Reversal of glial and neurovascular markers of unhealthy brain aging by exercise in middle-aged female mice
Healthy brain aging and cognitive function are promoted by exercise. The benefits of exercise are attributed to several mechanisms, many which highlight its neuroprotective role via actions that enhance neurogenesis, neuronal morphology and/or neurotrophin release. However, the brain is also compose...
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| Veröffentlicht in: | PloS one 2011-10, Vol.6 (10), p.e26812-e26812 |
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| creator | Latimer, Caitlin S Searcy, James L Bridges, Michael T Brewer, Lawrence D Popović, Jelena Blalock, Eric M Landfield, Philip W Thibault, Olivier Porter, Nada M |
| description | Healthy brain aging and cognitive function are promoted by exercise. The benefits of exercise are attributed to several mechanisms, many which highlight its neuroprotective role via actions that enhance neurogenesis, neuronal morphology and/or neurotrophin release. However, the brain is also composed of glial and vascular elements, and comparatively less is known regarding the effects of exercise on these components in the aging brain. Here, we show that aerobic exercise at mid-age decreased markers of unhealthy brain aging including astrocyte hypertrophy, a hallmark of brain aging. Middle-aged female mice were assigned to a sedentary group or provided a running wheel for six weeks. Exercise decreased hippocampal astrocyte and myelin markers of aging but increased VEGF, a marker of angiogenesis. Brain vascular casts revealed exercise-induced structural modifications associated with improved endothelial function in the periphery. Our results suggest that age-related astrocyte hypertrophy/reactivity and myelin dysregulation are aggravated by a sedentary lifestyle and accompanying reductions in vascular function. However, these effects appear reversible with exercise initiated at mid-age. As this period of the lifespan coincides with the appearance of multiple markers of brain aging, including initial signs of cognitive decline, it may represent a window of opportunity for intervention as the brain appears to still possess significant vascular plasticity. These results may also have particular implications for aging females who are more susceptible than males to certain risk factors which contribute to vascular aging. |
| doi_str_mv | 10.1371/journal.pone.0026812 |
| format | Article |
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The benefits of exercise are attributed to several mechanisms, many which highlight its neuroprotective role via actions that enhance neurogenesis, neuronal morphology and/or neurotrophin release. However, the brain is also composed of glial and vascular elements, and comparatively less is known regarding the effects of exercise on these components in the aging brain. Here, we show that aerobic exercise at mid-age decreased markers of unhealthy brain aging including astrocyte hypertrophy, a hallmark of brain aging. Middle-aged female mice were assigned to a sedentary group or provided a running wheel for six weeks. Exercise decreased hippocampal astrocyte and myelin markers of aging but increased VEGF, a marker of angiogenesis. Brain vascular casts revealed exercise-induced structural modifications associated with improved endothelial function in the periphery. Our results suggest that age-related astrocyte hypertrophy/reactivity and myelin dysregulation are aggravated by a sedentary lifestyle and accompanying reductions in vascular function. However, these effects appear reversible with exercise initiated at mid-age. As this period of the lifespan coincides with the appearance of multiple markers of brain aging, including initial signs of cognitive decline, it may represent a window of opportunity for intervention as the brain appears to still possess significant vascular plasticity. These results may also have particular implications for aging females who are more susceptible than males to certain risk factors which contribute to vascular aging.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0026812</identifier><identifier>PMID: 22046366</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Aging ; Aging - physiology ; Angiogenesis ; Animal cognition ; Animals ; Atherosclerosis ; Biology ; Biomarkers ; Brain ; Brain - blood supply ; Brain - pathology ; Brain - physiopathology ; Brain research ; Cardiovascular Physiological Phenomena ; Casts ; Cognitive ability ; Disease control ; Exercise ; Female ; Females ; Health care ; Hippocampus ; Hypertension ; Hypertrophy ; Laboratory animals ; Life span ; Males ; Markers ; Medicine ; Metabolism ; Mice ; Microscopy ; Middle age ; Musculoskeletal system ; Myelin ; Neurogenesis ; Neuroglia - pathology ; Neuronal-glial interactions ; Neurons ; Neurophysiology ; Neuroprotection ; Neurosciences ; Pharmacology ; Physical Conditioning, Animal - physiology ; Physical fitness ; Physical training ; Public health ; Risk analysis ; Risk factors ; Rodents ; Trends ; Vascular endothelial growth factor ; Wheel running ; Womens health</subject><ispartof>PloS one, 2011-10, Vol.6 (10), p.e26812-e26812</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Latimer et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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These results may also have particular implications for aging females who are more susceptible than males to certain risk factors which contribute to vascular aging.</description><subject>Age</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Angiogenesis</subject><subject>Animal cognition</subject><subject>Animals</subject><subject>Atherosclerosis</subject><subject>Biology</subject><subject>Biomarkers</subject><subject>Brain</subject><subject>Brain - blood supply</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Brain research</subject><subject>Cardiovascular Physiological Phenomena</subject><subject>Casts</subject><subject>Cognitive ability</subject><subject>Disease control</subject><subject>Exercise</subject><subject>Female</subject><subject>Females</subject><subject>Health care</subject><subject>Hippocampus</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>Laboratory animals</subject><subject>Life span</subject><subject>Males</subject><subject>Markers</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Microscopy</subject><subject>Middle age</subject><subject>Musculoskeletal system</subject><subject>Myelin</subject><subject>Neurogenesis</subject><subject>Neuroglia - 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The benefits of exercise are attributed to several mechanisms, many which highlight its neuroprotective role via actions that enhance neurogenesis, neuronal morphology and/or neurotrophin release. However, the brain is also composed of glial and vascular elements, and comparatively less is known regarding the effects of exercise on these components in the aging brain. Here, we show that aerobic exercise at mid-age decreased markers of unhealthy brain aging including astrocyte hypertrophy, a hallmark of brain aging. Middle-aged female mice were assigned to a sedentary group or provided a running wheel for six weeks. Exercise decreased hippocampal astrocyte and myelin markers of aging but increased VEGF, a marker of angiogenesis. Brain vascular casts revealed exercise-induced structural modifications associated with improved endothelial function in the periphery. Our results suggest that age-related astrocyte hypertrophy/reactivity and myelin dysregulation are aggravated by a sedentary lifestyle and accompanying reductions in vascular function. However, these effects appear reversible with exercise initiated at mid-age. As this period of the lifespan coincides with the appearance of multiple markers of brain aging, including initial signs of cognitive decline, it may represent a window of opportunity for intervention as the brain appears to still possess significant vascular plasticity. These results may also have particular implications for aging females who are more susceptible than males to certain risk factors which contribute to vascular aging.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22046366</pmid><doi>10.1371/journal.pone.0026812</doi><tpages>e26812</tpages><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Age Aging Aging - physiology Angiogenesis Animal cognition Animals Atherosclerosis Biology Biomarkers Brain Brain - blood supply Brain - pathology Brain - physiopathology Brain research Cardiovascular Physiological Phenomena Casts Cognitive ability Disease control Exercise Female Females Health care Hippocampus Hypertension Hypertrophy Laboratory animals Life span Males Markers Medicine Metabolism Mice Microscopy Middle age Musculoskeletal system Myelin Neurogenesis Neuroglia - pathology Neuronal-glial interactions Neurons Neurophysiology Neuroprotection Neurosciences Pharmacology Physical Conditioning, Animal - physiology Physical fitness Physical training Public health Risk analysis Risk factors Rodents Trends Vascular endothelial growth factor Wheel running Womens health |
| title | Reversal of glial and neurovascular markers of unhealthy brain aging by exercise in middle-aged female mice |
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