Mitochondrial dysfunction in Parkinson’s disease – a key disease hallmark with therapeutic potential

Molecular Neurodegeneration, Journal Year: 2023, Volume and Issue: 18(1)

Published: Nov. 11, 2023

Abstract Mitochondrial dysfunction is strongly implicated in the etiology of idiopathic and genetic Parkinson’s disease (PD). However, strategies aimed at ameliorating mitochondrial dysfunction, including antioxidants, antidiabetic drugs, iron chelators, have failed disease-modification clinical trials. In this review, we summarize cellular determinants impairment electron transport chain complex 1, increased oxidative stress, disturbed quality control mechanisms, bioenergetic deficiency. addition, outline pathways to neurodegeneration current context PD pathogenesis, review past treatment an attempt better understand why translational efforts thus far been unsuccessful.

Language: Английский

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Medicinal and food plant: Cistanches Herba, a potential therapeutic hope for Parkinson’s disease and related complications

Journal of Agriculture and Food Research, Journal Year: 2025, Volume and Issue: unknown, P. 101671 - 101671

Published: Jan. 1, 2025

Language: Английский

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Sensory quality and Metabolomic fingerprinting of Lacticaseibacillus paracasei-derived fermented soymilk beverages: Impact of starter strain and storage

Food Chemistry, Journal Year: 2025, Volume and Issue: 482, P. 144147 - 144147

Published: April 2, 2025

Language: Английский

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Integrative Metabolome and Proteome Analysis of Cerebrospinal Fluid in Parkinson’s Disease

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(21), P. 11406 - 11406

Published: Oct. 23, 2024

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons in substantia nigra. Recent studies have highlighted significant role cerebrospinal fluid (CSF) reflecting pathophysiological PD brain conditions analyzing components CSF. Based on published literature, we created single network with altered metabolites CSF patients PD. We analyzed biological functions related to transmembrane mitochondria, respiration neurodegeneration, and using bioinformatics tool. As proteome reflects phenotypes, collected data based papers, function showed similarities that metabolomic network. Then, integrated metabolome proteome. In silico predictions metabolomics proteomics neurodegeneration were predicted be activated. contrast, mitochondrial activity suppressed This review underscores importance omics analyses deciphering PD's complex biochemical networks underlying neurodegeneration.

Language: Английский

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Endoplasmic Reticulum Stress Signaling in the Regulation of Hepatic Pathological Responses

Stresses, Journal Year: 2024, Volume and Issue: 4(3), P. 481 - 504

Published: Aug. 1, 2024

The endoplasmic reticulum (ER) is a vital cell organelle that primarily involved in the processes of protein folding, maintenance intracellular calcium storage and lipid synthesis order to maintain cellular homeostasis. To achieve this meticulous order, several ER-dependent have be unison perfect harmony. However, persistent supply newly synthesized proteins strains ER mainly due accumulation unfolded proteins, thus ultimately leading an imbalance termed stress. Although misfolded frequent reason for initiation stress, it also induced by hyper-production reactive oxygen species, aberrant leakage from effect cytokines. stress signals are conveyed via three arms ER, namely PERK, IRE1 ATF6. Signal transduction form these signaling molecules often converges on transcriptional upregulation CHOP its related mechanisms. If unresolved, then can lead death through different mechanisms, including apoptosis, proptosis, etc. In liver, has been observed plays critical role hepatic damage under experimental conditions. This review highlights liver pathologies.

Language: Английский

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NR1H4 ameliorates Parkinson’s disease via inhibiting astrocyte activation and neuroinflammation in a CEBPβ/NF-κB dependent manner

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 142, P. 113087 - 113087

Published: Sept. 5, 2024

Language: Английский

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Lumbricus Extract Prevents LPS-Induced Inflammatory Activation of BV2 Microglia and Glutamate-Induced Hippocampal HT22 Cell Death by Suppressing MAPK/NF-κB/NLRP3 Signaling and Oxidative Stress

Current Issues in Molecular Biology, Journal Year: 2023, Volume and Issue: 45(12), P. 9926 - 9942

Published: Dec. 11, 2023

Microglia-induced inflammatory signaling and neuronal oxidative stress are mutually reinforcing processes central to the pathogenesis of neurodegenerative diseases. Recent studies have shown that extracts dried Pheretima aspergillum (Lumbricus) can inhibit tissue fibrosis, mitochondrial damage, asthma. However, effects Lumbricus on neuroinflammation damage not been previously studied. Therefore, evaluate therapeutic potential extract for diseases, current study assessed extract’s anti-inflammatory antioxidant activities in BV2 microglial cultures stimulated with lipopolysaccharide (LPS) along its neuroprotective efficacy mouse hippocampal HT22 cell treated excess glutamate. dose-dependently inhibited LPS-induced production multiple proinflammatory cytokines (tumor necrosis factor-α, interleukin (IL)-6, IL-1β) reversed upregulation enzymes (inducible nitric oxide synthase cyclooxygenase-2). also activated antioxidative nuclear factor erythroid 2-relayed 2/heme oxygenase-1 pathway activation factor-κB/mitogen-activated protein kinases/NOD-like receptor family pyrin domain containing 3 pathway. In addition, suppressed glutamate-induced necrotic apoptotic death cells, associated upregulated expression antiapoptotic proteins, downregulation pro-apoptotic reduced accumulation reactive oxygen species. Chromatography revealed contained uracil, hypoxanthine, uridine, xanthine, adenosine, inosine, guanosine. Its against excitotoxic reported herein support

Language: Английский

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Inosine exerts dopaminergic neuroprotective effects via mitigation of NLRP3 inflammasome activation

Neuropharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 110278 - 110278

Published: Dec. 1, 2024

Language: Английский

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