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Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 50322

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Dr. Anne Vejux

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Team “Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism”, Université de Bourgogne, 21000 Dijon, France
Interests: oxysterols; very-long-chain fatty acids; lipid metabolism; diet, peroxisomes; biotherapies; inflammation; cancer; cell cycle and apoptosis; autophagy; biological membranes; oxidative damage; biomarkers; neurodegenerative diseases
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Dear Colleagues,

This Special Issue is the continuation of our previous special issue "Cell Death and Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules".

Neurodegenerative diseases represent a major societal challenge. These are not diseases with a short, life-threatening prognosis, but they are very debilitating, inflicting heavy demands on carers and requiring the establishment of appropriate centers for patient care. It is, therefore, important to know even more about the mechanisms involved in the physiopathogenesis of these diseases.

Neurodegenerative diseases include demyelinating neurodegenerative diseases: multiple sclerosis and peroxysomal and nondemyelinating leukodystrophies—Alzheimer’s disease, Parkinson’s disease, Niemann–Pick disease, Huntington’s disease and amyotrophic lateral sclerosis or Charcot disease. Among the mechanisms involved in these pathologies, inflammation, oxidative stress and cell death play very important roles in the pathophysiology. It is, therefore, important to better understand the involvement of cell death, inflammation and oxidative stress, as well as the cellular and molecular mechanisms leading to it, and to identify the natural or unnatural molecules that can thwart these mechanisms. Apoptosis, autophagy, necroptosis or other forms of cell death can be interesting therapeutic targets to combat the development of these neurodegenerative diseases. Cytokinic and non-cytokinic inflammation, as well as processes generating oxidative stress, could also be interesting targets to fight these pathologies.

Dr. Anne Vejux
Guest Editor

Note: You are warmly welcomed to submit your woks to our new edition: Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules 2.0

Submission Deadline: 30 April 2022

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Note: You are warmly welcomed to submit your woks to our new edition: Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules 2.0

Submission Deadline: 30 April 2022

Related Special Issue

Cell Death and Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules in International Journal of Molecular Sciences (14 articles)

Published Papers (12 papers)

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Editorial

Jump to: Research, Review

3 pages, 177 KiB

Open AccessEditorial

Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules

by Anne Vejux

Int. J. Mol. Sci. 2021, 22(24), 13657; https://doi.org/10.3390/ijms222413657 - 20 Dec 2021

Cited by 7 | Viewed by 1531

Abstract

Neurodegenerative diseases are the most common chronic neurological pathologies associated with age, with a major impact on the patient’s quality of life [...] Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

Research

Jump to: Editorial, Review

20 pages, 6739 KiB

Open AccessArticle

Long-Term Effects of Repetitive Mild Traumatic Injury on the Visual System in Wild-Type and TDP-43 Transgenic Mice

by Kristina Pilipović, Jelena Rajič Bumber, Petra Dolenec, Nika Gržeta, Tamara Janković, Jasna Križ and Gordana Župan

Int. J. Mol. Sci. 2021, 22(12), 6584; https://doi.org/10.3390/ijms22126584 - 19 Jun 2021

Cited by 4 | Viewed by 2542

Abstract

Little is known about the impairments and pathological changes in the visual system in mild brain trauma, especially repetitive mild traumatic brain injury (mTBI). The goal of this study was to examine and compare the effects of repeated head impacts on the neurodegeneration, axonal integrity, and glial activity in the optic tract (OT), as well as on neuronal preservation, glial responses, and synaptic organization in the lateral geniculate nucleus (LGN) and superior colliculus (SC), in wild-type mice and transgenic animals with overexpression of human TDP-43 mutant protein (TDP-43^G348C) at 6 months after repeated closed head traumas. Animals were also assessed in the Barnes maze (BM) task. Neurodegeneration, axonal injury, and gliosis were detected in the OT of the injured animals of both genotypes. In the traumatized mice, myelination of surviving axons was mostly preserved, and the expression of neurofilament light chain was unaffected. Repetitive mTBI did not induce changes in the LGN and the SC, nor did it affect the performance of the BM task in the traumatized wild-type and TDP-43 transgenic mice. Differences in neuropathological and behavioral assessments between the injured wild-type and TDP-43^G348C mice were not revealed. Results of the current study suggest that repetitive mTBI was associated with chronic damage and inflammation in the OT in wild-type and TDP-43^G348C mice, which were not accompanied with behavioral problems and were not affected by the TDP-43 genotype, while the LGN and the SC remained preserved in the used experimental conditions. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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17 pages, 3123 KiB

Open AccessArticle

The Impact of High Glucose or Insulin Exposure on S100B Protein Levels, Oxidative and Nitrosative Stress and DNA Damage in Neuron-Like Cells

by Adriana Kubis-Kubiak, Benita Wiatrak and Agnieszka Piwowar

Int. J. Mol. Sci. 2021, 22(11), 5526; https://doi.org/10.3390/ijms22115526 - 24 May 2021

Cited by 7 | Viewed by 2493

Abstract

Alzheimer’s disease (AD) is attracting considerable interest due to its increasing number of cases as a consequence of the aging of the global population. The mainstream concept of AD neuropathology based on pathological changes of amyloid β metabolism and the formation of neurofibrillary tangles is under criticism due to the failure of Aβ-targeting drug trials. Recent findings have shown that AD is a highly complex disease involving a broad range of clinical manifestations as well as cellular and biochemical disturbances. The past decade has seen a renewed importance of metabolic disturbances in disease-relevant early pathology with challenging areas in establishing the role of local micro-fluctuations in glucose concentrations and the impact of insulin on neuronal function. The role of the S100 protein family in this interplay remains unclear and is the aim of this research. Intracellularly the S100B protein has a protective effect on neurons against the toxic effects of glutamate and stimulates neurites outgrowth and neuronal survival. At high concentrations, it can induce apoptosis. The aim of our study was to extend current knowledge of the possible impact of hyper-glycemia and -insulinemia directly on neuronal S100B secretion and comparison to oxidative stress markers such as ROS, NO and DBSs levels. In this paper, we have shown that S100B secretion decreases in neurons cultured in a high-glucose or high-insulin medium, while levels in cell lysates are increased with statistical significance. Our findings demonstrate the strong toxic impact of energetic disturbances on neuronal metabolism and the potential neuroprotective role of S100B protein. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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13 pages, 1749 KiB

Open AccessArticle

Discovery of a Necroptosis Inhibitor Improving Dopaminergic Neuronal Loss after MPTP Exposure in Mice

by Sara R. Oliveira, Pedro A. Dionísio, Maria M. Gaspar, Maria B. T. Ferreira, Catarina A. B. Rodrigues, Rita G. Pereira, Mónica S. Estevão, Maria J. Perry, Rui Moreira, Carlos A. M. Afonso, Joana D. Amaral and Cecília M. P. Rodrigues

Int. J. Mol. Sci. 2021, 22(10), 5289; https://doi.org/10.3390/ijms22105289 - 18 May 2021

Cited by 11 | Viewed by 2816

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, mainly characterized by motor deficits correlated with progressive dopaminergic neuronal loss in the substantia nigra pars compacta (SN). Necroptosis is a caspase-independent form of regulated cell death mediated by the concerted action of receptor-interacting protein 3 (RIP3) and the pseudokinase mixed lineage domain-like protein (MLKL). It is also usually dependent on RIP1 kinase activity, influenced by further cellular clues. Importantly, necroptosis appears to be strongly linked to several neurodegenerative diseases, including PD. Here, we aimed at identifying novel chemical inhibitors of necroptosis in a PD-mimicking model, by conducting a two-step screening. Firstly, we phenotypically screened a library of 31 small molecules using a cellular model of necroptosis and, thereafter, the hit compound effect was validated in vivo in a sub-acute 1-methyl-1-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) PD-related mouse model. From the initial compounds, we identified one hit—Oxa12—that strongly inhibited necroptosis induced by the pan-caspase inhibitor zVAD-fmk in the BV2 murine microglia cell line. More importantly, mice exposed to MPTP and further treated with Oxa12 showed protection against MPTP-induced dopaminergic neuronal loss in the SN and striatum. In conclusion, we identified Oxa12 as a hit compound that represents a new chemotype to tackle necroptosis. Oxa12 displays in vivo effects, making this compound a drug candidate for further optimization to attenuate PD pathogenesis. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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15 pages, 2170 KiB

Open AccessArticle

Epigallocatechin-3-Gallate-Loaded Liposomes Favor Anti-Inflammation of Microglia Cells and Promote Neuroprotection

by Chun-Yuan Cheng, Lassina Barro, Shang-Ting Tsai, Tai-Wei Feng, Xiao-Yu Wu, Che-Wei Chao, Ruei-Siang Yu, Ting-Yu Chin and Ming Fa Hsieh

Int. J. Mol. Sci. 2021, 22(6), 3037; https://doi.org/10.3390/ijms22063037 - 16 Mar 2021

Cited by 45 | Viewed by 3432

Abstract

Microglia-mediated neuroinflammation is recognized to mainly contribute to the progression of neurodegenerative diseases. Epigallocatechin-3-gallate (EGCG), known as a natural antioxidant in green tea, can inhibit microglia-mediated inflammation and protect neurons but has disadvantages such as high instability and low bioavailability. We developed an EGCG liposomal formulation to improve its bioavailability and evaluated the neuroprotective activity in in vitro and in vivo neuroinflammation models. EGCG-loaded liposomes have been prepared from phosphatidylcholine (PC) or phosphatidylserine (PS) coated with or without vitamin E (VE) by hydration and membrane extrusion method. The anti-inflammatory effect has been evaluated against lipopolysaccharide (LPS)-induced BV-2 microglial cells activation and the inflammation in the substantia nigra of Sprague Dawley rats. In the cellular inflammation model, murine BV-2 microglial cells changed their morphology from normal spheroid to activated spindle shape after 24 h of induction of LPS. In the in vitro free radical 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay, EGCG scavenged 80% of DPPH within 3 min. EGCG-loaded liposomes could be phagocytized by BV-2 cells after 1 h of cell culture from cell uptake experiments. EGCG-loaded liposomes improved the production of BV-2 microglia-derived nitric oxide and TNF-α following LPS. In the in vivo Parkinsonian syndrome rat model, simultaneous intra-nigral injection of EGCG-loaded liposomes attenuated LPS-induced pro-inflammatory cytokines and restored motor impairment. We demonstrated that EGCG-loaded liposomes exert a neuroprotective effect by modulating microglia activation. EGCG extracted from green tea and loaded liposomes could be a valuable candidate for disease-modifying therapy for Parkinson’s disease (PD). Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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22 pages, 3939 KiB

Open AccessArticle

Neuroprotective Effect of Apolipoprotein D in Cuprizone-Induced Cell Line Models: A Potential Therapeutic Approach for Multiple Sclerosis and Demyelinating Diseases

by Eva Martínez-Pinilla, Núria Rubio-Sardón, Rafael Peláez, Enrique García-Álvarez, Eva del Valle, Jorge Tolivia, Ignacio M. Larráyoz and Ana Navarro

Int. J. Mol. Sci. 2021, 22(3), 1260; https://doi.org/10.3390/ijms22031260 - 27 Jan 2021

Cited by 6 | Viewed by 3729

Abstract

Apolipoprotein D (Apo D) overexpression is a general finding across neurodegenerative conditions so the role of this apolipoprotein in various neuropathologies such as multiple sclerosis (MS) has aroused a great interest in last years. However, its mode of action, as a promising compound for the development of neuroprotective drugs, is unknown. The aim of this work was to address the potential of Apo D to prevent the action of cuprizone (CPZ), a toxin widely used for developing MS models, in oligodendroglial and neuroblastoma cell lines. On one hand, immunocytochemical quantifications and gene expression measures showed that CPZ compromised neural mitochondrial metabolism but did not induce the expression of Apo D, except in extremely high doses in neurons. On the other hand, assays of neuroprotection demonstrated that antipsychotic drug, clozapine, induced an increase in Apo D synthesis only in the presence of CPZ, at the same time that prevented the loss of viability caused by the toxin. The effect of the exogenous addition of human Apo D, once internalized, was also able to directly revert the loss of cell viability caused by treatment with CPZ by a reactive oxygen species (ROS)-independent mechanism of action. Taken together, our results suggest that increasing Apo D levels, in an endo- or exogenous way, moderately prevents the neurotoxic effect of CPZ in a cell model that seems to replicate some features of MS which would open new avenues in the development of interventions to afford MS-related neuroprotection. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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Review

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26 pages, 1768 KiB

Open AccessReview

Involvement of Microglia in Neurodegenerative Diseases: Beneficial Effects of Docosahexahenoic Acid (DHA) Supplied by Food or Combined with Nanoparticles

by Karine Charrière, Imen Ghzaiel, Gérard Lizard and Anne Vejux

Int. J. Mol. Sci. 2021, 22(19), 10639; https://doi.org/10.3390/ijms221910639 - 30 Sep 2021

Cited by 6 | Viewed by 2685

Abstract

Neurodegenerative diseases represent a major public health issue and require better therapeutic management. The treatments developed mainly target neuronal activity. However, an inflammatory component must be considered, and microglia may constitute an important therapeutic target. Given the difficulty in developing molecules that can cross the blood–brain barrier, the use of food-derived molecules may be an interesting therapeutic avenue. Docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid (22:6 omega-3), has an inhibitory action on cell death and oxidative stress induced in the microglia. It also acts on the inflammatory activity of microglia. These data obtained in vitro or on animal models are corroborated by clinical trials showing a protective effect of DHA. Whereas DHA crosses the blood–brain barrier, nutritional intake lacks specificity at both the tissue and cellular level. Nanomedicine offers new tools which favor the delivery of DHA at the cerebral level, especially in microglial cells. Because of the biological activities of DHA and the associated nanotargeting techniques, DHA represents a therapeutic molecule of interest for the treatment of neurodegenerative diseases. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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19 pages, 2078 KiB

Open AccessReview

Current Trends in Neurodegeneration: Cross Talks between Oxidative Stress, Cell Death, and Inflammation

by Tapan Behl, Rashita Makkar, Aayush Sehgal, Sukhbir Singh, Neelam Sharma, Gokhan Zengin, Simona Bungau, Felicia Liana Andronie-Cioara, Mihai Alexandru Munteanu, Mihaela Cristina Brisc, Diana Uivarosan and Ciprian Brisc

Int. J. Mol. Sci. 2021, 22(14), 7432; https://doi.org/10.3390/ijms22147432 - 11 Jul 2021

Cited by 47 | Viewed by 4139

Abstract

The human body is highly complex and comprises a variety of living cells and extracellular material, which forms tissues, organs, and organ systems. Human cells tend to turn over readily to maintain homeostasis in tissues. However, postmitotic nerve cells exceptionally have an ability to regenerate and be sustained for the entire life of an individual, to safeguard the physiological functioning of the central nervous system. For efficient functioning of the CNS, neuronal death is essential, but extreme loss of neurons diminishes the functioning of the nervous system and leads to the onset of neurodegenerative diseases. Neurodegenerative diseases range from acute to chronic severe life-altering conditions like Parkinson’s disease and Alzheimer’s disease. Millions of individuals worldwide are suffering from neurodegenerative disorders with little or negligible treatment available, thereby leading to a decline in their quality of life. Neuropathological studies have identified a series of factors that explain the etiology of neuronal degradation and its progression in neurodegenerative disease. The onset of neurological diseases depends on a combination of factors that causes a disruption of neurons, such as environmental, biological, physiological, and genetic factors. The current review highlights some of the major pathological factors responsible for neuronal degradation, such as oxidative stress, cell death, and neuroinflammation. All these factors have been described in detail to enhance the understanding of their mechanisms and target them for disease management. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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23 pages, 3315 KiB

Open AccessReview

Analyzing Olfactory Neuron Precursors Non-Invasively Isolated through NADH FLIM as a Potential Tool to Study Oxidative Stress in Alzheimer’s Disease

by Laura Gómez-Virgilio, Alejandro Luarte, Daniela P. Ponce, Bárbara A. Bruna and María I. Behrens

Int. J. Mol. Sci. 2021, 22(12), 6311; https://doi.org/10.3390/ijms22126311 - 12 Jun 2021

Cited by 7 | Viewed by 5222

Abstract

Among all the proposed pathogenic mechanisms to understand the etiology of Alzheimer’s disease (AD), increased oxidative stress seems to be a robust and early disease feature where many of those hypotheses converge. However, despite the significant lines of evidence accumulated, an effective diagnosis and treatment of AD are not yet available. This limitation might be partially explained by the use of cellular and animal models that recapitulate partial aspects of the disease and do not account for the particular biology of patients. As such, cultures of patient-derived cells of peripheral origin may provide a convenient solution for this problem. Peripheral cells of neuronal lineage such as olfactory neuronal precursors (ONPs) can be easily cultured through non-invasive isolation, reproducing AD-related oxidative stress. Interestingly, the autofluorescence of key metabolic cofactors such as reduced nicotinamide adenine dinucleotide (NADH) can be highly correlated with the oxidative state and antioxidant capacity of cells in a non-destructive and label-free manner. In particular, imaging NADH through fluorescence lifetime imaging microscopy (FLIM) has greatly improved the sensitivity in detecting oxidative shifts with minimal intervention to cell physiology. Here, we discuss the translational potential of analyzing patient-derived ONPs non-invasively isolated through NADH FLIM to reveal AD-related oxidative stress. We believe this approach may potentially accelerate the discovery of effective antioxidant therapies and contribute to early diagnosis and personalized monitoring of this devastating disease. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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13 pages, 263 KiB

Open AccessReview

Neuroinflammation as a Common Denominator of Complex Diseases (Cancer, Diabetes Type 2, and Neuropsychiatric Disorders)

by Serena Asslih, Odeya Damri and Galila Agam

Int. J. Mol. Sci. 2021, 22(11), 6138; https://doi.org/10.3390/ijms22116138 - 07 Jun 2021

Cited by 14 | Viewed by 2901

Abstract

The term neuroinflammation refers to inflammation of the nervous tissue, in general, and in the central nervous system (CNS), in particular. It is a driver of neurotoxicity, it is detrimental, and implies that glial cell activation happens prior to neuronal degeneration and, possibly, even causes it. The inflammation-like glial responses may be initiated in response to a variety of cues such as infection, traumatic brain injury, toxic metabolites, or autoimmunity. The inflammatory response of activated microglia engages the immune system and initiates tissue repair. Through translational research the role played by neuroinflammation has been acknowledged in different disease entities. Intriguingly, these entities include both those directly related to the CNS (commonly designated neuropsychiatric disorders) and those not directly related to the CNS (e.g., cancer and diabetes type 2). Interestingly, all the above-mentioned entities belong to the same group of “complex disorders”. This review aims to summarize cumulated data supporting the hypothesis that neuroinflammation is a common denominator of a wide variety of complex diseases. We will concentrate on cancer, type 2 diabetes (T2DM), and neuropsychiatric disorders (focusing on mood disorders). Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

16 pages, 792 KiB

Open AccessReview

Neuroinflammation in Post-Ischemic Neurodegeneration of the Brain: Friend, Foe, or Both?

by Ryszard Pluta, Sławomir Januszewski and Stanisław J. Czuczwar

Int. J. Mol. Sci. 2021, 22(9), 4405; https://doi.org/10.3390/ijms22094405 - 23 Apr 2021

Cited by 53 | Viewed by 2991

Abstract

One of the leading causes of neurological mortality, disability, and dementia worldwide is cerebral ischemia. Among the many pathological phenomena, the immune system plays an important role in the development of post-ischemic degeneration of the brain, leading to the development of neuroinflammatory changes in the brain. After cerebral ischemia, the developing neuroinflammation causes additional damage to the brain cells, but on the other hand it also plays a beneficial role in repair activities. Inflammatory mediators are sources of signals that stimulate cells in the brain and promote penetration, e.g., T lymphocytes, monocytes, platelets, macrophages, leukocytes, and neutrophils from systemic circulation to the brain ischemic area, and this phenomenon contributes to further irreversible ischemic brain damage. In this review, we focus on the issues related to the neuroinflammation that occurs in the brain tissue after ischemia, with particular emphasis on ischemic stroke and its potential treatment strategies. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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27 pages, 2666 KiB

Open AccessReview

Ferroptosis Mechanisms Involved in Neurodegenerative Diseases

by Cadiele Oliana Reichert, Fábio Alessandro de Freitas, Juliana Sampaio-Silva, Leonardo Rokita-Rosa, Priscila de Lima Barros, Debora Levy and Sérgio Paulo Bydlowski

Int. J. Mol. Sci. 2020, 21(22), 8765; https://doi.org/10.3390/ijms21228765 - 20 Nov 2020

Cited by 201 | Viewed by 14204

Abstract

Ferroptosis is a type of cell death that was described less than a decade ago. It is caused by the excess of free intracellular iron that leads to lipid (hydro) peroxidation. Iron is essential as a redox metal in several physiological functions. The brain is one of the organs known to be affected by iron homeostatic balance disruption. Since the 1960s, increased concentration of iron in the central nervous system has been associated with oxidative stress, oxidation of proteins and lipids, and cell death. Here, we review the main mechanisms involved in the process of ferroptosis such as lipid peroxidation, glutathione peroxidase 4 enzyme activity, and iron metabolism. Moreover, the association of ferroptosis with the pathophysiology of some neurodegenerative diseases, namely Alzheimer’s, Parkinson’s, and Huntington’s diseases, has also been addressed. Full article

(This article belongs to the Special Issue Cell Death, Inflammation and Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules)

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