Involvements of the lipid peroxidation product, HNE, in the pathogenesis and progression of Alzheimer's disease

被引：226

作者：

Butterfield, D. Allan ^{[1
]}

Lange, Miranda L. Bader ^{[1
]}

Sultana, Rukhsana ^{[1
]}

机构：

[1] Univ Kentucky, Sanders Brown Ctr Aging, Dept Chem, Ctr Membrane Sci, Lexington, KY 40506 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS | 2010年 / 1801卷 / 08期

基金：

美国国家卫生研究院;

关键词：

Lipid peroxidation; Alzheimer's disease; HNE; Amyloid beta-peptide; Proteomics; Oxidatively modified proteins; MILD COGNITIVE IMPAIRMENT; AMYLOID-BETA-PEPTIDE; (1-42)-INDUCED OXIDATIVE STRESS; MEMBRANE PHOSPHOLIPID ASYMMETRY; PROTEOMIC IDENTIFICATION; PHOSPHATIDYLSERINE EXTERNALIZATION; NEURONAL DEATH; BRAIN LEVELS; AMINOPHOSPHOLIPID TRANSLOCASE; HUMAN ERYTHROCYTES;

D O I：

10.1016/j.bbalip.2010.02.005

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：

Alzheimer's disease (AD) is an age-related neurodegenerative disorder. A number of hypotheses have been proposed to explain AD pathogenesis. One such hypothesis proposed to explain AD pathogenesis is the oxidative stress hypothesis. Increased levels of oxidative stress markers including the markers of lipid peroxidation such as acrolein, 4-hydroxy-2-trans-nonenal (HNE), malondialdehyde, etc. are found in brains of AD subjects. In this review, we focus principally on research conducted in the area of HNE in the central nervous system (CNS) of AD and mild cognitive impairment (MCI), and further, we discuss likely consequences of lipid peroxidation with respect to AD pathogenesis and progression. Based on the research conducted so far in the area of lipid peroxidation, it is suggested that lipid accessible antioxidant molecules could be a promising therapeutic approach to treat or slow progression of MCI and AD. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：924 / 929

页数：6

共 80 条

[1] Protection against amyloid beta-peptide (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes by tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester: Implications for Alzheimer's disease [J].

Abdul, HM ;

Butterfield, DA .

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2005, 1741 (1-2) :140-148

[2] Aminophospholipid asymmetry: A matter of life and death [J].

Balasubramanian, K ;

Schroit, AJ .

ANNUAL REVIEW OF PHYSIOLOGY, 2003, 65 :701-734

[3] Coenzyme Q, vitamin E and apo-E alleles in Alzheimer disease [J].

Battino, M ;

Bompadre, S ;

Leone, L ;

Devecchi, E ;

Degiuli, A ;

D'Agostino, F ;

Cambiè, G ;

D'Agostino, M ;

Faggi, L ;

Colturani, G ;

Gorini, A ;

Villa, RF .

BIOFACTORS, 2003, 18 (1-4) :277-281

[4] Role of phenylalanine 20 in Alzheimer's amyloid,β-peptide (1-42)-induced oxidative stress and neurotoxicity [J].

Boyd-Kimball, D ;

Abdul, HM ;

Reed, T ;

Sultana, R ;

Butterfield, DA .

CHEMICAL RESEARCH IN TOXICOLOGY, 2004, 17 (12) :1743-1749

[5] Proteomic identification of proteins specifically oxidized by intracerebral injection of amyloid β-peptide (1-42) into rat brain:: Implications for Alzheimer's disease [J].

Boyd-Kimball, D ;

Sultana, R ;

Poon, HF ;

Lynn, BC ;

Casamenti, F ;

Pepeu, G ;

Klein, JB ;

Butterfield, DA .

NEUROSCIENCE, 2005, 132 (02) :313-324

[6]

Butterfield D.A., 1997, ADV CELL AGING GERON, V2, P161

[7] Roles of amyloid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment [J].

Butterfield, D. Allan ;

Reed, Tanea ;

Newman, Shelley F. ;

Sultana, Rukhsana .

FREE RADICAL BIOLOGY AND MEDICINE, 2007, 43 (05) :658-677

[8] In vivo oxidative stress in brain of Alzheimer disease transgenic mice: Requirement for methionine 35 in amyloid β-peptide of APP [J].

Butterfield, D. Allan ;

Galvan, Veronica ;

Lange, Miranda Bader ;

Tang, Huidong ;

Sowell, Rena A. ;

Spilman, Patricia ;

Fombonne, Joanna ;

Gorostiza, Olivia ;

Zhang, Junli ;

Sultana, Rukhsana ;

Bredesen, Dale E. .

FREE RADICAL BIOLOGY AND MEDICINE, 2010, 48 (01) :136-144

[9] The critical role of methionine 35 in Alzheimer's amyloid-β-peptide (1-42)-induced oxidative stress and neurotoxicity [J].

Butterfield, DA ;

Boyd-Kimball, D .

BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS, 2005, 1703 (02) :149-156

[10]

Butterfield DA, 2002, NEUROBIOL AGING, V23, P655

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