Interplay between oxidative damage, protein synthesis, and protein degradation in Alzheimer's disease

被引:14
作者
Keller, Jeffrey N. [1 ]
机构
[1] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA
来源
JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY | 2006年
关键词
D O I
10.1155/JBB/2006/12129
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Protein synthesis and protein degradation are highly regulated cellular processes that are essential to maintaining cell viability. Numerous studies now indicate that protein synthesis and protein degradation are significantly altered in Alzheimer's disease (AD), with impairments in these two processes potentially contributing to AD pathogenesis. Alterations in steady state protein regulation may be a particularly important factor in regulating whether cells maintain homeostasis in response to oxidative damage, or conversely whether oxidative stress is induced by oxidative damage. The focus of this review is to discuss recent findings on each of these topics, and to discuss their importance to the onset and progression of AD. Copyright (c) 2006 Jeffrey N. Keller.
引用
收藏
页数:3
相关论文
共 20 条
[1]   The neuropathogenic contributions of lysosomal dysfunction [J].
Bahr, BA ;
Bendiske, J .
JOURNAL OF NEUROCHEMISTRY, 2002, 83 (03) :481-489
[2]   Ribosome dysfunction is an early event in Alzheimer's disease [J].
Ding, QX ;
Markesbery, WR ;
Chen, QH ;
Li, F ;
Keller, JN .
JOURNAL OF NEUROSCIENCE, 2005, 25 (40) :9171-9175
[3]   The relationship between oxidative/nitrative stress and pathological inclusions in Alzheimer's and Parkinson's diseases [J].
Giasson, BI ;
Ischiropoulos, H ;
Lee, VMY ;
Trojanowski, JQ .
FREE RADICAL BIOLOGY AND MEDICINE, 2002, 32 (12) :1264-1275
[4]   Selective degradation of oxidatively modified protein substrates by the proteasome [J].
Grune, T ;
Merker, K ;
Sandig, G ;
Davies, KJA .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 305 (03) :709-718
[5]   Ribosomal RNA in Alzheimer disease is oxidized by bound redox-active iron [J].
Honda, K ;
Smith, MA ;
Zhu, XW ;
Baus, D ;
Merrick, WC ;
Tartakoff, AM ;
Hattier, T ;
Harris, PL ;
Siedlak, SL ;
Fujioka, H ;
Liu, Q ;
Moreira, PI ;
Miller, FP ;
Nunomura, A ;
Shimohama, S ;
Perry, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (22) :20978-20986
[6]   Understanding cell death in Parkinson's disease [J].
Jenner, P ;
Olanow, CW .
ANNALS OF NEUROLOGY, 1998, 44 (03) :S72-S84
[7]   Evidence of increased oxidative damage in subjects with mild cognitive impairment [J].
Keller, JN ;
Schmitt, FA ;
Scheff, SW ;
Ding, Q ;
Chen, Q ;
Butterfield, DA ;
Markesbery, WR .
NEUROLOGY, 2005, 64 (07) :1152-1156
[8]   Remodeling Chromatin and Stress Resistance in the Central Nervous System: Histone Deacetylase Inhibitors as Novel and Broadly Effective Neuroprotective Agents [J].
Langley, Brett ;
Gensert, Joann M. ;
Beal, M. Flint ;
Ratan, Rajiv R. .
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS, 2005, 4 (01) :41-50
[9]   ALZHEIMERS DISEASE-ASSOCIATED REDUCTION OF POLYSOMAL MESSENGER-RNA TRANSLATION [J].
LANGSTROM, NS ;
ANDERSON, JP ;
LINDROOS, HG ;
WINBLAD, B ;
WALLACE, WC .
MOLECULAR BRAIN RESEARCH, 1989, 5 (04) :259-269
[10]   Lipid peroxidation is an early event in the brain in amnestic mild cognitive impairment [J].
Markesbery, WR ;
Kryscio, RJ ;
Lovell, MA ;
Morrow, JD .
ANNALS OF NEUROLOGY, 2005, 58 (05) :730-735