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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. [ABSTRACT FROM AUTHOR]

INTRODUCTION: This study investigated whether self‐reported sleep quality is associated with brain amyloid beta (Aβ) accumulation. METHODS: Linear mixed effect model analyses were conducted for 189 cognitively unimpaired (CU) older adults (mean ± standard deviation 74.0 ± 6.2; 53.2% female), with baseline self‐reported sleep data, and positron emission tomography‐determined brain Aβ measured over a minimum of three time points (range 33.3–72.7 months). Analyses included random slopes and intercepts, interaction for apolipoprotein E (APOE) ε4 allele status, and time, adjusting for sex and baseline age. RESULTS: Sleep duration <6 hours, in APOE ε4 carriers, and sleep efficiency <65%, in the whole sample and APOE ε4 non‐carriers, is associated with faster accumulation of brain Aβ. DISCUSSION: These findings suggest a role for self‐reported suboptimal sleep efficiency and duration in the accumulation of Alzheimer's disease (AD) neuropathology in CU individuals. Additionally, poor sleep efficiency represents a potential route via which individuals at lower genetic risk may progress to preclinical AD. Highlights: In cognitively unimpaired older adults self‐report sleep is associated with brain amyloid beta (Aβ) accumulation.Across sleep characteristics, this relationship differs by apolipoprotein E (APOE) genotype.Sleep duration <6 hours is associated with faster brain Aβ accumulation in APOE ε4 carriers.Sleep efficiency < 65% is associated with faster brain Aβ accumulation in APOE ε4 non‐carriers.Personalized sleep interventions should be studied for potential to slow Aβ accumulation. [ABSTRACT FROM AUTHOR]

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., (© 2024 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)

Introduction: Non-exercise estimates of cardiorespiratory fitness hold great utility for epidemiological research and clinical practice. Older adults may yield the greatest benefit from fitness estimates due to limited capacity to undergo strenuous maximal exercise testing, however, few of the previously developed non-exercise equations are suitable for use in older adults. Thus, the current study developed a non-exercise equation for estimating cardiorespiratory fitness in older adults derived from the widely used International Physical Activity Questionnaire (IPAQ)., Methods: This study was a secondary analysis of baseline data from a randomized controlled trial. Participants were community-dwelling, cognitively unimpaired older adults aged 60-80 years ( n  = 92). They completed the IPAQ and underwent maximal exercise testing on a cycle ergometer. Stepwise linear regression was used to determine the equation in a randomly selected, sex-balanced, derivation subset of participants ( n  = 60), and subsequently validated using a second subset of participants ( n  = 32)., Results: The final equation included age, sex, body mass index and leisure time activity from the IPAQ and explained 61% and 55% of the variance in the derivation and validation groups, respectively (standard error of estimates = 3.9, 4.0). Seventy-seven and 81% of the sample fell within ±1SD (5.96 and 6.28 ml·kg-1·min-1) of measured VO 2peak for the derivation and validation subgroups. The current equation showed better performance compared to equations from Wier et al. (2006), Jackson et al. (1990), and Schembre & Riebe (2011), although it is acknowledged previous equations were developed for different populations., Conclusions: Using non-exercise, easily accessible measures can yield acceptable estimates of cardiorespiratory fitness in older adults, which should be further validated in other samples and examined in relation to public health outcomes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Sewell, Peiffer, Markovic and Brown.)

Introduction: This study investigated whether self-reported sleep quality is associated with brain amyloid beta (Aβ) accumulation., Methods: Linear mixed effect model analyses were conducted for 189 cognitively unimpaired (CU) older adults (mean ± standard deviation 74.0 ± 6.2; 53.2% female), with baseline self-reported sleep data, and positron emission tomography-determined brain Aβ measured over a minimum of three time points (range 33.3-72.7 months). Analyses included random slopes and intercepts, interaction for apolipoprotein E ( APOE ) ε4 allele status, and time, adjusting for sex and baseline age., Results: Sleep duration <6 hours, in APOE ε4 carriers, and sleep efficiency <65%, in the whole sample and APOE ε4 non-carriers, is associated with faster accumulation of brain Aβ., Discussion: These findings suggest a role for self-reported suboptimal sleep efficiency and duration in the accumulation of Alzheimer's disease (AD) neuropathology in CU individuals. Additionally, poor sleep efficiency represents a potential route via which individuals at lower genetic risk may progress to preclinical AD., Highlights: In cognitively unimpaired older adults self-report sleep is associated with brain amyloid beta (Aβ) accumulation.Across sleep characteristics, this relationship differs by apolipoprotein E ( APOE ) genotype.Sleep duration <6 hours is associated with faster brain Aβ accumulation in APOE ε4 carriers.Sleep efficiency < 65% is associated with faster brain Aβ accumulation in APOE ε4 non-carriers.Personalized sleep interventions should be studied for potential to slow Aβ accumulation., Competing Interests: L.N.P., B.M.B., K.R.S., J.D.D., V.D., M.W., H.R.S., S.L.G., R.S.B., S.M.L., K.T., and S.R.R.S. report no disclosures. V.L.V. is and has been a consultant or paid speaker at sponsored conference sessions for Eli Lilly, Life Molecular Imaging, ACE Barcelona, and IXICO. P.M. is a full‐time employee of Cogstate Ltd. C.L.M. is an advisor to Prana Biotechnology Ltd and a consultant to Eli Lilly. C.C.R. has served on scientific advisory boards for Bayer Pharma, Elan Corporation, GE Healthcare, and AstraZeneca; has received speaker honoraria from Bayer Pharma and GE Healthcare; and has received research support from Bayer Pharma, GE Healthcare, Piramal Lifesciences, and Avid Radiopharmaceuticals. R.N.M. is founder of, and owns stock in, Alzhyme, and is a co‐founder of the KaRa Institute of Neurological Diseases. Author disclosures are available in the supporting information, (© 2024 The Authors. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)

Objectives: Observational studies consistently demonstrate that physical activity is associated with elevated cognitive function, however, there remains significant heterogeneity in cognitive outcomes from randomized exercise interventions. Individual variation in sleep behaviours may be a source of variability in the effectiveness of exercise-induced cognitive change, however this has not yet been investigated. The current study aimed to (1) investigate the influence of a 6-month exercise intervention on sleep, assessed pre- and post-intervention and, (2) investigate whether baseline sleep measures moderate exercise-induced cognitive changes., Methods: We utilised data from the Intense Physical Activity and Cognition (IPAC) study (n = 89), a 6-month moderate intensity and high intensity exercise intervention, in cognitively unimpaired community-dwelling older adults aged 60-80 (68.76 ± 5.32). Exercise was supervised and completed on a stationary exercise bicycle, and cognitive function was measured using a comprehensive neuropsychological battery administered pre- and post-intervention. Sleep was measured using the Pittsburgh sleep quality index. There was no effect of the exercise intervention on any sleep outcomes from pre- to post-intervention., Results: There was a significant moderating effect of baseline sleep efficiency on both episodic memory and global cognition within the moderate intensity exercise group, such that those with poorer sleep efficiency at baseline showed greater exercise-induced improvements in episodic memory., Conclusions: These results suggest that those with poorer sleep may have the greatest exercise-induced cognitive benefits and that baseline sleep behaviours may be an important source of heterogeneity in previous exercise interventions targeting cognitive outcomes., (© 2023 The Authors. International Journal of Geriatric Psychiatry published by John Wiley & Sons Ltd.)