Loss of proteins regulating synaptic plasticity in normal aging of the human brain and in Alzheimer disease
Loss of proteins regulating synaptic plasticity in normal aging of the human brain and in Alzheimer disease
复制标题
DOI：
10.1097/00005072-199906000-00008
复制
发表时间：
1999-06-01
影响因子：
3.2
通讯作者：
Rapoport, SI
中科院分区：
文献类型：
--
作者：
Hatanpää, K;Isaacs, KR;Rapoport, SI
最近的研究表明，与正常衰老相关的认知障碍是由于神经元功能障碍，而不是神经元或突触的丢失。为了表征这种功能障碍，在大脑皮层的尸检样品中定量神经元功能的分子指标。在正常衰老过程中，最显着的下降是在参与轴突和树突的结构可塑性（重塑）的突触蛋白水平。阿尔茨海默病是老年痴呆症最常见的原因，与dreplastin水平额外下降81%有关，dreplastin是一种调节突触后可塑性的蛋白质。可塑性机制的紊乱可能导致衰老和阿尔茨海默病期间的认知功能障碍。
Recent studies suggest that the cognitive impairment associated with normal aging is due to neuronal dysfunction rather than to loss of neurons or synapses. To characterize this dysfunction, molecular indices of neuronal function were quantified in autopsy samples of cerebral cortex. During normal aging, the most dramatic decline was found in levels of synaptic proteins involved in structural plasticity (remodeling) of axons and dendrites. Alzheimer disease, the most common cause of dementia in the elderly, was associated with an additional 81% decrease in levels of drebrin, a protein regulating postsynaptic plasticity. Disturbed mechanisms of plasticity may contribute to cognitive dysfunction during aging and in Alzheimer disease.