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Synchronizing an aging brain: can entraining circadian clocks by food slow Alzheimer's disease?

Kent BA - Front Aging Neurosci (2014)

Bottom Line: Until effective treatments are developed, promoting overall health may hold potential for delaying the onset or preventing neurodegenerative diseases such as AD.It is well reported that AD is associated with disrupted circadian functioning to a greater extent than normal aging.If the uncoupling of rhythms is contributing to AD progression or exacerbating symptoms, then it may be possible to draw from the food-entrainment literature to identify mechanisms for re-synchronizing rhythms to improve overall health and reduce the severity of symptoms.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, University of Cambridge Cambridge, UK.

ABSTRACT
Alzheimer's disease (AD) is a global epidemic. Unfortunately, we are still without effective treatments or a cure for this disease, which is having devastating consequences for patients, their families, and societies around the world. Until effective treatments are developed, promoting overall health may hold potential for delaying the onset or preventing neurodegenerative diseases such as AD. In particular, chronobiological concepts may provide a useful framework for identifying the earliest signs of age-related disease as well as inexpensive and noninvasive methods for promoting health. It is well reported that AD is associated with disrupted circadian functioning to a greater extent than normal aging. However, it is unclear if the central circadian clock (i.e., the suprachiasmatic nucleus) is dysfunctioning, or whether the synchrony between the central and peripheral clocks that control behavior and metabolic processes are becoming uncoupled. Desynchrony of rhythms can negatively affect health, increasing morbidity and mortality in both animal models and humans. If the uncoupling of rhythms is contributing to AD progression or exacerbating symptoms, then it may be possible to draw from the food-entrainment literature to identify mechanisms for re-synchronizing rhythms to improve overall health and reduce the severity of symptoms. The following review will briefly summarize the circadian system, its potential role in AD, and propose using a feeding-related neuropeptide, such as ghrelin, to synchronize uncoupled rhythms. Synchronizing rhythms may be an inexpensive way to promote healthy aging and delay the onset of neurodegenerative disease such as AD.

No MeSH data available.


Related in: MedlinePlus

Hypothesized link between ghrelin and symptoms often associated with aging and Alzheimer’s disease. Ghrelin has been shown to directly affect hippocampal plasticity and neurogenesis, hunger-levels, and circadian processes. Both aging and Alzheimer’s disease (AD) are associated with lower levels of circulating ghrelin. Low ghrelin levels may result in reduced hippocampal plasticity and neurogenesis, and contribute to the cognitive deficits associated with old-age and AD. Lower circulating levels of ghrelin may also reduce hunger levels, and may partially underlie the weight loss associated with older age and AD. Finally, if ghrelin acts to enhance feeding-related zeitgebers, then reductions in circulating ghrelin could dampen food-entrained oscillators and disrupt circadian rhythmicity.
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Figure 2: Hypothesized link between ghrelin and symptoms often associated with aging and Alzheimer’s disease. Ghrelin has been shown to directly affect hippocampal plasticity and neurogenesis, hunger-levels, and circadian processes. Both aging and Alzheimer’s disease (AD) are associated with lower levels of circulating ghrelin. Low ghrelin levels may result in reduced hippocampal plasticity and neurogenesis, and contribute to the cognitive deficits associated with old-age and AD. Lower circulating levels of ghrelin may also reduce hunger levels, and may partially underlie the weight loss associated with older age and AD. Finally, if ghrelin acts to enhance feeding-related zeitgebers, then reductions in circulating ghrelin could dampen food-entrained oscillators and disrupt circadian rhythmicity.

Mentions: Importantly, weight loss may precede the memory loss associated with dementia (Buchman et al., 2005; Stewart et al., 2005; Johnson et al., 2006; Knopman et al., 2007). Because ghrelin is an important regulator of appetite, the age-related weight loss is in agreement with the finding of an age-related decline of plasma ghrelin concentrations as well as the age-related decline in growth-hormone releasing effect of ghrelin (Figure 2; Rigamonti et al., 2002; Broglio et al., 2003). AD patients compared with age-matched controls, also show a reduction in local ghrelin production in the brain (Gahete et al., 2010). Because weight loss appears to precede cognitive impairment in patients with AD (Knopman et al., 2007), metabolic changes could be targets for early detection and prevention of cognitive decline.


Synchronizing an aging brain: can entraining circadian clocks by food slow Alzheimer's disease?

Kent BA - Front Aging Neurosci (2014)

Hypothesized link between ghrelin and symptoms often associated with aging and Alzheimer’s disease. Ghrelin has been shown to directly affect hippocampal plasticity and neurogenesis, hunger-levels, and circadian processes. Both aging and Alzheimer’s disease (AD) are associated with lower levels of circulating ghrelin. Low ghrelin levels may result in reduced hippocampal plasticity and neurogenesis, and contribute to the cognitive deficits associated with old-age and AD. Lower circulating levels of ghrelin may also reduce hunger levels, and may partially underlie the weight loss associated with older age and AD. Finally, if ghrelin acts to enhance feeding-related zeitgebers, then reductions in circulating ghrelin could dampen food-entrained oscillators and disrupt circadian rhythmicity.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150207&req=5

Figure 2: Hypothesized link between ghrelin and symptoms often associated with aging and Alzheimer’s disease. Ghrelin has been shown to directly affect hippocampal plasticity and neurogenesis, hunger-levels, and circadian processes. Both aging and Alzheimer’s disease (AD) are associated with lower levels of circulating ghrelin. Low ghrelin levels may result in reduced hippocampal plasticity and neurogenesis, and contribute to the cognitive deficits associated with old-age and AD. Lower circulating levels of ghrelin may also reduce hunger levels, and may partially underlie the weight loss associated with older age and AD. Finally, if ghrelin acts to enhance feeding-related zeitgebers, then reductions in circulating ghrelin could dampen food-entrained oscillators and disrupt circadian rhythmicity.
Mentions: Importantly, weight loss may precede the memory loss associated with dementia (Buchman et al., 2005; Stewart et al., 2005; Johnson et al., 2006; Knopman et al., 2007). Because ghrelin is an important regulator of appetite, the age-related weight loss is in agreement with the finding of an age-related decline of plasma ghrelin concentrations as well as the age-related decline in growth-hormone releasing effect of ghrelin (Figure 2; Rigamonti et al., 2002; Broglio et al., 2003). AD patients compared with age-matched controls, also show a reduction in local ghrelin production in the brain (Gahete et al., 2010). Because weight loss appears to precede cognitive impairment in patients with AD (Knopman et al., 2007), metabolic changes could be targets for early detection and prevention of cognitive decline.

Bottom Line: Until effective treatments are developed, promoting overall health may hold potential for delaying the onset or preventing neurodegenerative diseases such as AD.It is well reported that AD is associated with disrupted circadian functioning to a greater extent than normal aging.If the uncoupling of rhythms is contributing to AD progression or exacerbating symptoms, then it may be possible to draw from the food-entrainment literature to identify mechanisms for re-synchronizing rhythms to improve overall health and reduce the severity of symptoms.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, University of Cambridge Cambridge, UK.

ABSTRACT
Alzheimer's disease (AD) is a global epidemic. Unfortunately, we are still without effective treatments or a cure for this disease, which is having devastating consequences for patients, their families, and societies around the world. Until effective treatments are developed, promoting overall health may hold potential for delaying the onset or preventing neurodegenerative diseases such as AD. In particular, chronobiological concepts may provide a useful framework for identifying the earliest signs of age-related disease as well as inexpensive and noninvasive methods for promoting health. It is well reported that AD is associated with disrupted circadian functioning to a greater extent than normal aging. However, it is unclear if the central circadian clock (i.e., the suprachiasmatic nucleus) is dysfunctioning, or whether the synchrony between the central and peripheral clocks that control behavior and metabolic processes are becoming uncoupled. Desynchrony of rhythms can negatively affect health, increasing morbidity and mortality in both animal models and humans. If the uncoupling of rhythms is contributing to AD progression or exacerbating symptoms, then it may be possible to draw from the food-entrainment literature to identify mechanisms for re-synchronizing rhythms to improve overall health and reduce the severity of symptoms. The following review will briefly summarize the circadian system, its potential role in AD, and propose using a feeding-related neuropeptide, such as ghrelin, to synchronize uncoupled rhythms. Synchronizing rhythms may be an inexpensive way to promote healthy aging and delay the onset of neurodegenerative disease such as AD.

No MeSH data available.


Related in: MedlinePlus