Lipid Peroxidation Products in the Blood Plasma of Patients with Parkinson’s Disease as Possible Biomarkers of Different Stages of the Disease

Федорова, Т. Н.; Logvinenko, A.; Полещук, В.В.; Muzychuk, O. A.; Шабалина, А.А.; Иллариошкин, С. Н.

doi:10.1134/s1819712419040020

Cited by 10 publications

(11 citation statements)

References 33 publications

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“…It is known that these radicals can lead to neuronal death through different pathways. The 4-Hydroxynonenal (4-HNE), one of the products of LP secondary to the activity of these oxidant species, can induce apoptosis through the intrinsic pathway involving the release of cytochrome C into the cytosol and the consequent activation of associated caspases [ 48 ]. Similarly, proinflammatory cytokines released by astrocytes in response to pathological α-syn aggregates can activate the caspase/cytochrome C signaling cascade [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress and Mitochondrial Complex I Dysfunction Correlate with Neurodegeneration in an α-Synucleinopathy Animal Model

Morales-Martínez

Martínez-Gómez

Martínez‐Fong

et al. 2022

IJMS

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The α-synucleinopathies constitute a subset of neurodegenerative disorders, of which Parkinson’s disease (PD) is the most common worldwide, characterized by the accumulation of misfolded α-synuclein in the cytoplasm of neurons, which spreads in a prion-like manner to anatomically interconnected brain areas. However, it is not clear how α-synucleinopathy triggers neurodegeneration. We recently developed a rat model through a single intranigral administration of the neurotoxic β-sitosterol β-D-glucoside (BSSG), which produces α-synucleinopathy. In this model, we aimed to evaluate the temporal pattern of levels in oxidative and nitrosative stress and mitochondrial complex I (CI) dysfunction and how these biochemical parameters are associated with neurodegeneration in different brain areas with α-synucleinopathy (Substantia nigra pars compacta, the striatum, in the hippocampus and the olfactory bulb, where α-syn aggregation spreads). Interestingly, an increase in oxidative stress and mitochondrial CI dysfunction accompanied neurodegeneration in those brain regions. Furthermore, in silico analysis suggests a high-affinity binding site for BSSG with peroxisome proliferator-activated receptors (PPAR) alpha (PPAR-α) and gamma (PPAR-γ). These findings will contribute to elucidating the pathophysiological mechanisms associated with α-synucleinopathies and lead to the identification of new early biomarkers and therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress and Mitochondrial Complex I Dysfunction Correlate with Neurodegeneration in an α-Synucleinopathy Animal Model

Morales-Martínez

Martínez-Gómez

Martínez‐Fong

et al. 2022

IJMS

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“…PUFA levels were found to decrease in the SN, along with increased MDA levels, suggesting increased lipid peroxidation and oxidative damage in the dopaminergic neurons of patients with PD [ 175 ]. Additionally, Fedorova et al demonstrated a reciprocal increase in lipid peroxidation products with clinical PD-advancing stages in the peripheral blood of 240 patients with PD [ 33 ]. A reduction in antioxidative protective systems was also found in a post-mortem study, and the SN from patients with PD possessed reduced GSH levels compared to the control group [ 176 , 177 ].…”

Section: Iron Deposition α-Synuclein Aggregation Lipid Peroxidation A...mentioning

confidence: 99%

“…Iron chelators, antioxidative system x c − , and antioxidants such as coenzyme Q10 (CoQ10) inhibit ferroptosis, while ferroptosis inducers work in the opposite fashion [ 27 , 29 ]. Lately, the connections between PD and ferroptosis were supported by the correlation of iron accumulation with α-synuclein aggregation and the elevation of lipid peroxidation products in the post-mortem SN of patients with PD [ 30 , 31 , 32 , 33 ].…”

Section: Introductionmentioning

confidence: 99%

Iron Brain Menace: The Involvement of Ferroptosis in Parkinson Disease

Lin

Chen

Lin

et al. 2022

Cells

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Parkinson disease (PD) is the second-most common neurodegenerative disease. The characteristic pathology of progressive dopaminergic neuronal loss in people with PD is associated with iron accumulation and is suggested to be driven in part by the novel cell death pathway, ferroptosis. A unique modality of cell death, ferroptosis is mediated by iron-dependent phospholipid peroxidation. The mechanisms of ferroptosis inhibitors enhance antioxidative capacity to counter the oxidative stress from lipid peroxidation, such as through the system xc−/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis and the coenzyme Q10 (CoQ10)/FSP1 pathway. Another means to reduce ferroptosis is with iron chelators. To date, there is no disease-modifying therapy to cure or slow PD progression, and a recent topic of research seeks to intervene with the development of PD via regulation of ferroptosis. In this review, we provide a discussion of different cell death pathways, the molecular mechanisms of ferroptosis, the role of ferroptosis in blood–brain barrier damage, updates on PD studies in ferroptosis, and the latest progress of pharmacological agents targeting ferroptosis for the intervention of PD in clinical trials.

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“…The modified oligomers are toxic and may contribute to the deterioration of neurons [ 152 ]. It was found that HNE modifies the transport and possibly the loss of dopamine since its content increases proportionally to the severity stages of PD [ 153 ]. Elevated HNE, protein accumulation, and dopamine loss probably affect the physical capabilities and the process of learning in patients with PD [ 147 ].…”

Section: Parkinson’s Diseasementioning

confidence: 99%

Lipid Peroxidation and Antioxidant Supplementation in Neurodegenerative Diseases: A Review of Human Studies

et al. 2020

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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.

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Lipid Peroxidation Products in the Blood Plasma of Patients with Parkinson’s Disease as Possible Biomarkers of Different Stages of the Disease

Cited by 10 publications

References 33 publications

Oxidative Stress and Mitochondrial Complex I Dysfunction Correlate with Neurodegeneration in an α-Synucleinopathy Animal Model

Oxidative Stress and Mitochondrial Complex I Dysfunction Correlate with Neurodegeneration in an α-Synucleinopathy Animal Model

Iron Brain Menace: The Involvement of Ferroptosis in Parkinson Disease

Lipid Peroxidation and Antioxidant Supplementation in Neurodegenerative Diseases: A Review of Human Studies

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