Accumulated hippocampal formaldehyde induces age-dependent memory decline
Accumulated hippocampal formaldehyde induces age-dependent memory decline
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海马甲醛累积导致年龄依赖性记忆衰退
DOI：
10.1007/s11357-012-9388-8
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发表时间：
2013-06-01
期刊：
影响因子：
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通讯作者：
He, Rongqiao
中科院分区：
文献类型：
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作者：
Tong, Zhiqian;Han, Chanshuai;He, Rongqiao
衰老是老年动物和人类记忆衰退以及阿尔茨海默病中的重要因素，并且与海马长时程增强（LTP）受损和NR 1/NR 2B表达下调相关。已知气态甲醛暴露会诱导动物记忆丧失和人类认知能力下降;然而，尚不清楚海马体中内源性甲醛的浓度是否升高，以及过量甲醛如何影响衰老过程中的LTP和记忆形成。在目前的研究中，我们报告海马甲醛积累在记忆恶化的疾病，如年龄相关性痴呆。持续腹腔注射甲醛可使正常SD大鼠的空间记忆能力逐渐受损。此外，过量甲醛处理抑制海马LTP的形成，通过阻断N-甲基-d-天冬氨酸（NMDA）受体。超过30天的慢性过量甲醛治疗显着降低海马的活力和下调NMDA受体的NR 1和NR 2B亚基的表达。我们的研究结果表明，过量的内源性甲醛是与年龄相关的记忆衰退疾病的记忆丧失的一个关键因素。
Aging is an important factor in memory decline in aged animals and humans and in Alzheimer's disease and is associated with the impairment of hippocampal long-term potentiation (LTP) and down-regulation of NR1/NR2B expression. Gaseous formaldehyde exposure is known to induce animal memory loss and human cognitive decline; however, it is unclear whether the concentrations of endogenous formaldehyde are elevated in the hippocampus and how excess formaldehyde affects LTP and memory formation during the aging process. In the present study, we report that hippocampal formaldehyde accumulated in memory-deteriorating diseases such as age-related dementia. Spatial memory performance was gradually impaired in normal Sprague-Dawley rats by persistent intraperitoneal injection with formaldehyde. Furthermore, excess formaldehyde treatment suppressed the hippocampal LTP formation by blocking N-methyl-d-aspartate (NMDA) receptor. Chronic excess formaldehyde treatment over a period of 30 days markedly decreased the viability of the hippocampus and down-regulated the expression of the NR1 and NR2B subunits of the NMDA receptor. Our results indicate that excess endogenous formaldehyde is a critical factor in memory loss in age-related memory-deteriorating diseases.