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.

中文翻译：

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微血管在衰老中的可塑性。

了解与衰老有关的认知下降的基础仍然是神经生物学的主要挑战。定量研究表明，大部分大脑中神经元或突触的数量变化不大，但它们正在进行的替代却减少了，导致衰老时神经元可塑性的显着丧失。衰老还可能以神经元及其联系的解剖学研究无法发现的方式改变神经元的功能和可塑性。由于神经系统依赖于稳定的血液供应，因此任何与衰老相关的微脉管系统变化都可能影响神经元功能。多项研究表明，随着神经系统的衰老，大脑某些区域的微脉管系统会变得稀少，而其余血管的结构也会发生变化。这些变化导致脑血流量（CBF）下降，从而减少了对神经信号的代谢支持，尤其是在神经元活动水平较高时。除了对微血管的直接影响外，衰老还会降低微血管的可塑性和血管对代谢需求变化做出适当反应的能力。微血管可塑性的丧失对神经元信号的代谢支持具有重要的意义，因为成年大脑中的神经发生与毛细血管的生长协调。