Sleep quality decreases with aging and thus sleep complaints are prevalent in older adults, particularly for those with cognitive impairment and dementia. For older adults, emerging evidence suggests poor sleep quality increases risk of developing cognitive impairment and dementia. Given the aging population—and the impending economic burden associated with increasing numbers of dementia patients—there is pressing need to improve sleep quality among older adults. As such, research efforts have increased focus on investigating the association between age-related sleep changes and cognitive decline in older adults. Sleep quality is a complex construct to evaluate empirically, and yet the Pittsburg Sleep Quality Index (PSQI) is commonly used in studies as their only measure of sleep quality. Furthermore, the PSQI may not be the best sleep quality measure for older adults, due to its reliance on the cognitive capacity to reflect on the past month. Further study is needed to determine the PSQI's validity among older adults. Thus, the current study examined sleep quality for 78 community dwelling adults 55+ to determine the PSQI's predictive validity for objective sleep quality (as measured by actigraphy). We compared two subjective measures of sleep quality—the PSQI and Consensus Sleep Diary (CSD)—with actigraphy (MotionWatch 8©; camntech). Our results suggest perceived sleep quality is quite different from objective reality, at least for adults 55+. Importantly, we show this difference is unrelated to age, gender, education, or cognitive status (assessed using standard screens). Previous studies have shown the PSQI to be a valuable tool for assessing subjective sleep quality; however, our findings indicate for older adults the PSQI should not be used as a substitute for actigraphy, or vice versa. Hence, we conclude best practice is to include both subjective and objective measures when examining sleep quality in older adults (i.e., the PSQI, CSD, and actigraphy).
Persistence of a behavioral food-anticipatory circadian rhythm following dorsomedial hypothalamic ablation in rats. Am J Physiol Regul Integr Comp Physiol 290: R1527-R1534, 2006. First published January 19, 2006 doi:10.1152/ajpregu.00874.2005.-Circadian rhythms of behavior in rodents are regulated by a system of circadian oscillators, including a master light-entrainable pacemaker in the suprachiasmatic nucleus that mediates synchrony to the day-night cycle, and food-entrainable oscillators located elsewhere that generate rhythms of food-anticipatory activity (FAA) synchronized to daily feeding schedules. Despite progress in elucidating neural and molecular mechanisms of circadian oscillators, localization of food-entrainable oscillators driving FAA remains an enduring problem. Recent evidence suggests that the dorsomedial hypothalamic nucleus (DMH) may function as a final common output for behavioral rhythms and may be critical for the expression of FAA (Gooley JJ, Schomer A, and Saper CB. Nat Neurosci 9: 398 -407, 2006). To determine whether the reported loss of FAA by DMH lesions is specific to one behavioral measure or generalizes to other measures, rats received large radiofrequency lesions aimed at the DMH and were recorded in cages with movement sensors. Total and partial DMH ablation was associated with a significant attenuation of light-dark-entrained activity rhythms during ad libitum food access, because of a selective reduction in nocturnal activity. When food was restricted to a single 3-h daily meal in the middle of the lights-on period, all DMH and intact rats exhibited significant FAA. The rhythm of FAA persisted during a 48-h food deprivation test and reappeared during a 72-h deprivation test after ad libitum food access. The DMH is not the site of oscillators or entrainment pathways necessary for all manifestations of FAA, but may participate on the output side of this circadian function. food entrainment; food-anticipatory activity; food-entrainable oscillator CIRCADIAN RHYTHMS IN MAMMALS are generated by a system of cell-autonomous circadian oscillators distributed within the brain and in peripheral organs (32,57). A population of oscillators located in the retino-recipient hypothalamic suprachiasmatic nucleus (SCN) function as a master pacemaker critical for normal circadian organization of behavior and physiology and for entrainment of rhythms to daily light-dark (LD) cycles (34). Circadian rhythms can also be entrained by daily feeding schedules. If food access is restricted to a narrow daily temporal window (typically 2-4 h in the middle of the lights-on period), nocturnal rodents, such as rats, mice, and hamsters, become behaviorally active in anticipation of the feeding time. This daily rhythm of food-anticipatory activity (FAA) takes a few circadian cycles to emerge, exhibits gradual shifting (transients) if mealtime is shifted, persists for at least 5 days during total food deprivation, and does not emerge if the interval between mealtimes is outside of the circadian range or its har...
Restricted daytime feeding generates food-anticipatory activity (FAA) by entrainment of a circadian pacemaker separate from the light-entrainable pacemaker located in the SCN. The dorsomedial hypothalamic nucleus (DMH) has been proposed as the site of food-entrainable oscillators critical for the expression of FAA, but another study found no effects of complete DMH ablation on FAA. To account for these different results, the authors examined methodological factors, including (1) cage configuration and feeding method and (2) use of social cues. Intact and DMH-ablated rats were maintained on one 4-h daily meal in the middle of the light period, using caging and feeding methods matching those of Gooley et al. (2006). Rats with partial or complete DMH ablation were less nocturnal during ad lib food access but exhibited normal FAA during restricted feeding, as quantified by FAA magnitude, ratios, latency to appearance, duration, and precision. To evaluate the use of social cues, intact rats naive to restricted-feeding schedules were food deprived for 72 h on 4 tests. Daytime activity increased during food deprivation, but the magnitude and waveform of this activity was not influenced by the presence of food-entrained rats exhibiting robust FAA in adjacent cages. Thus, hungry intact rats do not use social cues to anticipate a daily mealtime, suggesting that DMH-ablated rats do not anticipate meals by reacting to sounds from food-entrained intact rats in adjacent cabinets. These results confirm our previous finding that the DMH is not critical for normal expression of FAA in rats, and this observation is extended to food restriction methodologies used by other labs. The methodological differences that do underlie discrepant results remain unresolved, as does the location of food-entrainable oscillators, input pathways, and output pathways critical for FAA.
As of 2010, the worldwide economic impact of dementia was estimated at $604 billion USD; and without discovery of a cure or effective interventions to delay disease progression, dementia’s annual global economic impact is expected to surpass $1 trillion USD as early as 2030. Alzheimer’s disease (AD) is the leading cause of dementia accounting for over 75% of all cases. Toxic accumulation of amyloid beta (Aβ), either by overproduction or some clearance failure, is thought to be an underlying mechanism of the neuronal cell death characteristic of AD—though this amyloid hypothesis has been increasingly challenged in recent years. A compelling alternative hypothesis points to chronic neuroinflammation as a common root in late-life degenerative diseases including AD. Apolipoprotein-E (APOE) genotype is the strongest genetic risk factor for AD: APOE-ε4 is proinflammatory and individuals with this genotype accumulate more Aβ, are at high risk of developing AD, and almost half of all AD patients have at least one ε4 allele. Recent studies suggest a bidirectional relationship exists between sleep and AD pathology. Sleep may play an important role in Aβ clearance, and getting good quality sleep vs. poor quality sleep might reduce the AD risk associated with neuroinflammation and the ε4 allele. Taken together, these findings are particularly important given the sleep disruptions commonly associated with AD and the increased burden disrupted sleep poses for AD caregivers. The current review aims to: (1) identify individuals at high risk for dementia who may benefit most from sleep interventions; (2) explore the role poor sleep quality plays in exacerbating AD type dementia; (3) examine the science of sleep interventions to date; and (4) provide a road map in pursuit of comprehensive sleep interventions, specifically targeted to promote cognitive function and delay progression of dementia.
Participants with probable MCI were less active and more sedentary. The relationships of these behaviors with cognitive function differed by MCI status; associations were found only in participants without MCI.
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