Agnati L F, Leo G, Genedani S, Piron L, Rivera A, Guidolin D, Fuxe K
Department of BioMedical Sciences, University of Modena, Via Campi 287, 41100 Modena, Italy.
J Neural Transm (Vienna). 2009 Aug;116(8):953-74. doi: 10.1007/s00702-008-0150-4. Epub 2008 Nov 19.
In this paper a hypothesis that some special signals ("key-signals" excito-amino acids, beta-amyloid peptides and alpha-synuclein) are not only involved in information handling by the neuronal circuits, but also trigger out substantial structural and/or functional changes in the Central Nervous System (CNS) is introduced. This forces the neuronal circuits to move from one stable state towards a new state, but in doing so these signals became potentially dangerous. Several mechanisms are put in action to protect neurons and glial cells from these potentially harmful signals. However, in agreement with the Red Queen Theory of Ageing (Agnati et al. in Acta Physiol Scand 145:301-309, 1992), it is proposed that during ageing these neuroprotective processes become less effective while, in the meantime, a shortage of brain plasticity occurs together with an increased need of plasticity for repairing the wear and tear of the CNS. The paper presents findings supporting the concept that such key-signals in instances such as ageing may favour neurodegenerative processes in an attempt of maximizing neuronal plasticity.
本文提出了一种假说，即某些特殊信号（“关键信号”——兴奋性氨基酸、β-淀粉样肽和α-突触核蛋白）不仅参与神经回路的信息处理，还会引发中枢神经系统（CNS）实质性的结构和/或功能变化。这迫使神经回路从一种稳定状态转变为一种新状态，但在此过程中，这些信号可能会变得危险。机体启动了多种机制来保护神经元和神经胶质细胞免受这些潜在有害信号的影响。然而，根据衰老的红皇后理论（阿尼亚蒂等人，《生理学杂志》，145:301 - 309，1992年），有人提出，在衰老过程中，这些神经保护过程的效果会降低，与此同时，大脑可塑性会出现不足，而修复中枢神经系统磨损所需的可塑性需求却在增加。本文呈现的研究结果支持了这样一种观点，即在衰老等情况下，此类关键信号可能会促进神经退行性过程，以试图最大化神经元可塑性。
