Disorders of Endogenous and Exogenous Antioxidants in Neurological Diseases DOI Creative Commons
Izabela Korczowska-Łącka, Bartosz Słowikowski, Thomas Piekut

et al.

Antioxidants, Journal Year: 2023, Volume and Issue: 12(10), P. 1811 - 1811

Published: Sept. 29, 2023

In diseases of the central nervous system, such as Alzheimer's disease (AD), Parkinson's (PD), stroke, amyotrophic lateral sclerosis (ALS), Huntington's (HD), and even epilepsy migraine, oxidative stress load commonly surpasses endogenous antioxidative capacity. While processes have been robustly implicated in pathogenesis these diseases, significance particular antioxidants, both especially exogenous, maintaining redox homeostasis requires further research. Among enzymes catalase, superoxide dismutase, glutathione peroxidase are to disabling free radicals, thereby preventing damage cellular lipids, proteins, nucleic acids. Whether supplementation with endogenously occurring antioxidant compounds melatonin carries any benefit, however, remains equivocal. Similarly, while health benefits certain exogenous including ascorbic acid (vitamin C), carotenoids, polyphenols, sulforaphanes, anthocyanins touted, their clinical efficacy effectiveness neurological contexts need be more defined. Here, we review current literature on mechanisms mitigating comment possible benefit most common antioxidants AD, PD, ALS, HD, epilepsy, migraine. We selected a basically neurodegenerative nature.

Language: Английский

Nutritional and Metabolic Control of Ferroptosis DOI
Eikan Mishima, Marcus Conrad

Annual Review of Nutrition, Journal Year: 2022, Volume and Issue: 42(1), P. 275 - 309

Published: June 2, 2022

Ferroptosis is a type of regulated cell death characterized by an excessive lipid peroxidation cellular membranes caused the disruption antioxidant defense system and/or imbalanced metabolism. differentiates from other forms in that several metabolic pathways and nutritional aspects, including endogenous antioxidants (such as coenzyme Q10, vitamin E, di/tetrahydrobiopterin), iron handling, energy sensing, selenium utilization, amino acids, fatty directly regulate cells' sensitivity to ferroptosis. As hallmarks ferroptosis have been documented variety diseases, neurodegeneration, acute organ injury, therapy-resistant tumors, modulation using pharmacological tools or reprogramming holds great potential for treatment ferroptosis-associated diseases cancer therapy. Hence, this review focuses on regulation cues discusses interventions therapy targeting

Language: Английский

Citations

62

Identification of Ferroptosis-Related Genes in Alzheimer’s Disease Based on Bioinformatic Analysis DOI Creative Commons
Ying Wāng, Guohua Chen, Wei Shao

et al.

Frontiers in Neuroscience, Journal Year: 2022, Volume and Issue: 16

Published: Feb. 7, 2022

Introduction Alzheimer’s disease (AD) is the most prevalent cause of dementia, and emerging evidence suggests that ferroptosis involved in pathological process AD. Materials Methods Three microarray datasets (GSE122063, GSE37263, GSE140829) about AD were collected from GEO database. AD-related module genes identified through a weighted gene co-expression network analysis (WGCNA). The ferroptosis-related extracted FerrDb. apoptosis-related downloaded UniProt as control to show specificity ferroptosis. overlap was performed obtain associated with apoptosis. Then Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analyses protein-protein interaction (PPI) conducted. Cytoscape CytoHubba used identify hub genes, Logistic regression distinguish patients controls. Results 53 obtained. GO revealed response oxidative stress starvation, multicellular organismal homeostasis highly enriched terms. KEGG showed these overlapped not only renal cell carcinoma pathways central carbon metabolism cancer, but also autophagy-related Ferroptosis-related (JUN, SLC2A1, TFRC, ALB, NFE2L2) finally identified, which could controls (P < 0.05). area under ROC curve (AUC) 0.643. Apoptosis-related (STAT1, MCL1, BCL2L11) AUC 0.608, less than former value, suggesting more special apoptosis Conclusion We five are closely can differentiate JUN, NFE2L2 thus potential biomarkers for diagnosis therapeutic monitoring.

Language: Английский

Citations

43

Brain Iron Metabolism, Redox Balance and Neurological Diseases DOI Creative Commons
Guofen Gao, Linhao You, J. J. Zhang

et al.

Antioxidants, Journal Year: 2023, Volume and Issue: 12(6), P. 1289 - 1289

Published: June 16, 2023

The incidence of neurological diseases, such as Parkinson’s disease, Alzheimer’s disease and stroke, is increasing. An increasing number studies have correlated these diseases with brain iron overload the resulting oxidative damage. Brain deficiency has also been closely linked to neurodevelopment. These disorders seriously affect physical mental health patients bring heavy economic burdens families society. Therefore, it important maintain homeostasis understand mechanism affecting reactive oxygen species (ROS) balance, in neural damage, cell death and, ultimately, leading development disease. Evidence shown that many therapies targeting ROS imbalances good preventive therapeutic effects on diseases. This review highlights molecular mechanisms, pathogenesis treatment strategies metabolism

Language: Английский

Citations

36

Porphyromonas gingivalis and the pathogenesis of Alzheimer’s disease DOI Creative Commons
Sixin Liu, Catherine A. Butler, Scott Ayton

et al.

Critical Reviews in Microbiology, Journal Year: 2023, Volume and Issue: 50(2), P. 127 - 137

Published: Jan. 4, 2023

The cause of Alzheimer's disease (AD), and the pathophysiological mechanisms involved, remain major unanswered questions in medical science. Oral bacteria, especially those species associated with chronic periodontitis particularly Porphyromonas gingivalis, are being linked causally to AD pathophysiology a subpopulation susceptible individuals. P. gingivalis produces large amounts proteolytic enzymes, haem iron capture proteins, adhesins internalins that secreted attached cell surface concentrated onto outer membrane vesicles (OMVs). These enzymes adhesive proteins have been shown host tissue damage stimulate inflammatory responses. ecological roles OMVs, their ability disperse widely throughout deliver functional lead proposal they may be link between focal infection subgingivae during neurodegeneration AD. OMVs can cross blood brain barrier accelerate AD-specific neuropathology by increasing neuroinflammation, plaque/tangle formation dysregulation homeostasis, thereby inducing ferroptosis leading neuronal death neurodegeneration.

Language: Английский

Citations

33

Disorders of Endogenous and Exogenous Antioxidants in Neurological Diseases DOI Creative Commons
Izabela Korczowska-Łącka, Bartosz Słowikowski, Thomas Piekut

et al.

Antioxidants, Journal Year: 2023, Volume and Issue: 12(10), P. 1811 - 1811

Published: Sept. 29, 2023

In diseases of the central nervous system, such as Alzheimer's disease (AD), Parkinson's (PD), stroke, amyotrophic lateral sclerosis (ALS), Huntington's (HD), and even epilepsy migraine, oxidative stress load commonly surpasses endogenous antioxidative capacity. While processes have been robustly implicated in pathogenesis these diseases, significance particular antioxidants, both especially exogenous, maintaining redox homeostasis requires further research. Among enzymes catalase, superoxide dismutase, glutathione peroxidase are to disabling free radicals, thereby preventing damage cellular lipids, proteins, nucleic acids. Whether supplementation with endogenously occurring antioxidant compounds melatonin carries any benefit, however, remains equivocal. Similarly, while health benefits certain exogenous including ascorbic acid (vitamin C), carotenoids, polyphenols, sulforaphanes, anthocyanins touted, their clinical efficacy effectiveness neurological contexts need be more defined. Here, we review current literature on mechanisms mitigating comment possible benefit most common antioxidants AD, PD, ALS, HD, epilepsy, migraine. We selected a basically neurodegenerative nature.

Language: Английский

Citations

31