously shown that exercise is particularly beneficial for older, cognitively unimpaired apolipoprotein E4 ( Design: CYCLE-AD is a randomized, single-blind, single-center, controlled trial of a home-based, high-intensity exercise intervention involving 150 older ε4 carriers (ages 65-80 years) who are healthy, cognitively unimpaired, and physically inactive. Participants are randomized into two groups: indoor cycling (IC) or usual and customary care (UCC) (target of 75 each). IC participants exercise 3×/week on an upright stationary cycle ergometer at a moderate-vigorous intensity for 18 months. Those in the UCC group are expected to maintain enrollment levels of activity. Outcomes: Comparison of IC and UCC groups on change in primary and secondary outcomes over baseline, 9-month, and 18-month evaluations. Primary outcomes are VO Hypotheses: Over an 18-month interval, physically inactive ε4 carriers who engage in high-intensity aerobic exercise will demonstrate less cognitive decline and hippocampal atrophy than physically inactive ε4 carriers who did not participate in a formal exercise program. Conclusion: Successful demonstration of a scalable, home-based, high-intensity aerobic exercise intervention in altering the trajectory of AD pathophysiology and its effects on cognitive functioning will transform AD treatment, improve patient outcomes and quality of life, and reduce healthcare costs.
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