Barrientos Ruth M, Frank Matthew G, Watkins Linda R, Maier Steven F
Department of Psychology and Neuroscience, University of Colorado at Boulder, Boulder, CO 80309, USA.
Aging Dis. 2010 Jan 1;1(3):212-231.
Healthy aged individuals are more likely to suffer profound memory impairments following a challenging life event such as a severe bacterial infection, surgery, or an intense psychological stressor, than are younger adults. These peripheral challenges are capable of producing a neuroinflammatory response, (e.g., increased pro-inflammatory cytokines), and in the healthy aged brain this response is exaggerated and prolonged. Normal aging primes or sensitizes microglia and this appears to be the source of this amplified response. Among the outcomes of this exaggerated neuroinflammatory response is an impairment in synaptic plasticity, and a reduction in key downstream mediators such as Arc and BDNF. Each of these mechanisms is important for long-term memory formation, and is compromised by elevated pro-inflammatory cytokines. Pharmacological, dietary and physical interventions are discussed as potential therapies to abrogate the challenge-induced neuroinflammatory response, thereby preventing or reducing memory deficits in aged subjects.
与年轻人相比，健康的老年人在经历具有挑战性的生活事件（如严重细菌感染、手术或强烈心理应激源）后更有可能遭受严重的记忆障碍。这些外周挑战能够产生神经炎症反应（例如促炎细胞因子增加），在健康的老年大脑中，这种反应会被放大和延长。正常衰老会使小胶质细胞致敏，这似乎是这种放大反应的根源。这种过度的神经炎症反应的后果之一是突触可塑性受损，以及关键下游介质如Arc和BDNF的减少。这些机制中的每一个对于长期记忆形成都很重要，并且会因促炎细胞因子升高而受到损害。文中讨论了药物、饮食和身体干预作为潜在疗法，以消除挑战诱导的神经炎症反应，从而预防或减少老年受试者的记忆缺陷。
