Microvascular plasticity in aging.
Understanding the bases of aging-related cognitive decline remains a central challenge in neurobiology. Quantitative studies reveal little change in the number of neurons or synapses in most of the brain but their ongoing replacement is reduced, resulting in a significant loss of neuronal plasticity with senescence. Aging also may alter neuronal function and plasticity in ways that are not evident from anatomical studies of neurons and their connections. Since the nervous system is dependent upon a consistent blood supply, any aging-related changes in the microvasculature could affect neuronal function. Several studies suggest that, as the nervous system ages, there is a rarefaction of the microvasculature in some regions of the brain, as well as changes in the structure of the remaining vessels. These changes contribute to a decline in cerebral blood flow (CBF) that reduces metabolic support for neural signaling, particularly when levels of neuronal activity are high. In addition to direct effects on the microvasculature, aging reduces microvascular plasticity and the ability of the vessels to respond appropriately to changes in metabolic demand. This loss of microvascular plasticity has significance beyond metabolic support for neuronal signaling, since neurogenesis in the adult brain is regulated coordinately with capillary growth.
Riddle
David R
DR
Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1010, USA. driddle@wfubmc.edu
Sonntag
William E
WE
Lichtenwalner
Robin J
RJ
D000375:Aging / Q000502:physiology*; D000818:Animals; D001808:Blood Vessels / Q000502:physiology*; D001921:Brain / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006801:Humans; D008833:Microcirculation / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D015398:Signal Transduction