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
相关论文
共 52 条
[41]   EXPRESSION OF THE LOW-AFFINITY NERVE GROWTH-FACTOR RECEPTOR ENHANCES BETA-AMYLOID PEPTIDE TOXICITY [J].
RABIZADEH, S ;
BITLER, CM ;
BUTCHER, LL ;
BREDESEN, DE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (22) :10703-10706
[42]   A DOUBLE-BLIND, PLACEBO CONTROLLED-STUDY OF GINKGO-BILOBA EXTRACT (TANAKAN) IN ELDERLY OUTPATIENTS WITH MILD TO MODERATE MEMORY IMPAIRMENT [J].
RAI, GS ;
SHOVLIN, C ;
WESNES, KA .
CURRENT MEDICAL RESEARCH AND OPINION, 1991, 12 (06) :350-355
[43]   Transforming growth factors-beta protect primary rat hippocampal neuronal cultures from degeneration induced by beta-amyloid peptide [J].
Ren, RF ;
Flanders, KC .
BRAIN RESEARCH, 1996, 732 (1-2) :16-24
[44]  
RODRIGUEZTARDUCHY G, 1992, J IMMUNOL, V149, P535
[45]   BETA-AMYLOID-(1-42) IS A MAJOR COMPONENT OF CEREBROVASCULAR AMYLOID DEPOSITS - IMPLICATIONS FOR THE PATHOLOGY OF ALZHEIMER-DISEASE [J].
ROHER, AE ;
LOWENSON, JD ;
CLARKE, S ;
WOODS, AS ;
COTTER, RJ ;
GOWING, E ;
BALL, MJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (22) :10836-10840
[46]   EFFECT OF AGING ON THE KINETIC CHARACTERISTICS OF THE INSULIN-RECEPTOR AUTOPHOSPHORYLATION IN RAT ADIPOCYTES [J].
RUIZ, P ;
PULIDO, JA ;
MARTINEZ, C ;
CARRASCOSA, JM ;
SATRUSTEGUI, J ;
ANDRES, A .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1992, 296 (01) :231-238
[47]   NORMAL AND ABNORMAL BIOLOGY OF THE BETA-AMYLOID PRECURSOR PROTEIN [J].
SELKOE, DJ .
ANNUAL REVIEW OF NEUROSCIENCE, 1994, 17 :489-517
[48]  
SELL C, 1995, CANCER RES, V55, P303
[49]   The neuroprotective properties of the Ginkgo biloba leaf: A review of the possible relationship to platelet-activating factor (PAF) [J].
Smith, PF ;
Maclennan, K ;
Darlington, CL .
JOURNAL OF ETHNOPHARMACOLOGY, 1996, 50 (03) :131-139
[50]   Insulin and epidermal growth factor receptors regulate distinct pools of Grb2-SOS in the control of ras activation [J].
Waters, SB ;
Chen, D ;
Kao, AW ;
Okada, S ;
Holt, KH ;
Pessin, JE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (30) :18224-18230