SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close DOI Creative Commons
Gaber El‐Saber Batiha, Hayder M. Al‐kuraishy, Ali I. Al‐Gareeb

et al.

Inflammopharmacology, Journal Year: 2022, Volume and Issue: 31(1), P. 37 - 56

Published: Dec. 29, 2022

Abstract Silent information regulator (SIRT) has distinctive enzymatic activities and physiological functions to control cell-cycle progression, gene expression, DNA stability by targeting histone non-histone proteins. SIRT1 enhances synaptic formation activity, therefore, can reduce the progression of various degenerative brain diseases including Parkinson’s disease (PD). activity is decreased aging with a subsequent increased risk for development diseases. Inhibition promotes inflammatory reactions since inhibits transcription nuclear factor kappa B (NF-κB) which also activation via microRNA miR-34a NAD synthesis. highly expressed in microglia as well neurons, antioxidant anti-inflammatory effects. Therefore, this review aimed find possible role PD neuropathology. neuroprotective effects; downregulation during p53 expression may increase vulnerability neuronal cell deaths. neuropathology linked sequence changes release pro-inflammatory cytokines due signaling pathways. In addition, oxidative stress, disorders, mitochondrial dysfunction, apoptosis contribute mutually Thus, activators play crucial mitigation through amelioration apoptosis,

Language: Английский

Oxidative stress mitigation by antioxidants - An overview on their chemistry and influences on health status DOI
Aurelia Magdalena Pisoschi,

Aneta Pop,

Florin Iordache

et al.

European Journal of Medicinal Chemistry, Journal Year: 2020, Volume and Issue: 209, P. 112891 - 112891

Published: Sept. 30, 2020

Language: Английский

Citations

602
Oxidative Stress in Parkinson's Disease: A Systematic Review and Meta-Analysis DOI Creative Commons

Ze‐Xu Wei,

Xiaowan Li, Xixi Li

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2018, Volume and Issue: 11

Published: July 5, 2018

Oxidative stress has been suggested to play a key role in Parkinson's disease, but inconsistent results were found clinical studies. This study sought quantitatively summarize the blood and cerebrospinal fluid (CSF) oxidative marker data PD patients. We performed systematic search of Pubmed Web Science, studies included if they provided on peripheral CSF concentrations patients healthy control (HC) subjects. Data extracted by three independent investigators from 80 encompassing 7212 6037 HC Of 22 markers analyzed, random effects meta-analysis showed that 8-OhdG, MDA, nitrite ferritin increased with compared In contrast, we levels catalase, uric acid, glutathione total-cholesterol significantly down-regulated when controls. There no significant differences between subjects for blood, Mn, Cu, Zn, Fe, SOD, albumin, peroxidase, vitamin E, ceruloplasmin, triglycerides, lactoferrin, transferrin, LDL-cholesterol HDL-cholesterol. Due limited number small sample size, this only non-significant association 8-OhdG PD. The findings our demonstrated higher ferritin, lower patients, strengthening evidence is accompanied stress.

Language: Английский

Citations

252
Selenium, selenoproteins and neurodegenerative diseases DOI Creative Commons
Bárbara Rita Cardoso, Blaine R. Roberts, Ashley I. Bush

et al.

Metallomics, Journal Year: 2015, Volume and Issue: 7(8), P. 1213 - 1228

Published: May 13, 2015

Abstract It is unsurprising that our understanding of the role selenium in neurological function somewhat immature, considering its relatively recent discovery as an essential element to human health. Selenocysteine, 21st amino acid, defining feature 25 selenoprotein-encoding genes so far discovered within genome. The low abundance these proteins brain belies integral they play normal function, from well-characterised antioxidant activity periphery poorly understood mechanisms modulate mitochondrial and response pathology. Selenium has been identified playing a several neurodegenerative disorders, including Alzheimer's Parkinson's disease, though ‘cause or effect’ disease process remains unclear. This review discusses metabolism detail, specifically with regard it plays central nervous system, examines most current literature investigating how may be involved chronic diseases system.

Language: Английский

Citations

243
The Role of Selenium in Pathologies: An Updated Review DOI Creative Commons

Giulia Barchielli,

Antonella Capperucci, Damiano Tanini

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(2), P. 251 - 251

Published: Jan. 27, 2022

Selenium is an essential microelement required for a number of biological functions. Selenium-and more specifically the amino acid selenocysteine-is present in at least 25 human selenoproteins involved wide variety functions, ranging from regulation reactive oxygen species (ROS) concentration to biosynthesis hormones. These processes also play central role preventing and modulating clinical outcome several diseases, including cancer, diabetes, Alzheimer's disease, mental disorders, cardiovascular fertility impairments, inflammation, infections (including SARS-CoV-2). Over past years, studies focusing on relationship between selenium such pathologies have been reported. Generally, adequate nutritional state-and some cases supplementation-have related improved prognostic reduced risk developing diseases. On other hand, supra-nutritional levels might adverse effects. The results recent these topics are summarized discussed this review, with particular emphasis advances achieved last decade.

Language: Английский

Citations

232
Mitochondrial dysfunction in Parkinson’s disease DOI Creative Commons
Qingsong Hu, Guanghui Wang

Translational Neurodegeneration, Journal Year: 2016, Volume and Issue: 5(1)

Published: July 22, 2016

Parkinson's disease (PD) is the second most common neurodegenerative disease, which characterized by loss of dopaminergic (DA) neurons in substantia nigra pars compacta and formation Lewy bodies neurites surviving DA cases. Although cause PD still unclear, remarkable advances have been made understanding possible causative mechanisms pathogenesis. Numerous studies showed that dysfunction mitochondria may play key roles neuronal loss. Both genetic environmental factors are associated with contribute to mitochondrial The induction neurotoxins inhibit complex I provides direct evidence linking PD. Decrease activity present brain neurotoxin- or factor-induced cellular animal models. Moreover, PINK1 parkin, two autosomal recessive gene products, important mitophagy, a process clear damaged mitochondria. activates parkin ubiquitinate outer membrane proteins induce selective degradation autophagy. In this review, we summarize recent

Language: Английский

Citations

181
Neuroprotection Against Oxidative Stress: Phytochemicals Targeting TrkB Signaling and the Nrf2-ARE Antioxidant System DOI Creative Commons
Md. Abdul Hannan, Raju Dash, Abdullah Al Mamun Sohag

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2020, Volume and Issue: 13

Published: July 2, 2020

Oxidative stress (OS) plays a critical role in the pathophysiology of several brain-related disorders, including neurodegenerative diseases and ischemic stroke, which are major causes dementia. The Nrf2-ARE (nuclear factor erythroid-2-related 2 (Nrf2)/antioxidant responsive element (ARE) antioxidant) system, primary cellular defense against OS, an essential neuroprotection by regulating expressions antioxidant molecules enzymes. However, simultaneous events resulting overproduction reactive oxygen species (ROS) deregulation system damage cell components cause loss neuron structural functional integrity. On other hand, TrkB (tropomyosin-related kinase B) signaling, classical neurotrophin signaling pathway, regulates neuronal survival synaptic plasticity, play pivotal roles memory cognition. Also, specifically TrkB/PI3K/Akt (TrkB-phosphatidylinositol 3 kinase/protein pathway promotes activation nuclear translocation Nrf2, thus, confers OS. is also known to be downregulated brain disorders due lack support. Therefore, activations offer potential approach design novel therapeutic agents for disorders. Here, we briefly overview development OS association between pathogenesis injury. We propose signaling-mediated systems considered pharmacological targets treatment diseases, review literature on neuroprotective effects phytochemicals that can co-activate these systems.

Language: Английский

Citations

156
The complex relationship between obesity and neurodegenerative diseases: an updated review DOI Creative Commons
Alexandre Neto, Adelaide Fernandes, Andreia Barateiro

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2023, Volume and Issue: 17

Published: Nov. 9, 2023

Obesity is a global epidemic, affecting roughly 30% of the world’s population and predicted to rise. This disease results from genetic, behavioral, societal, environmental factors, leading excessive fat accumulation, due insufficient energy expenditure. The adipose tissue, once seen as simple storage depot, now recognized complex organ with various functions, including hormone regulation modulation metabolism, inflammation, homeostasis. associated low-grade inflammatory state has been linked neurodegenerative diseases like multiple sclerosis (MS), Alzheimer’s (AD), Parkinson’s (PD). Mechanistically, reduced expandability leads hypertrophic adipocytes, triggering insulin leptin resistance, blood-brain barrier disruption, altered brain neuronal atrophy, cognitive decline. impacts disorders through shared underlying mechanisms, underscoring its potential modifiable risk factor for these diseases. Nevertheless, further research needed fully grasp intricate connections between obesity neurodegeneration. Collaborative efforts in this field hold promise innovative strategies address relationship develop effective prevention treatment methods, which also includes specific diets physical activities, ultimately improving quality life health.

Language: Английский

Citations

48
Superoxide dismutase and neurological disorders DOI Creative Commons
Saravana Babu Chidambaram, Nikhilesh Anand, Sudhir Varma

et al.

IBRO Neuroscience Reports, Journal Year: 2024, Volume and Issue: 16, P. 373 - 394

Published: Jan. 23, 2024

Superoxide dismutase (SOD) is a common antioxidant enzyme found majorly in living cells. The main physiological role of SOD detoxification and maintain the redox balance, acts as first line defence against Reactive nitrogen species (RNS), oxygen (ROS), other such potentially hazardous molecules. catalyses conversion superoxide anion free radicals (O

Language: Английский

Citations

40
The impact of obesity on neurodegenerative diseases DOI

Janaína Niero Mazon,

Aline Haas de Mello, Gabriela K. Ferreira

et al.

Life Sciences, Journal Year: 2017, Volume and Issue: 182, P. 22 - 28

Published: June 3, 2017

Language: Английский

Citations

154
Coronavirus S protein-induced fusion is blocked prior to hemifusion by Abl kinase inhibitors DOI Open Access
Jeanne M. Sisk, Matthew B. Frieman, Carolyn E. Machamer

et al.

Journal of General Virology, Journal Year: 2018, Volume and Issue: 99(5), P. 619 - 630

Published: March 20, 2018

Enveloped viruses gain entry into host cells by fusing with cellular membranes, a step that is required for virus replication. Coronaviruses, including the severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East (MERS-CoV) and infectious bronchitis (IBV), fuse at plasma membrane or use receptor-mediated endocytosis endosomes, depending on cell tissue type. The spike (S) protein mediates fusion membrane. We have shown previously an Abelson (Abl) kinase inhibitor, imatinib, significantly reduces SARS-CoV MERS-CoV viral titres prevents endosomal HIV SARS S MERS pseudotyped virions. are classified as BSL-3 viruses, which makes experimentation mechanisms involved in infection more challenging. Here, we IBV, BSL-2 virus, model studying role of Abl activity during infection. found imatinib two specific inhibitors, GNF2 GNF5, reduce IBV blocking first round Additionally, all three drugs prevented S-induced syncytia formation prior to hemifusion step. Our results indicate (both virus-cell cell-cell) blocked presence inhibitors. Studying effects inhibitors will be useful identifying pathways This provide insight possible therapeutic targets treat infections current well newly emerging coronaviruses.

Language: Английский

Citations

154