Protective and rescuing abilities of IGF-I and some putative free radical scavengers against β-amyloid-inducing toxicity in neurons

被引:34
作者
Doré, S [1 ]
Bastianetto, S [1 ]
Kar, S [1 ]
Quirion, R [1 ]
机构
[1] McGill Univ, Douglas Hosp, Res Ctr, Verdun, PQ H4H 1R3, Canada
来源
NEUROPROTECTIVE AGENTS: FOURTH INTERNATIONAL CONFERENCE | 1999年 / 890卷
关键词
D O I
10.1111/j.1749-6632.1999.tb08015.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
beta-Amyloid (A beta) peptides are most likely involved in the neurodegenerative process occurring in Alzheimer's Disease (AD) and are enriched in senile plaques, The mechanisms of A beta toxicity are not clear but likely involve free radicals and apoptosis. Much interest is currently aiming at developing effective approaches to block A beta toxicity in order to slow down disease progression. In that context, we are particularly interested in studying the role of insulin like growth factors, particularly IGF-I and purported free radical scavengers including a Gingko biloba extract (EGb761) as blocker of A beta toxicity in a simple irt vitro model of hippocampal primary cultures, We observed that both IGF-I and EGb761 are unique in that they are able not only to protect but even to rescue neurons against A beta toxicity. These results are summarized here and possible mechanisms of action are discussed to explain the protective properties of these two classes of agents.
引用
收藏
页码:356 / 364
页数:9
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