Longitudinal associations between exercise and biomarkers in autosomal dominant Alzheimer's disease
INTRODUCTION We investigated longitudinal associations between self‐reported exercise and Alzheimer's disease (AD)‐related biomarkers in individuals with autosomal dominant AD (ADAD) mutations. METHODS Participants were 308 ADAD mutation carriers aged 39.7 ± 10.8 years from the Dominantly Inher...
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Veröffentlicht in: | Alzheimer's & dementia 2024-11, Vol.20 (11), p.7923-7939 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | INTRODUCTION
We investigated longitudinal associations between self‐reported exercise and Alzheimer's disease (AD)‐related biomarkers in individuals with autosomal dominant AD (ADAD) mutations.
METHODS
Participants were 308 ADAD mutation carriers aged 39.7 ± 10.8 years from the Dominantly Inherited Alzheimer's Network. Weekly exercise volume was measured via questionnaire and associations with brain volume (magnetic resonance imaging), cerebrospinal fluid biomarkers, and brain amyloid beta (Aβ) measured by positron emission tomography were investigated.
RESULTS
Greater volume of weekly exercise at baseline was associated with slower accumulation of brain Aβ at preclinical disease stages β = –0.16 [–0.23 to –0.08], and a slower decline in multiple brain regions including hippocampal volume β = 0.06 [0.03 to 0.08].
DISCUSSION
Exercise is associated with more favorable profiles of AD‐related biomarkers in individuals with ADAD mutations. Exercise may have therapeutic potential for delaying the onset of AD; however, randomized controlled trials are vital to determine a causal relationship before a clinical recommendation of exercise is implemented.
Highlights
Greater self‐reported weekly exercise predicts slower declines in brain volume in autosomal dominant Alzheimer's disease (ADAD).
Greater self‐reported weekly exercise predicts slower accumulation of brain amyloid beta in ADAD.
Associations varied depending on closeness to estimated symptom onset. |
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ISSN: | 1552-5260 1552-5279 1552-5279 |
DOI: | 10.1002/alz.14270 |