Molecular mechanisms of brain aging and neurodegenerative disorders: lessons from dietary restriction

被引:126
作者
Prolla, TA
Mattson, MP
机构
[1] Univ Wisconsin, Dept Genet, Madison, WI 53706 USA
[2] Univ Wisconsin, Dept Med Genet, Madison, WI 53706 USA
[3] NIA, Neurosci Lab, Gerontol Res Ctr, Baltimore, MD 21224 USA
[4] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
关键词
D O I
10.1016/S0166-2236(00)01957-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The application of modern molecular and cell biology technologies to studies of the neurobiology of aging provides a window on the molecular substrates of successful brain aging and neurodegenerative disorders. Aging is associated with increased oxidative stress, disturbances in energy metabolism and inflammation-like processes. Dietary restriction (DR) can extends lifespan and might increase the resistance of the nervous system to age-related neurodegenerative disorders. The neuroprotective effect of DR involves a preconditioning response in which the production of neurotrophic factors and protein chaperones is increased resulting in protection against oxyradical production, stabilization of cellular calcium homeostasis, and inhibition of apoptosis. DR might also enhance neurogenesis, synaptic plasticity and self-repair mechanisms.
引用
收藏
页码:S21 / S31
页数:11
相关论文
共 86 条
[1]   Inflammation and Alzheimer's disease [J].
Akiyama, H ;
Barger, S ;
Barnum, S ;
Bradt, B ;
Bauer, J ;
Cole, GM ;
Cooper, NR ;
Eikelenboom, P ;
Emmerling, M ;
Fiebich, BL ;
Finch, CE ;
Frautschy, S ;
Griffin, WST ;
Hampel, H ;
Hull, M ;
Landreth, G ;
Lue, LF ;
Mrak, R ;
Mackenzie, IR ;
McGeer, PL ;
O'Banion, MK ;
Pachter, J ;
Pasinetti, G ;
Plata-Salaman, C ;
Rogers, J ;
Rydel, R ;
Shen, Y ;
Streit, W ;
Strohmeyer, R ;
Tooyoma, I ;
Van Muiswinkel, FL ;
Veerhuis, R ;
Walker, D ;
Webster, S ;
Wegrzyniak, B ;
Wenk, G ;
Wyss-Coray, T .
NEUROBIOLOGY OF AGING, 2000, 21 (03) :383-421
[2]   Regulation of lifespan by sensory perception in Caenorhabditis elegans [J].
Apfeld, J ;
Kenyon, C .
NATURE, 1999, 402 (6763) :804-809
[3]   Proteomics: new perspectives, new biomedical opportunities [J].
Banks, RE ;
Dunn, MJ ;
Hochstrasser, DF ;
Sanchez, JC ;
Blackstock, W ;
Pappin, DJ ;
Selby, PJ .
LANCET, 2000, 356 (9243) :1749-1756
[4]  
Black IB, 1999, J NEUROBIOL, V41, P108, DOI 10.1002/(SICI)1097-4695(199910)41:1<108::AID-NEU14>3.0.CO
[5]  
2-U
[6]  
Bruce-Keller AJ, 1999, ANN NEUROL, V45, P8, DOI 10.1002/1531-8249(199901)45:1<8::AID-ART4>3.0.CO
[7]  
2-V
[8]   A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease [J].
Chen, GQ ;
Chen, KS ;
Knox, J ;
Inglis, J ;
Bernard, A ;
Martin, SJ ;
Justice, A ;
McConlogue, L ;
Games, D ;
Freedman, SB ;
Morris, RGM .
NATURE, 2000, 408 (6815) :975-979
[9]   POSITIVE CONTROL OF A REGULON FOR DEFENSES AGAINST OXIDATIVE STRESS AND SOME HEAT-SHOCK PROTEINS IN SALMONELLA-TYPHIMURIUM [J].
CHRISTMAN, MF ;
MORGAN, RW ;
JACOBSON, FS ;
AMES, BN .
CELL, 1985, 41 (03) :753-762
[10]   Alzheimer's disease - Etiologies, pathophysiology, cognitive reserve, and treatment opportunities [J].
Cummings, JL ;
Vinters, HV ;
Cole, GM ;
Khachaturian, ZS .
NEUROLOGY, 1998, 51 (01) :S2-S17