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Antioxidants
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Lipid Peroxidation in Neurodegeneration
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Lipid Peroxidation in Neurodegeneration

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 25449

Special Issue Editor

Dr. Consuelo Cháfer-Pericás

E-Mail Website
Guest Editor
Neonatal Research Unit, Health Research Institute La Fe, Valencia, Spain

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases have great social and economic impacts on society as they are the cause of millions of deaths every year. The potential molecular mechanisms that generate these pathologies have been widely studied and have shown that lipid peroxidation plays an important role in neurodegeneration. More specifically, the mechanisms that could relate lipid peroxidation with neurodegeneration are ferroptosis and mitochondrial dysfunction. In addition, lipid peroxidation compounds in minimally invasive samples could be good indicators of the effectiveness of different treatments and could serve as diagnostic and/or prognostic biomarkers. In this sense, lipid peroxidation requires evaluation in different neurodegenerative conditions, as well as from different points of view.

Dr. Consuelo Cháfer-Pericás
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodegenerative disease
  • lipid peroxidation
  • biomarker
  • diagnosis
  • prognosis
  • follow-up

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

2 pages, 181 KiB  
Editorial
Lipid Peroxidation in Neurodegeneration
by Consuelo Cháfer-Pericás
Antioxidants 2021, 10(3), 484; https://doi.org/10.3390/antiox10030484 - 19 Mar 2021
Cited by 6 | Viewed by 1595
Abstract
Neurodegenerative diseases have multiple social and economic impacts on society, and they are the cause of millions of deaths every year [...] Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)

Research

Jump to: Editorial, Review

21 pages, 4642 KiB  
Article
Comparative Proteomics Unveils LRRFIP1 as a New Player in the DAPK1 Interactome of Neurons Exposed to Oxygen and Glucose Deprivation
by Núria DeGregorio-Rocasolano, Verónica Guirao, Jovita Ponce, Marc Melià-Sorolla, Alicia Aliena-Valero, Alexia García-Serran, Juan B. Salom, Antoni Dávalos, Octavi Martí-Sistac and Teresa Gasull
Antioxidants 2020, 9(12), 1202; https://doi.org/10.3390/antiox9121202 - 30 Nov 2020
Cited by 6 | Viewed by 3666
Abstract
Death-associated protein kinase 1 (DAPK1) is a pleiotropic hub of a number of networked distributed intracellular processes. Among them, DAPK1 is known to interact with the excitotoxicity driver NMDA receptor (NMDAR), and in sudden pathophysiological conditions of the brain, e.g., stroke, several lines [...] Read more.
Death-associated protein kinase 1 (DAPK1) is a pleiotropic hub of a number of networked distributed intracellular processes. Among them, DAPK1 is known to interact with the excitotoxicity driver NMDA receptor (NMDAR), and in sudden pathophysiological conditions of the brain, e.g., stroke, several lines of evidence link DAPK1 with the transduction of glutamate-induced events that determine neuronal fate. In turn, DAPK1 expression and activity are known to be affected by the redox status of the cell. To delineate specific and differential neuronal DAPK1 interactors in stroke-like conditions in vitro, we exposed primary cultures of rat cortical neurons to oxygen/glucose deprivation (OGD), a condition that increases reactive oxygen species (ROS) and lipid peroxides. OGD or control samples were co-immunoprecipitated separately, trypsin-digested, and proteins in the interactome identified by high-resolution LC-MS/MS. Data were processed and curated using bioinformatics tools. OGD increased total DAPK1 protein levels, cleavage into shorter isoforms, and dephosphorylation to render the active DAPK1 form. The DAPK1 interactome comprises some 600 proteins, mostly involving binding, catalytic and structural molecular functions. OGD up-regulated 190 and down-regulated 192 candidate DAPK1-interacting proteins. Some differentially up-regulated interactors related to NMDAR were validated by WB. In addition, a novel differential DAPK1 partner, LRRFIP1, was further confirmed by reverse Co-IP. Furthermore, LRRFIP1 levels were increased by pro-oxidant conditions such as ODG or the ferroptosis inducer erastin. The present study identifies novel partners of DAPK1, such as LRRFIP1, which are suitable as targets for neuroprotection. Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)
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12 pages, 7548 KiB  
Article
Dopamine Therapy and the Regulation of Oxidative Stress and Mitochondrial DNA Copy Number in Patients with Parkinson’s Disease
by Shih-Hsuan Chen, Chung-Wen Kuo, Tsu-Kung Lin, Meng-Han Tsai and Chia-Wei Liou
Antioxidants 2020, 9(11), 1159; https://doi.org/10.3390/antiox9111159 - 20 Nov 2020
Cited by 9 | Viewed by 2142
Abstract
Few studies have reported on changes to oxidative stress and mitochondrial DNA copy numbers in patients with Parkinson’s disease (PD), particularly those undergoing long-term dopamine therapy. This study measured mitochondrial copy numbers, thiobarbituric acid reactive substances (TBARS), and thiols in 725 PD patients [...] Read more.
Few studies have reported on changes to oxidative stress and mitochondrial DNA copy numbers in patients with Parkinson’s disease (PD), particularly those undergoing long-term dopamine therapy. This study measured mitochondrial copy numbers, thiobarbituric acid reactive substances (TBARS), and thiols in 725 PD patients and 744 controls. The total prescribed dopamine dose was calculated for each PD patient. A decreased mitochondrial copy number and antioxidant thiols level, but an elevated oxidative TBARS level presented in PD patients. Stratification into age subgroups revealed a consistently lower mitochondrial copy number and thiols in all PD subgroups, but increased TBARS levels compared with those of the controls. Further study found an association between lower serum TBARS and dopamine administration. There appears to be an indirect relationship with the mitochondrial copy number, where a decrease in TBARS was found to diminish the effect of pathogenetic and age-related decrease in mitochondrial copy number in PD patients. Follow-up evaluations noted more significant decreases of mitochondrial copy numbers in PD patients over time; meanwhile, dopamine administration was associated with an initial decrease of the TBARS level which attenuated with high-dose and long-term therapy. Our study provides evidence that moderate dopamine dose therapy benefits PD patients through attenuation of oxidative stress and manipulation of the mitochondrial copy number. Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)
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12 pages, 773 KiB  
Article
Clinical Utility of Plasma Lipid Peroxidation Biomarkers in Alzheimer’s Disease Differential Diagnosis
by Carmen Peña-Bautista, Lourdes Álvarez, Thierry Durand, Claire Vigor, Ana Cuevas, Miguel Baquero, Máximo Vento, David Hervás and Consuelo Cháfer-Pericás
Antioxidants 2020, 9(8), 649; https://doi.org/10.3390/antiox9080649 - 22 Jul 2020
Cited by 10 | Viewed by 2964
Abstract
Background: Differential diagnosis of Alzheimer’s disease (AD) is a complex task due to the clinical similarity among neurodegenerative diseases. Previous studies showed the role of lipid peroxidation in early AD development. However, the clinical validation of potential specific biomarkers in minimally invasive samples [...] Read more.
Background: Differential diagnosis of Alzheimer’s disease (AD) is a complex task due to the clinical similarity among neurodegenerative diseases. Previous studies showed the role of lipid peroxidation in early AD development. However, the clinical validation of potential specific biomarkers in minimally invasive samples constitutes a great challenge in early AD diagnosis. Methods: Plasma samples from participants classified into AD (n = 138), non-AD (including MCI and other dementias not due to AD) (n = 70) and healthy (n = 50) were analysed. Lipid peroxidation compounds (isoprostanes, isofurans, neuroprostanes, neurofurans) were determined by ultra-performance liquid chromatography coupled with tandem mass spectrometry. Statistical analysis for biomarkers’ clinical validation was based on Elastic Net. Results: A two-step diagnosis model was developed from plasma lipid peroxidation products to diagnose early AD specifically, and a bootstrap validated AUC of 0.74 was obtained. Conclusion: A promising AD differential diagnosis model was developed. It was clinically validated as a screening test. However, further external validation is required before clinical application. Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)
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11 pages, 285 KiB  
Article
Isoprostanoids Levels in Cerebrospinal Fluid Do Not Reflect Alzheimer’s Disease
by Carmen Peña-Bautista, Miguel Baquero, Marina López-Nogueroles, Máximo Vento, David Hervás and Consuelo Cháfer-Pericás
Antioxidants 2020, 9(5), 407; https://doi.org/10.3390/antiox9050407 - 10 May 2020
Cited by 4 | Viewed by 2446
Abstract
Previous studies showed a relationship between lipid oxidation biomarkers from plasma samples and Alzheimer’s Disease (AD), constituting a promising diagnostic tool. In this work we analyzed whether these plasma biomarkers could reflect specific brain oxidation in AD. In this work lipid peroxidation compounds [...] Read more.
Previous studies showed a relationship between lipid oxidation biomarkers from plasma samples and Alzheimer’s Disease (AD), constituting a promising diagnostic tool. In this work we analyzed whether these plasma biomarkers could reflect specific brain oxidation in AD. In this work lipid peroxidation compounds were determined in plasma and cerebrospinal fluid (CSF) samples from AD and non-AD (including other neurological pathologies) participants, by means of an analytical method based on liquid chromatography coupled with mass spectrometry. Statistical analysis evaluated correlations between biological matrices. The results did not show satisfactory correlations between plasma and CSF samples for any of the studied lipid peroxidation biomarkers (isoprostanes, neuroprostanes, prostaglandines, dihomo-isoprostanes). However, some of the analytes showed correlations with specific CSF biomarkers for AD and with neuropsychological tests (Mini-Mental State Examination (MMSE), Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)). In conclusion, lipid peroxidation biomarkers in CSF samples do not reflect their levels in plasma samples, and no significant differences were observed between participant groups. However, some of the analytes could be useful as cognitive decline biomarkers. Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)
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Review

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19 pages, 752 KiB  
Review
The Neuromelanin Paradox and Its Dual Role in Oxidative Stress and Neurodegeneration
by Alexandra Moreno-García, Alejandra Kun, Miguel Calero and Olga Calero
Antioxidants 2021, 10(1), 124; https://doi.org/10.3390/antiox10010124 - 16 Jan 2021
Cited by 27 | Viewed by 5932
Abstract
Aging is associated with an increasing dysfunction of key brain homeostasis mechanisms and represents the main risk factor across most neurodegenerative disorders. However, the degree of dysregulation and the affectation of specific pathways set apart normal aging from neurodegenerative disorders. In particular, the [...] Read more.
Aging is associated with an increasing dysfunction of key brain homeostasis mechanisms and represents the main risk factor across most neurodegenerative disorders. However, the degree of dysregulation and the affectation of specific pathways set apart normal aging from neurodegenerative disorders. In particular, the neuronal metabolism of catecholaminergic neurotransmitters appears to be a specifically sensitive pathway that is affected in different neurodegenerations. In humans, catecholaminergic neurons are characterized by an age-related accumulation of neuromelanin (NM), rendering the soma of the neurons black. This intracellular NM appears to serve as a very efficient quencher for toxic molecules. However, when a neuron degenerates, NM is released together with its load (many undegraded cellular components, transition metals, lipids, xenobiotics) contributing to initiate and worsen an eventual immune response, exacerbating the oxidative stress, ultimately leading to the neurodegenerative process. This review focuses on the analysis of the role of NM in normal aging and neurodegeneration related to its capabilities as an antioxidant and scavenging of harmful molecules, versus its involvement in oxidative stress and aberrant immune response, depending on NM saturation state and its extracellular release. Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)
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27 pages, 1129 KiB  
Review
Lipid Peroxidation and Antioxidant Supplementation in Neurodegenerative Diseases: A Review of Human Studies
by Snjezana Petrovic, Aleksandra Arsic, Danijela Ristic-Medic, Zorica Cvetkovic and Vesna Vucic
Antioxidants 2020, 9(11), 1128; https://doi.org/10.3390/antiox9111128 - 13 Nov 2020
Cited by 52 | Viewed by 5986
Abstract
Being characterized by progressive and severe damage in neuronal cells, neurodegenerative diseases (NDDs) are the major cause of disability and morbidity in the elderly, imposing a significant economic and social burden. As major components of the central nervous system, lipids play important roles [...] Read more.
Being characterized by progressive and severe damage in neuronal cells, neurodegenerative diseases (NDDs) are the major cause of disability and morbidity in the elderly, imposing a significant economic and social burden. As major components of the central nervous system, lipids play important roles in neural health and pathology. Disturbed lipid metabolism, particularly lipid peroxidation (LPO), is associated with the development of many NDDs, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), all of which show elevated levels of LPO products and LPO-modified proteins. Thus, the inhibition of neuronal oxidation might slow the progression and reduce the severity of NDD; natural antioxidants, such as polyphenols and antioxidant vitamins, seem to be the most promising agents. Here, we summarize current literature data that were derived from human studies on the effect of natural polyphenols and vitamins A, C, and E supplementation in patients with AD, PD, and ALS. Although these compounds may reduce the severity and slow the progression of NDD, research gaps remain in antioxidants supplementation in AD, PD, and ALS patients, which indicates that further human studies applying antioxidant supplementation in different forms of NDDs are urgently needed. Full article
(This article belongs to the Special Issue Lipid Peroxidation in Neurodegeneration)
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