Potential Effects of Leukotriene Receptor Antagonist Montelukast in Treatment of Neuroinflammation in Parkinson’s Disease

Wallin, Johan; Svenningsson, Per

doi:10.3390/ijms22115606

Cited by 19 publications

(12 citation statements)

References 99 publications

(118 reference statements)

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“…Furthermore, several other agents have been proven to exert a neuroprotective action on PD, including celecoxib (a selective COX-2 inhibitor) [ 185 ], montelukast (a leukotriene receptor antagonist) [ 186 , 187 , 188 , 193 ], and tocopherol (vitamin E) [ 194 , 195 ]. Therapy with the aid of celecoxib (< 20 μM) has been shown to reinstate SH-SY5Y cells that had been potentially subjected to paraquat and 6-OHDA prompted damage [ 185 ].…”

Section: Experimental Studies Portraying the Deep Insights Into The Neuroprotective Role Of Ppar Agonists In Pdmentioning

confidence: 99%

Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

Behl

Madaan

Sehgal

et al. 2021

IJMS

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One of the utmost frequently emerging neurodegenerative diseases, Parkinson’s disease (PD) must be comprehended through the forfeit of dopamine (DA)-generating nerve cells in the substantia nigra pars compacta (SN-PC). The etiology and pathogenesis underlying the emergence of PD is still obscure. However, expanding corroboration encourages the involvement of genetic and environmental factors in the etiology of PD. The destruction of numerous cellular components, namely oxidative stress, ubiquitin-proteasome system (UPS) dysfunction, autophagy-lysosome system dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction partake in the pathogenesis of PD. Present-day pharmacotherapy can alleviate the manifestations, but no therapy has been demonstrated to cease disease progression. Peroxisome proliferator-activated receptors (PPARs) are ligand-directed transcription factors pertaining to the class of nuclear hormone receptors (NHR), and are implicated in the modulation of mitochondrial operation, inflammation, wound healing, redox equilibrium, and metabolism of blood sugar and lipids. Numerous PPAR agonists have been recognized to safeguard nerve cells from oxidative destruction, inflammation, and programmed cell death in PD and other neurodegenerative diseases. Additionally, various investigations suggest that regular administration of PPAR-activating non-steroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, indomethacin), and leukotriene receptor antagonists (montelukast) were related to the de-escalated evolution of neurodegenerative diseases. The present review elucidates the emerging evidence enlightening the neuroprotective outcomes of PPAR agonists in in vivo and in vitro models experiencing PD. Existing articles up to the present were procured through PubMed, MEDLINE, etc., utilizing specific keywords spotlighted in this review. Furthermore, the authors aim to provide insight into the neuroprotective actions of PPAR agonists by outlining the pharmacological mechanism. As a conclusion, PPAR agonists exhibit neuroprotection through modulating the expression of a group of genes implicated in cellular survival pathways, and may be a propitious target in the therapy of incapacitating neurodegenerative diseases like PD.

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Section: Experimental Studies Portraying the Deep Insights Into The Neuroprotective Role Of Ppar Agonists In Pdmentioning

confidence: 99%

Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

Behl

Madaan

Sehgal

et al. 2021

IJMS

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“…The pattern of serum TNF-α concentration increment through the 5 th , 10 th , and 15 th day after diagnosis, (A) for COVID without chronic disease group, (B) for COVID with chronic disease group TNF-α concentration was evaluated for all age subgroups on the 5th, 10th, and 15th days after diagnosis; the results showed no significant difference among the different age subgroups on the 5th and 10th days for COVID without chronic disease. While on the 15th day, a significant (P<0.01-P<0.001) difference was found between the (60-69) age subgroup and the (40-49), (30)(31)(32)(33)(34)(35)(36)(37)(38)(39), (20-29) age subgroup as shown in (Figure -8-). For COVID with chronic disease in the (60-69) age subgroups, the TNF-α concentration was significantly (P<0.05-P<0.0001) higher than in other age subgroups.…”

Section: Figurementioning

confidence: 79%

measurement of some cytokines can predict the severity of COVID-19 infection among different age groups

Rahim

Farhan

2022

ijhs

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Coronavirus disease 2019 (COVID-19. Outbreak of severe acute respiratory syndrome (SARS-CoV-2)) started in Wuhan, the capital of Hubei Province, Republic of China, and has spread worldwide. Pandemic 11 March 2020 is closely related to the pangolin and the bat virus and is also believed to be of zoonotic origin.Symptoms include cough, muscle aches, sputum production, headache, hemoptysis, diarrhea, shortness of breath, and in some cases, acute respiratory distress syndrome (ARDS). Acute respiratory distress syndrome (ARDS), sudden heart damage, or secondary infection can happen to affected people. This study provides evidence that inflammation reflected by cytokine storms in COVID-19 patients could have contributed to disease exacerbations, so we analyzed the gene expression predictive values of (IL-6 and INF α). A cytokine storm can occur due to an infection, autoimmune condition, or other diseases. It may also occur after treatment with some types of immunotherapy. Symptoms include high fever, inflammation (redness and swelling), severe fatigue, and nausea. Sometimes, a cytokine storm may be severe or life-threatening and lead to multiple organ failures. Also called hyper cytokines. Recent studies on COVID-19 infected patients have shown that these individuals exhibit high levels of both pro-inflammatory cytokines, which include IFN-γ, IL-1β, IL-6, IL-2, and chemokine's

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“…Employment of agents pertaining to the class of monoamine oxidase B (MAO-B) and catechol-O-methyltransferase (COMT) blockers can successfully regulate DA deprivation in the brain [ 82 ]. Aside from that, non-steroidal anti-inflammatory drugs (NSAIDs) (aspirin and ibuprofen) [ 83 ], leukotriene receptor antagonist (montelukast) [ 84 ], vitamins (B 3 , D, E, and C) [ 85 ], alcohol imbibing [ 86 ], smoking [ 86 ], caffeine intake [ 87 ], and physical exercise [ 88 ] have been demonstrated to render significant neuronal protection in PD. Recent investigation has revealed that escalated alcohol consumption possesses safeguarding effect over the risk of PD (with odds ratio 0.79; 95% confidence interval 0.65–0.96; probability value = 0.021), with the significant involvement of alcohol dehydrogenase 1B [ 86 ].…”

Section: Parkinson’s Disease: Etiological Factors Pathogenic Events and Treatmentmentioning

confidence: 99%

Mechanistic Insights Expatiating the Redox-Active-Metal-Mediated Neuronal Degeneration in Parkinson’s Disease

Behl

Madaan

Sehgal

et al. 2022

IJMS

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Parkinson’s disease (PD) is a complicated and incapacitating neurodegenerative malady that emanates following the dopaminergic (DArgic) nerve cell deprivation in the substantia nigra pars compacta (SN-PC). The etiopathogenesis of PD is still abstruse. Howbeit, PD is hypothesized to be precipitated by an amalgamation of genetic mutations and exposure to environmental toxins. The aggregation of α-synucelin within the Lewy bodies (LBs), escalated oxidative stress (OS), autophagy-lysosome system impairment, ubiquitin-proteasome system (UPS) impairment, mitochondrial abnormality, programmed cell death, and neuroinflammation are regarded as imperative events that actively participate in PD pathogenesis. The central nervous system (CNS) relies heavily on redox-active metals, particularly iron (Fe) and copper (Cu), in order to modulate pivotal operations, for instance, myelin generation, synthesis of neurotransmitters, synaptic signaling, and conveyance of oxygen (O2). The duo, namely, Fe and Cu, following their inordinate exposure, are viable of permeating across the blood–brain barrier (BBB) and moving inside the brain, thereby culminating in the escalated OS (through a reactive oxygen species (ROS)-reliant pathway), α-synuclein aggregation within the LBs, and lipid peroxidation, which consequently results in the destruction of DArgic nerve cells and facilitates PD emanation. This review delineates the metabolism of Fe and Cu in the CNS, their role and disrupted balance in PD. An in-depth investigation was carried out by utilizing the existing publications obtained from prestigious medical databases employing particular keywords mentioned in the current paper. Moreover, we also focus on decoding the role of metal complexes and chelators in PD treatment. Conclusively, metal chelators hold the aptitude to elicit the scavenging of mobile/fluctuating metal ions, which in turn culminates in the suppression of ROS generation, and thereby prelude the evolution of PD.

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Potential Effects of Leukotriene Receptor Antagonist Montelukast in Treatment of Neuroinflammation in Parkinson’s Disease

Cited by 19 publications

References 99 publications

Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

measurement of some cytokines can predict the severity of COVID-19 infection among different age groups

Mechanistic Insights Expatiating the Redox-Active-Metal-Mediated Neuronal Degeneration in Parkinson’s Disease

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