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The impact of dietary energy intake on cognitive aging.

Mattson MP - Front Aging Neurosci (2010)

Bottom Line: Our findings from studies of animal models suggest that dietary energy restriction can enhance neural plasticity and reduce the vulnerability of the brain to age-related dysfunction and disease.Dietary energy restriction may exert beneficial effects on the brain by engaging adaptive cellular stress response pathways resulting in the up-regulation of genes that encode proteins that promote neural plasticity and cell survival (e.g., neurotrophic factors, protein chaperones and redox enzymes).Alternate day calorie restriction, novel insulin-sensitizing and neuroprotective agents, and drugs that activate adaptive stress response pathways, are examples of approaches for preserving cognitive function that show promise in preclinical studies.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Neurosciences, National Institute on Aging Intramural Research Program Baltimore, MD, USA.

ABSTRACT
Rodents that are insulin resistant and obese as the result of genetic factors, overeating and/or a sedentary lifestyle, exhibit cognitive deficits that worsen with advancing age compared to their more svelte counterparts. Data from epidemiological and clinical studies suggest similar adverse effects of excessive dietary energy intake and insulin resistance on cognition in humans. Our findings from studies of animal models suggest that dietary energy restriction can enhance neural plasticity and reduce the vulnerability of the brain to age-related dysfunction and disease. Dietary energy restriction may exert beneficial effects on the brain by engaging adaptive cellular stress response pathways resulting in the up-regulation of genes that encode proteins that promote neural plasticity and cell survival (e.g., neurotrophic factors, protein chaperones and redox enzymes). Two energy state-sensitive factors that are proving particularly important in regulating energy balance and improving/preserving cognitive function are brain-derived neurotrophic factor and glucagon-like peptide 1. Alternate day calorie restriction, novel insulin-sensitizing and neuroprotective agents, and drugs that activate adaptive stress response pathways, are examples of approaches for preserving cognitive function that show promise in preclinical studies.

No MeSH data available.


Related in: MedlinePlus

Pivotal roles for brain-derived neurotrophic factor in the integration of CNS neuroplasticity and peripheral energy metabolism. The production of BDNF by neurons in the central nervous system (CNS) is increased in response to the metabolic and electrochemical challenged imposed upon the neurons by dietary energy restriction, exercise and cognitive stimulation. BDNF acts a multiple levels of the nervous system to engage adaptive responses to the environmental demands. BDNF acts on: neurons in the hypothalamus to reduce appetite; cells in the hippocampus to enhance synaptic plasticity, neurogenesis and learning and memory ability; neurons in the autonomic nervous system (ANS) which innervate peripheral organs (heart, muscle, pancreas, liver and others); and neurons in the peripheral nervous system (e.g., lower motor neurons that innervate skeletal muscle cells). As of one or more of these actions, BDNF improves peripheral insulin sensitivity. By direct actions within the CNS, and by indirect effects on energy metabolism, BDNF may protect the nervous system against injury and disease. BDNF is also produced by peripheral cells and circulates in the blood, although its functions in the periphery are not known. PNS, peripheral nervous system.
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Figure 3: Pivotal roles for brain-derived neurotrophic factor in the integration of CNS neuroplasticity and peripheral energy metabolism. The production of BDNF by neurons in the central nervous system (CNS) is increased in response to the metabolic and electrochemical challenged imposed upon the neurons by dietary energy restriction, exercise and cognitive stimulation. BDNF acts a multiple levels of the nervous system to engage adaptive responses to the environmental demands. BDNF acts on: neurons in the hypothalamus to reduce appetite; cells in the hippocampus to enhance synaptic plasticity, neurogenesis and learning and memory ability; neurons in the autonomic nervous system (ANS) which innervate peripheral organs (heart, muscle, pancreas, liver and others); and neurons in the peripheral nervous system (e.g., lower motor neurons that innervate skeletal muscle cells). As of one or more of these actions, BDNF improves peripheral insulin sensitivity. By direct actions within the CNS, and by indirect effects on energy metabolism, BDNF may protect the nervous system against injury and disease. BDNF is also produced by peripheral cells and circulates in the blood, although its functions in the periphery are not known. PNS, peripheral nervous system.

Mentions: BDNF may also act centrally to affect energy metabolism more directly and acutely. Infusion of BDNF into the brains of diabetic mice improved their peripheral insulin sensitivity, apparently by a mechanism independent of a change in food intake (Nonomura et al., 2001). One possible mechanism by which this might occur involves modulation of the autonomic nervous system (Figure 3). Indeed, by comparing the heart rate variability (HRV) of mice on ad libitum control diet with the HRV of mice on either ADF or limited daily feeding dietary restriction, we showed that dietary energy restriction results in a reduction in resting heart rate and an increase of HRV in rats (Mager et al., 2006). Data in the latter study suggested that dietary energy restriction shifts the autonomic control of the heart such that parasympathetic (acetylcholine) activity is increased. More recently, we found that heart rate is reduced and HRV increased, within minutes of infusion of BDNF into the third ventricle of mice (author's unpublished data).


The impact of dietary energy intake on cognitive aging.

Mattson MP - Front Aging Neurosci (2010)

Pivotal roles for brain-derived neurotrophic factor in the integration of CNS neuroplasticity and peripheral energy metabolism. The production of BDNF by neurons in the central nervous system (CNS) is increased in response to the metabolic and electrochemical challenged imposed upon the neurons by dietary energy restriction, exercise and cognitive stimulation. BDNF acts a multiple levels of the nervous system to engage adaptive responses to the environmental demands. BDNF acts on: neurons in the hypothalamus to reduce appetite; cells in the hippocampus to enhance synaptic plasticity, neurogenesis and learning and memory ability; neurons in the autonomic nervous system (ANS) which innervate peripheral organs (heart, muscle, pancreas, liver and others); and neurons in the peripheral nervous system (e.g., lower motor neurons that innervate skeletal muscle cells). As of one or more of these actions, BDNF improves peripheral insulin sensitivity. By direct actions within the CNS, and by indirect effects on energy metabolism, BDNF may protect the nervous system against injury and disease. BDNF is also produced by peripheral cells and circulates in the blood, although its functions in the periphery are not known. PNS, peripheral nervous system.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2874403&req=5

Figure 3: Pivotal roles for brain-derived neurotrophic factor in the integration of CNS neuroplasticity and peripheral energy metabolism. The production of BDNF by neurons in the central nervous system (CNS) is increased in response to the metabolic and electrochemical challenged imposed upon the neurons by dietary energy restriction, exercise and cognitive stimulation. BDNF acts a multiple levels of the nervous system to engage adaptive responses to the environmental demands. BDNF acts on: neurons in the hypothalamus to reduce appetite; cells in the hippocampus to enhance synaptic plasticity, neurogenesis and learning and memory ability; neurons in the autonomic nervous system (ANS) which innervate peripheral organs (heart, muscle, pancreas, liver and others); and neurons in the peripheral nervous system (e.g., lower motor neurons that innervate skeletal muscle cells). As of one or more of these actions, BDNF improves peripheral insulin sensitivity. By direct actions within the CNS, and by indirect effects on energy metabolism, BDNF may protect the nervous system against injury and disease. BDNF is also produced by peripheral cells and circulates in the blood, although its functions in the periphery are not known. PNS, peripheral nervous system.
Mentions: BDNF may also act centrally to affect energy metabolism more directly and acutely. Infusion of BDNF into the brains of diabetic mice improved their peripheral insulin sensitivity, apparently by a mechanism independent of a change in food intake (Nonomura et al., 2001). One possible mechanism by which this might occur involves modulation of the autonomic nervous system (Figure 3). Indeed, by comparing the heart rate variability (HRV) of mice on ad libitum control diet with the HRV of mice on either ADF or limited daily feeding dietary restriction, we showed that dietary energy restriction results in a reduction in resting heart rate and an increase of HRV in rats (Mager et al., 2006). Data in the latter study suggested that dietary energy restriction shifts the autonomic control of the heart such that parasympathetic (acetylcholine) activity is increased. More recently, we found that heart rate is reduced and HRV increased, within minutes of infusion of BDNF into the third ventricle of mice (author's unpublished data).

Bottom Line: Our findings from studies of animal models suggest that dietary energy restriction can enhance neural plasticity and reduce the vulnerability of the brain to age-related dysfunction and disease.Dietary energy restriction may exert beneficial effects on the brain by engaging adaptive cellular stress response pathways resulting in the up-regulation of genes that encode proteins that promote neural plasticity and cell survival (e.g., neurotrophic factors, protein chaperones and redox enzymes).Alternate day calorie restriction, novel insulin-sensitizing and neuroprotective agents, and drugs that activate adaptive stress response pathways, are examples of approaches for preserving cognitive function that show promise in preclinical studies.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Neurosciences, National Institute on Aging Intramural Research Program Baltimore, MD, USA.

ABSTRACT
Rodents that are insulin resistant and obese as the result of genetic factors, overeating and/or a sedentary lifestyle, exhibit cognitive deficits that worsen with advancing age compared to their more svelte counterparts. Data from epidemiological and clinical studies suggest similar adverse effects of excessive dietary energy intake and insulin resistance on cognition in humans. Our findings from studies of animal models suggest that dietary energy restriction can enhance neural plasticity and reduce the vulnerability of the brain to age-related dysfunction and disease. Dietary energy restriction may exert beneficial effects on the brain by engaging adaptive cellular stress response pathways resulting in the up-regulation of genes that encode proteins that promote neural plasticity and cell survival (e.g., neurotrophic factors, protein chaperones and redox enzymes). Two energy state-sensitive factors that are proving particularly important in regulating energy balance and improving/preserving cognitive function are brain-derived neurotrophic factor and glucagon-like peptide 1. Alternate day calorie restriction, novel insulin-sensitizing and neuroprotective agents, and drugs that activate adaptive stress response pathways, are examples of approaches for preserving cognitive function that show promise in preclinical studies.

No MeSH data available.


Related in: MedlinePlus