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Article: Oxidative Stress in Brain in Amnestic Mild Cognitive Impairment.

Butterfield, D Allan

2023 Volume 12, Issue 2

Abstract: Amnestic mild cognitive impairment (MCI), arguably the earliest clinical stage of Alzheimer disease (AD), is characterized by normal activities of daily living but with memory issues but no dementia. Oxidative stress, with consequent damaged key proteins ...

Abstract	Amnestic mild cognitive impairment (MCI), arguably the earliest clinical stage of Alzheimer disease (AD), is characterized by normal activities of daily living but with memory issues but no dementia. Oxidative stress, with consequent damaged key proteins and lipids, are prominent even in this early state of AD. This review article outlines oxidative stress in MCI and how this can account for neuronal loss and potential therapeutic strategies to slow progression to AD.
Language	English
Publishing date	2023-02-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12020462
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Article ; Online: Oxidative Stress in Brain in Amnestic Mild Cognitive Impairment

Butterfield, D. Allan

Antioxidants. 2023 Feb. 11, v. 12, no. 2

2023

Abstract	Amnestic mild cognitive impairment (MCI), arguably the earliest clinical stage of Alzheimer disease (AD), is characterized by normal activities of daily living but with memory issues but no dementia. Oxidative stress, with consequent damaged key proteins and lipids, are prominent even in this early state of AD. This review article outlines oxidative stress in MCI and how this can account for neuronal loss and potential therapeutic strategies to slow progression to AD.
Keywords	Alzheimer disease ; brain ; cognitive disorders ; memory ; neurons ; oxidative stress ; therapeutics
Language	English
Dates of publication	2023-0211
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12020462
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Article ; Online: Ubiquitin carboxyl-terminal hydrolase L-1 in brain: Focus on its oxidative/nitrosative modification and role in brains of subjects with Alzheimer disease and mild cognitive impairment.

Butterfield, D Allan

Free radical biology & medicine

2021 Volume 177, Page(s) 278–286

Abstract: Neurons must remove aggregated, damaged proteins in order to survive. Among the ways of facilitating this protein quality control is the ubiquitin-proteasomal system (UPS). Aggregated, damaged proteins are targeted for destruction by the UPS by acquiring ...

Abstract	Neurons must remove aggregated, damaged proteins in order to survive. Among the ways of facilitating this protein quality control is the ubiquitin-proteasomal system (UPS). Aggregated, damaged proteins are targeted for destruction by the UPS by acquiring a polymer of ubiquitin residues that serves as a signal for transport to the UPS. However, before this protein degradation can occur, the polyubiquitin chain must be removed, one residue at a time, a reaction facilitated by the enzyme, ubiquitin C-terminal hydrolase (UCH-L1). In Alzheimer disease brain, this normally abundant protein is both of lower levels and oxidatively and nitrosatively modified than in control brain. This causes diminished function of the pleiotropic UCH-L1 enzyme with consequent pathological alterations in AD brain, and the author asserts the oxidative and nitrosative alterations of UCH-L1 are major contributors to mechanisms of neuronal death in this devastating dementing disorder and its earlier stage, mild cognitive impairment (MCI). This review paper outlines these findings in AD and MCI brain.
MeSH term(s)	Alzheimer Disease/genetics ; Brain/metabolism ; Cognitive Dysfunction/genetics ; Humans ; Oxidative Stress ; Ubiquitin/metabolism ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	Ubiquitin ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2021-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2021.10.036
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Article ; Online: Neurodegeneration and regeneration: Antioxidants and redox signaling.

Zarkovic, Neven / Butterfield, D Allan

Free radical biology & medicine

2022 Volume 189, Page(s) 154–156

MeSH term(s)	Antioxidants/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Signal Transduction
Chemical Substances	Antioxidants
Language	English
Publishing date	2022-08-01
Publishing country	United States
Document type	Editorial
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2022.07.017
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Article ; Online: Brain lipid peroxidation and alzheimer disease: Synergy between the Butterfield and Mattson laboratories.

Butterfield, D Allan

Ageing research reviews

2020 Volume 64, Page(s) 101049

Abstract: ... that is highly neurotoxic and critical to the pathophysiology of AD. The Butterfield laboratory is one ...

Abstract	Brains from persons with Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI), exhibit high levels of oxidative damage, including that to phospholipids. One type of oxidative damage is lipid peroxidation, the most important index of which is protein-bound 4-hydroxy-2-trans-nonenal (HNE). This highly reactive alkenal changes the conformations and lowers the activities of brain proteins to which HNE is covalently bound. Evidence exists that suggests that lipid peroxidation is the first type of oxidative damage associated with amyloid β-peptide (Aβ), a 38-42 amino acid peptide that is highly neurotoxic and critical to the pathophysiology of AD. The Butterfield laboratory is one of, if not the, first research group to show that Aβ42 oligomers led to lipid peroxidation and to demonstrate this modification in brains of subjects with AD and MCI. The Mattson laboratory, particularly when Dr. Mattson was a faculty member at the University of Kentucky, also showed evidence for lipid peroxidation associated with Aβ peptides, mostly in in vitro systems. Consequently, there is synergy between our two laboratories. Since this special tribute issue of Aging Research Reviews is dedicated to the career of Dr. Mattson, a review of some aspects of this synergy of lipid peroxidation and its relevance to AD, as well as the role of lipid peroxidation in the progression of this dementing disorder seems germane. Accordingly, this review outlines some of the individual and/or complementary research on lipid peroxidation related to AD published from our two laboratories either separately or jointly.
MeSH term(s)	Alzheimer Disease ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Humans ; Laboratories ; Lipid Peroxidation ; Oxidative Stress
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2020-03-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2020.101049
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Article ; Online: Cellular Stress Response (Hormesis) in Response to Bioactive Nutraceuticals with Relevance to Alzheimer Disease.

Butterfield, D Allan / Boyd-Kimball, Debra / Reed, Tanea T

Antioxidants & redox signaling

2023 Volume 38, Issue 7-9, Page(s) 643–669

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Animals ; Alzheimer Disease/metabolism ; NF-E2-Related Factor 2/metabolism ; Hormesis ; Heme Oxygenase-1/metabolism ; Oxidative Stress ; Dietary Supplements
Chemical Substances	NF-E2-Related Factor 2 ; Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2023-01-13
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2022.0214
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Article ; Online: Altered Metabolism in Alzheimer Disease Brain: Role of Oxidative Stress.

Rummel, Nicole G / Butterfield, D Allan

Antioxidants & redox signaling

2021 Volume 36, Issue 16-18, Page(s) 1289–1305

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Aged ; Alzheimer Disease/metabolism ; Brain/metabolism ; Humans ; Oxidation-Reduction ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2021-12-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2021.0177
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Article ; Online: Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.

Perluigi, Marzia / Di Domenico, Fabio / Butterfield, D Allan

Physiological reviews

2023 Volume 104, Issue 1, Page(s) 103–197

Abstract: Alzheimer disease (AD) is associated with multiple etiologies and pathological mechanisms, among which oxidative stress (OS) appears as a major determinant. Intriguingly, OS arises in various pathways regulating brain functions, and it seems to link ... ...

Abstract	Alzheimer disease (AD) is associated with multiple etiologies and pathological mechanisms, among which oxidative stress (OS) appears as a major determinant. Intriguingly, OS arises in various pathways regulating brain functions, and it seems to link different hypotheses and mechanisms of AD neuropathology with high fidelity. The brain is particularly vulnerable to oxidative damage, mainly because of its unique lipid composition, resulting in an amplified cascade of redox reactions that target several cellular components/functions ultimately leading to neurodegeneration. The present review highlights the "OS hypothesis of AD," including amyloid beta-peptide-associated mechanisms, the role of lipid and protein oxidation unraveled by redox proteomics, and the antioxidant strategies that have been investigated to modulate the progression of AD. Collected studies from our groups and others have contributed to unraveling the close relationships between perturbation of redox homeostasis in the brain and AD neuropathology by elucidating redox-regulated events potentially involved in both the pathogenesis and progression of AD. However, the complexity of AD pathological mechanisms requires an in-depth understanding of several major intracellular pathways affecting redox homeostasis and relevant for brain functions. This understanding is crucial to developing pharmacological strategies targeting OS-mediated toxicity that may potentially contribute to slow AD progression as well as improve the quality of life of persons with this severe dementing disorder.
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Quality of Life ; Oxidative Stress/physiology ; Oxidation-Reduction ; Lipids
Chemical Substances	Amyloid beta-Peptides ; Lipids
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00030.2022
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Article ; Online: Perspectives on Oxidative Stress in Alzheimer's Disease and Predictions of Future Research Emphases.

Butterfield, D Allan

Journal of Alzheimer's disease : JAD

2018 Volume 64, Issue s1, Page(s) S469–S479

Abstract: ... The Butterfield laboratory discovered the oxidative stress associated with oligomeric amyloid-β peptide manifested ... The importance and significance of the research emanating from the Butterfield laboratory rest on the paradigm ...

Abstract	Oxidative stress, an overproduction of free radicals or a diminution of free radical scavenging ability relative to those of cognitively aged-matched controls, is widely recognized as a critical component of the pathogenesis and progression of Alzheimer's disease (AD). This recognition arose in significant part from the work in the author's laboratory, complemented by research from others' laboratories. The Butterfield laboratory discovered the oxidative stress associated with oligomeric amyloid-β peptide manifested primarily as elevated oxidative modification of proteins and peroxidation of lipids. Such oxidative damage caused neuronal death, which undoubtedly underlies the progressive loss of cognition in AD. Identification of specific oxidatively modified brain proteins in subjects with AD or amnestic mild cognitive impairment was achieved by the methods of redox proteomics, pioneered in the author's laboratory. The importance and significance of the research emanating from the Butterfield laboratory rest on the paradigm shift of thinking regarding the roles of oxidative stress and resulting damage to key proteins and biochemical pathways in the pathogenesis and progression of AD. Predictions of future research directions also are presented. Given the enormous financial and personal burden placed upon citizens (and governments) of the US from AD, and the surety that the number of AD patients will greatly increase over the next 20-30 years, greater understanding of the molecular basis of pathogenesis and progression of AD is essential. Our laboratory is privileged to have contributed to better understanding of AD and provided rationales to identify effective therapeutic targets for this devastating dementing disorder.
MeSH term(s)	Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Humans ; Oxidative Stress/physiology
Language	English
Publishing date	2018-03-04
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-179912
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Article ; Online: Phosphoproteomics of Alzheimer disease brain: Insights into altered brain protein regulation of critical neuronal functions and their contributions to subsequent cognitive loss.

Butterfield, D Allan

Biochimica et biophysica acta. Molecular basis of disease

2018 Volume 1865, Issue 8, Page(s) 2031–2039

Abstract: Alzheimer disease (AD) is the major locus of dementia worldwide. In the USA there are nearly 6 million persons with this disorder, and estimates of 13-20 million AD cases in the next three decades. The molecular bases for AD remain unknown, though ... ...

Abstract	Alzheimer disease (AD) is the major locus of dementia worldwide. In the USA there are nearly 6 million persons with this disorder, and estimates of 13-20 million AD cases in the next three decades. The molecular bases for AD remain unknown, though processes involving amyloid beta-peptide as small oligomeric forms are gaining attention as known agents to both lead to oxidative stress and synaptic dysfunction associated with cognitive dysfunction in AD and its earlier forms, including amnestic mild cognitive impairment (MCI) and possibly preclinical Alzheimer disease (PCAD). Altered brain protein phosphorylation is a hallmark of AD, and phosphoproteomics offers an opportunity to identify these altered phosphoproteins in order to gain more insights into molecular mechanisms of neuronal dysfunction and death that lead to cognitive loss. This paper reviews what, to this author, are believed to be the known phosphoproteomics studies related to in vitro and in vivo models of AD as well as phosphoproteomics studies of brains from subjects with AD, and in at least one case in MCI and PCAD as well. The results of this review are discussed with relevance to new insights into AD brain protein dysregulation in critical neuronal functions and to potential therapeutic targets to slow, or in favorable cases, halt progression of this dementing disorder that affects millions of persons and their families worldwide.
MeSH term(s)	Alzheimer Disease/complications ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Animals ; Brain/metabolism ; Brain/physiopathology ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/physiopathology ; Humans ; Neurons/metabolism ; Neurons/pathology ; Oxidative Stress ; Phosphorylation ; Proteins/metabolism ; Proteomics
Chemical Substances	Proteins
Language	English
Publishing date	2018-08-29
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2018.08.035
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