内源性甲醛异常蓄积与记忆衰退

Excess Endogenous Formaldehyde Induces Memory Decline

近期,本实验室报道了内源性甲醛浓度与认知功能损伤程度之间的关系(Neurobiol Aging,2011,32(1):31-41).观察到转基因痴呆小鼠(APP、APP/PS1)及衰老加速型(SAMP8)小鼠脑内甲醛浓度较对照组显著升高.参照痴呆鼠脑内甲醛浓度,实验人员对正常成年小鼠进行注射,导致其视觉空间记忆能力减退.注射甲醛消除剂可以降低老龄大鼠体内甲醛浓度、减少APP痴呆模型小鼠脑内的老年斑,且能观察到记忆功能的改善.临床观察显示,老年痴呆患者尿甲醛浓度与认知功能损伤程度之间呈正相关.甲醛的过量蓄积造成脑慢性损伤,可能是散发性老年记忆衰退的机制之一.

This review focuses on the relationship between excess endogenous formaldehyde and memory decline, as well as multi-factors inducing formaldehyde abnormal accumulation and cognitive impairments. Elevation of endogenous formaldehyde concentrations in Alzheimer＇s animal models and clinical patients was discussed. Injection with formaldehyde （referred to the detected level in the AD animal models） into normal mice obviously induced spatial memory decline. Aging, and some of genetic factors, diet and environmental pollutants led to formaldehyde abnormal accumulation. Formaldehyde scavengers could rescue spatial memory of APP-transgenic mice. These studies addressed that excess formaldehyde-induced damage of brain is one of the critical factors of cognitive impairments of sporadic senile dementia. Scavenging excess formaldehyde may be a novel therapy for Alzheimer＇s disease.