Amyloid<i>β</i>-Peptide (1–42)-Induced Oxidative Stress in Alzheimer Disease: Importance in Disease Pathogenesis and Progression

Butterfield, D. Allan; Swomley, Aaron M.; Sultana, Rukhsana

doi:10.1089/ars.2012.5027

Cited by 468 publications

(358 citation statements)

References 175 publications

(132 reference statements)

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“…High levels of HNE have been detected in amyloid b plaques and in the cerebrospinal fluid in Alzheimer's patients. 27 The accumulation of HNE-modified amyloid b-peptides has been shown to inhibit the proteasome, 28 and the resulting accumulation of ubiquitinated modified proteins leads to a proinflammatory response (cyclo-oxygenase 2, prostaglandins). This contributes to neurodegeneration.…”

Section: Hne and Diseases Associated With Oxidative Damage: Links To mentioning

confidence: 99%

Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance

et al. 2013

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During the last three decades, 4-hydroxy-2-nonenal (HNE), a major a,b-unsaturated aldehyde product of n-6 fatty acid oxidation, has been shown to be involved in a great number of pathologies such as metabolic diseases, neurodegenerative diseases and cancers. These multiple pathologies can be explained by the fact that HNE is a potent modulator of numerous cell processes such as oxidative stress signaling, cell proliferation, transformation or cell death. The main objective of this review is to focus on the different aspects of HNE-induced cell death, with a particular emphasis on apoptosis. HNE is a special apoptotic inducer because of its abilities to form protein adducts and to propagate oxidative stress. It can stimulate intrinsic and extrinsic apoptotic pathways and interact with typical actors such as tumor protein 53, JNK, Fas or mitochondrial regulators. At the same time, due to its oxidant status, it can also induce some cellular defense mechanisms against oxidative stress, thus being involved in its own detoxification. These processes in turn limit the apoptotic potential of HNE. These dualities can imbalance cell fate, either toward cell death or toward survival, depending on the cell type, the metabolic state and the ability to detoxify.

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Section: Hne and Diseases Associated With Oxidative Damage: Links To mentioning

confidence: 99%

Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance

et al. 2013

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“…Aβ plays a central role in the pathogenesis of AD, by causing neurodegeneration and disrupting the cognitive function although the molecular pathways leading to neuronal impairment are not yet fully elucidated. It has been shown that early formed pre-fibrillar aggregates of Aβ are mainly endowed with cytotoxicity, whereas mature fibrils are much less toxic or even harmless [86][87][88].…”

Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationmentioning

confidence: 99%

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Cavallaro¹,

Fuso²,

D’Erme³

et al. 2016

Int J Clin Nutr Diet

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S-adenosyl-L-methionine (SAM) is the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. SAM level in the organism decreases with aging and restoring the original levels through exogenous supplementation is an important tool for the improvement of many vital functions. Indeed, SAM deficiency may contribute to the onset of several diseases, i.e. depression, liver diseases, osteoarthritis and senile neurological disorders such as Alzheimer's and Parkinson's diseases. Recent evidences indicate that SAM may have an involvement in oxidative stress, a process which typically involves an alteration of cellular sulfur amino acids homeostasis. SAM is not only the principal methyl donor, but also a precursor of glutathione, the major endogenous antioxidant, whose role in counteracting oxidative stress is well known. In this review we will highlight the role of SAM not just as a methyl-donor but also as a regulator of different metabolic pathways involved in the antioxidant response in brain related disorders. Role of S-adenosylmethionine in the Modulation of Oxidative StressRelated Neurodegeneration Review ArticleOpen Access IntroductionThe interaction between environmental and genetic factors plays a fundamental role in inducing and modulating the aging processes towards brain disorders. Among environmental factors, diet and nutritional lifestyle have a key role in brain health through the alteration of the intake or the bioavailability of metabolites and cofactors. Specific nutritional factors have particular impact on one-carbon metabolism, which is a complex biochemical pathway regulated by the presence of folate, vitamin B12 and B6 (among other metabolites) and leading to the production of S-adenosyl-L-methionine (SAM), the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. This metabolism involves three interrelated biochemical pathways: folate cycle, transsulfuration pathway and methionine cycle. These three metabolic sequences were first combined and correlated in 1964 by Laster's group [1][2][3] giving the integrated point of view of transmethylation and transsulfuration pathways, linking sulfur amino acid metabolism to the provision of methyl groups for many biochemical processes. Normal functioning of this metabolic cycle is essential for growth and development and impairment of this metabolism; transmethylation efficiency is associated with many diseases like cardiovascular diseases [4][5], liver diseases [6-9], neural tube defects [10] and brain diseases [11][12][13][14][15][16]. One-carbon metabolism alterations, low methylation and oxidative stress are all linked to Late Onset Alzheimer's Disease (LOAD) [17][18][19][20][21][22][23][24] Moreover, wide confirmed reports underline the role of SAM dependent reactions in age related neurodegeneration also showi...

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“…Aβ 1-42 -induced oxidative stress was considered as crucial to the pathophysiology of AD [6]. In this study, oxidative stress was assessed by measuring the intracellular ROS level using the ROS-sensitive fluorescence probe DCF.…”

Section: Cntf Protects Sh-sy5y Cells From Aβ 1-42 -Induced Oxidative mentioning

confidence: 99%

Ciliary neurotrophic factor protects SH-SY5Y neuroblastoma cells against Aβ 1-42 -induced neurotoxicity via activating the JAK2/STAT3 axis

Wang¹,

Xie²,

Zhu³

et al. 2015

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A b s t r a c t The neurotoxicity of aggregated amyloid beta (Aβ) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD), which leads to neuronal cell damage by inducing oxidative stress and consequently triggering cell apoptosis. Recently, Aβ-dependent inactivation of the Janus tyrosine kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway was found to play a critical role in the memory impairment related to AD. Previous research indicated that JAK2/STAT3 axis inactivation might be the result of aberrant reactive oxygen species (ROS) generation induced by Aβ in neurons. As the JAK2/STAT3 axis is a major transducer of ciliary neurotrophic factor (CNTF)-

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Amyloidβ-Peptide (1–42)-Induced Oxidative Stress in Alzheimer Disease: Importance in Disease Pathogenesis and Progression

Cited by 468 publications

References 175 publications

Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance

Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Ciliary neurotrophic factor protects SH-SY5Y neuroblastoma cells against Aβ 1-42 -induced neurotoxicity via activating the JAK2/STAT3 axis

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