Alzheimer’s And Exercise

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Alzheimer's And Exercise

If you carried a gene that doubled your likelihood of getting Alzheimer’s disease, would you want to know? What if there was a simple lifestyle change that virtually abolished that elevated risk? People with a gene known as APOE e4 have a higher risk of cognitive impairment and dementia in old age. Even before behavioral symptoms appear, their brains show reduced metabolism, altered activity and more deterioration than those without the high-risk gene. Yet accumulating research is showing that carrying this gene is not necessarily a sentence for memory loss and confusion—if you know how to work it to your advantage with exercise. Scientists have long known that exercise can help stave off cognitive decline. Over the past decade evidence has mounted suggesting that this benefit is even greater for those at higher genetic risk for Alzheimer’s. For example, two studies by a team in Finland and Sweden found that exercising at least twice a week in midlife lowers one’s chance of getting dementia more than 20 years later, and this protective effect is stronger in people with the APOE e4 gene. Several others reported that frequent exercise—at least three times a week in some studies; up to more than an hour a day in others—can slow cognitive decline only in those carrying the high-risk gene. Furthermore, for those who carry the gene, being sedentary is associated with increased brain accumulation of the toxic protein beta-amyloid, a hallmark of Alzheimer’s. More recent studies, including a 2012 paper published in Alzheimer’s & Dementia and a 2011 paper in NeuroImage, found that high-risk individuals who exercise have greater brain activity and glucose uptake during a memory task compared with their less active counterparts or with those at low genetic risk. This link to metabolism may help explain why exercise protects APOE e4 carriers. According to a theory proposed in May by anthropologist David Raichlen and psychologist Gene Alexander, both at the University of Arizona, the answer lies in our evolutionary past. Two million years ago, when our ancestors were much more physically active—for example, perhaps running long distances to hunt prey—only the high-risk gene variant existed, they argue. The gene allowed for better metabolism during intense activity, and its downside, faster cognitive decline, was counteracted by our ancestors’ active way of life. As humans adopted more sedentary habits, other variants of the gene appeared, and in modern times we are now seeing the negative effect of the high-risk gene more often than its benefit. Although these studies suggest that exercise is exceptionally protective for those at highest risk, some findings buck the trend. One large-scale study reported that high levels of leisure-time activity reduced risk of dementia five years later but only in those who did not carry the high-risk APOE e4 gene. These inconsistencies suggest the interaction may be complex, although most of the evidence still indicates that an active lifestyle has great value. Exercise is important for healthy aging, regardless of genetics, but Raichlen emphasizes that “for individuals that are APOE e4 carriers, studies certainly underline the importance of maintaining physical activity across the life span.” And with further research, he suggests, “a better understanding of the evolutionary origins of genotype-lifestyle interactions will help identify populations that may particularly benefit from behavioral changes.”
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Alzheimer's And Exercise

DiscussionThis pilot, randomized, controlled trial provides preliminary evidence that 6-months of AEx benefits functional ability in early-stage AD compared to a ST control intervention. Furthermore, we found evidence that improvements in cardiorespiratory fitness were related to benefits in memory performance and brain volume change. These data fit with a growing body of evidence that enhancing cardiorespiratory fitness through exercise may be important in attaining maximal brain benefits of exercise. Our primary finding is that 26 weeks of AEx was associated with increased functional ability compared to the ST control. Our measure of functional ability was the Disability Assessment for Dementia, a caregiver-based assessment of activities of daily living, that predicts earlier time to institutionalization. Individuals with mild to moderate AD typically decline approximately 1 point per month on this scale (100 equates to full functional ability). We found that the AEx group increased 1.5 points while the ST group decreased 4.5 points over the course of the intervention suggesting a meaningful effect on sustained independence. This also extends prior findings suggesting that exercise promotes function in AD. We also found that exercise-related change in the gold standard measure of cardiorespiratory fitness (peak VO2) was related to change in both memory performance and bilateral hippocampal volume. This observation supports the concept, reported widely in animal data, that exercise may attenuate AD-related brain and cognitive decline although CR fitness gains may be necessary to achieve these benefits These findings thus support the cardiorespiratory fitness hypothesis, which posits that improved fitness as a result of aerobic exercise is essential and causally related to attaining exercise-related cognitive benefits. The cardiorespiratory fitness hypothesis is also supported by human studies that suggest cardiorespiratory fitness gains may be important in mediating physiological benefits to brain health. Gains in cardiorespiratory fitness may reflect complex systemic changes necessary to impact brain physiology or reflect an individual’s ability to attain sufficient levels of exercise necessary to impact brain structure and function. Surprisingly, we did not observe significant group differences in exercise-related gains in cardiorespiratory fitness (peak VO2) for the AEx group (3% gain) compared to the ST group (0.03%). The modest 3% gain in cardiorespiratory fitness for the AEx group is lower than what we achieve in cognitively normal older adults following a similar protocol despite good compliance with the exercise protocol and an increase in our secondary measure of functional fitness, the 6-minute walk test. This lack of a robust peak VO2 response suggests that individuals with early AD may have a limited, or more variable, physiologic response to aerobic exercise than cognitively normal individuals. We have previously reported that individuals with AD exhibit lower cross-sectional peak VO2 and significantly greater longitudinal peak VO2 decline than cognitively normal older adults. This suggests that there may be inherent physiological differences, beyond behavioral issues, that may limit cardiorespiratory fitness responses. The primary limitation for this pilot study is a relatively small sample size that limits our power to detect significant group effects. The exercise interventions were delivered in the community, enhancing generalizability but possibly introducing variability in execution, though we have previously demonstrated that our community-based methods can deliver a rigorously-controlled intervention of various exercise doses producing linearly increasing responses to cardiorespiratory fitness. Our findings of a relationship of change in cardiorespiratory fitness with memory change and hippocampal atrophy are suggestive but do not prove cause and effect. For instance, it remains unclear whether improvement in cardiorespiratory fitness drives memory improvement or whether a decline in memory (or more severely progressive dementia) influences measured cardiorespiratory fitness as indexed by peak VO2. Reverse causation cannot be ruled out as an explanation for these secondary findings, although these relationships remained significant even when controlling for baseline MMSE or baseline CDR (as an index of baseline disease severity). Finally, it is important to note that we made no correction for multiple tests, raising the potential for false positives. While multiple outcomes are not ideal for a clinical trial, we felt it important to explore in this pilot study the various aspects of function that have previously been shown to benefit from aerobic exercise. In conclusion, findings from this pilot randomized controlled trial were consistent with previous work showing aerobic exercise benefits functional ability in individuals with early-stage AD. Further, we found indirect evidence that exercise-related increases in cardiorespiratory fitness may be important to improving memory performance and reducing hippocampal atrophy. These effects should be explored in a definitive trial of aerobic exercise for individuals with early-stage AD. We have provided effect size estimates and confidence intervals to inform these future studies.
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Alzheimer's And Exercise

You won’t find articles in popular magazines that discuss the benefits of exercise for persons with Alzheimer’s Disease. In fact, as of February 2001, only two articles in professional journals documented the multiple benefits of physical fitness training for non-institutionalized early- to moderate-stage persons with Alzheimer’s Disease. The author’s Alzheimer’s Disease Rehab by Students program (Arkin, 1999) showed dramatic gains in physical fitness and mood, maintenance of function in multiple language measures, and a slower than typical decline in mental status after a year of exercise. An Italian research group (Palleschi, Vetta, Degennaro, Idone, Sottosanti, Gianni, & Marigliano, 1996) found a significant improvement on four cognitive measures after three months of aerobic exercise.
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Alzheimer's And Exercise

Abstract Background There is increasing interest in the role of physical exercise as a therapeutic strategy for individuals with Alzheimer’s disease (AD). We assessed the effect of 26 weeks (6 months) of a supervised aerobic exercise program on memory, executive function, functional ability and depression in early AD. Methods and findings This study was a 26-week randomized controlled trial comparing the effects of 150 minutes per week of aerobic exercise vs. non-aerobic stretching and toning control intervention in individuals with early AD. A total of 76 well-characterized older adults with probable AD (mean age 72.9 ) were enrolled and 68 participants completed the study. Exercise was conducted with supervision and monitoring by trained exercise specialists. Neuropsychological tests and surveys were conducted at baseline,13, and 26 weeks to assess memory and executive function composite scores, functional ability (Disability Assessment for Dementia), and depressive symptoms (Cornell Scale for Depression in Dementia). Cardiorespiratory fitness testing and brain MRI was performed at baseline and 26 weeks. Aerobic exercise was associated with a modest gain in functional ability (Disability Assessment for Dementia) compared to individuals in the ST group (X2 = 8.2, p = 0.02). There was no clear effect of intervention on other primary outcome measures of Memory, Executive Function, or depressive symptoms. However, secondary analyses revealed that change in cardiorespiratory fitness was positively correlated with change in memory performance and bilateral hippocampal volume. Conclusions Aerobic exercise in early AD is associated with benefits in functional ability. Exercise-related gains in cardiorespiratory fitness were associated with improved memory performance and reduced hippocampal atrophy, suggesting cardiorespiratory fitness gains may be important in driving brain benefits. Trial registration ClinicalTrials.gov NCT01128361

Alzheimer's And Exercise

Alzheimer's And Exercise
Alzheimer's And Exercise
Alzheimer's And Exercise

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