Evidence of oxidative damage in Alzheimer's disease brain: Central role for amyloid β-peptide

D. Allan Butterfield; Jennifer Drake; Chava Pocernich; Alessandra Castegna

doi:10.1016/S1471-4914(01)02173-6

Evidence of oxidative damage in Alzheimer's disease brain: Central role for amyloid β-peptide

D. Allan Butterfield, Jennifer Drake, Chava Pocernich, Alessandra Castegna

Research output: Contribution to journal › Review article › peer-review

1070 Citations (SciVal)

Abstract

Amyloid β-peptide (Aβ) is heavily deposited in the brains of Alzheimer's disease (AD) patients. Free-radical oxidative stress, particularly of neuronal lipids, proteins and DNA, is extensive in those AD brain areas in which Aβ is abundant. Recent research suggests that these observations might be linked, and it is postulated that Aβ-induced oxidative stress leads to neurodegeneration in AD brain. Consonant with this postulate, Aβ leads to neuronal lipid peroxidation, protein oxidation and DNA oxidation by means that are inhibited by free-radical antioxidants. Here, we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Aβ in this oxidative stress.

Original language	English
Pages (from-to)	548-554
Number of pages	7
Journal	Trends in Molecular Medicine
Volume	7
Issue number	12
DOIs	https://doi.org/10.1016/S1471-4914(01)02173-6
State	Published - 2001

Bibliographical note

Funding Information:
This work was supported in part by NIH grants to D.A.B. (AG-05119, AG-10836, AG-12423). We thank William Markesbery and Mark Lovell for useful discussions.

ASJC Scopus subject areas

Molecular Medicine
Molecular Biology

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10.1016/S1471-4914(01)02173-6

Cite this

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title = "Evidence of oxidative damage in Alzheimer's disease brain: Central role for amyloid β-peptide",

abstract = "Amyloid β-peptide (Aβ) is heavily deposited in the brains of Alzheimer's disease (AD) patients. Free-radical oxidative stress, particularly of neuronal lipids, proteins and DNA, is extensive in those AD brain areas in which Aβ is abundant. Recent research suggests that these observations might be linked, and it is postulated that Aβ-induced oxidative stress leads to neurodegeneration in AD brain. Consonant with this postulate, Aβ leads to neuronal lipid peroxidation, protein oxidation and DNA oxidation by means that are inhibited by free-radical antioxidants. Here, we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Aβ in this oxidative stress.",

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AU - Drake, Jennifer

AU - Pocernich, Chava

AU - Castegna, Alessandra

N1 - Funding Information: This work was supported in part by NIH grants to D.A.B. (AG-05119, AG-10836, AG-12423). We thank William Markesbery and Mark Lovell for useful discussions.

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AB - Amyloid β-peptide (Aβ) is heavily deposited in the brains of Alzheimer's disease (AD) patients. Free-radical oxidative stress, particularly of neuronal lipids, proteins and DNA, is extensive in those AD brain areas in which Aβ is abundant. Recent research suggests that these observations might be linked, and it is postulated that Aβ-induced oxidative stress leads to neurodegeneration in AD brain. Consonant with this postulate, Aβ leads to neuronal lipid peroxidation, protein oxidation and DNA oxidation by means that are inhibited by free-radical antioxidants. Here, we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Aβ in this oxidative stress.

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Evidence of oxidative damage in Alzheimer's disease brain: Central role for amyloid β-peptide

Abstract

Bibliographical note

ASJC Scopus subject areas

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