Wilson Iain A, Gallagher Michela, Eichenbaum Howard, Tanila Heikki
Department of Neuroscience and Neurology, University of Kuopio, Kuopio 70211, Finland.
Trends Neurosci. 2006 Dec;29(12):662-70. doi: 10.1016/j.tins.2006.10.002. Epub 2006 Oct 13.
Normal aging is often accompanied by impairments in forming new memories, and studies of aging rodents have revealed structural and functional changes to the hippocampus that might point to the mechanisms behind such memory loss. In this article, we synthesize recent neurobiological and neurophysiological findings into a model of the information-processing circuit of the aging hippocampus. The key point of the model is that small concurrent changes during aging strengthen the auto-associative network of the CA3 subregion at the cost of processing new information coming in from the entorhinal cortex. As a result of such reorganization in aged memory-impaired individuals, information that is already stored would become the dominant pattern of the hippocampus to the detriment of the ability to encode new information.
正常衰老往往伴随着形成新记忆的能力受损,对衰老啮齿动物的研究揭示了海马体的结构和功能变化,这些变化可能指向这种记忆丧失背后的机制。在本文中,我们将近期的神经生物学和神经生理学研究结果综合成一个衰老海马体信息处理回路的模型。该模型的关键点在于,衰老过程中同时发生的微小变化以处理来自内嗅皮质的新信息为代价,强化了CA3子区域的自联想网络。由于老年记忆受损个体中的这种重组,已经存储的信息将成为海马体的主导模式,从而损害编码新信息的能力。