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Volume 10, Issue 3 (Summer 2024)
Caspian J Neurol Sci 2024, 10(3): 151-168 |
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Kosari M, Asgari Taei A, Klegeris A, Soleimani S, Tavasol A, Jazi K, et al . The Role of Dysregulated Neuroinflammatory Molecular Pathways in Parkinson Disease: A Systematic Review. Caspian J Neurol Sci 2024; 10 (3) :151-168
URL: http://cjns.gums.ac.ir/article-1-712-en.html
URL: http://cjns.gums.ac.ir/article-1-712-en.html
Mohammadreza Kosari1 
, Afsaneh Asgari Taei2 , Andis Klegeris3 , Sevim Soleimani4 , Arian Tavasol4 , Kimia Jazi5 , Kimia Eyvani6 , Ashkan Bahrami7 , Zahra Farrokhi8 , Farnoosh Vosough9 , Faraz Rahmani Khajeh10 , Saleh Behzadi11 , Zohreh Zamani *12
, Afsaneh Asgari Taei2 , Andis Klegeris3 , Sevim Soleimani4 , Arian Tavasol4 , Kimia Jazi5 , Kimia Eyvani6 , Ashkan Bahrami7 , Zahra Farrokhi8 , Farnoosh Vosough9 , Faraz Rahmani Khajeh10 , Saleh Behzadi11 , Zohreh Zamani *12
1- Tongji Medical College, Wuhan Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
2- Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3- Department of Biology, Faculty of Science, University of British Columbia Okanagan Campus, Kelowna, Canada.
4- School of Medicine, Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
5- Student Research Committee, School of Medicine, Qom University of Medical Sciences, Qom, Iran.
6- Student Research Committee, Faculty of Medicine,Guilan University of Medical Sciences, Rasht, Iran.
7- Student Research Committee, Faculty of Medicine, Kashan University of Medical Science, Kashan, Iran.
8- Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
9- Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
10- Student Research Committee, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
11- Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
12- Department of Neurology, Firoozabadi Clinical Research Development Unit (FACRDU), Iran University of Medical Sciences, Tehran, Iran. ,zamani.zhrh@gmail.com
2- Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3- Department of Biology, Faculty of Science, University of British Columbia Okanagan Campus, Kelowna, Canada.
4- School of Medicine, Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
5- Student Research Committee, School of Medicine, Qom University of Medical Sciences, Qom, Iran.
6- Student Research Committee, Faculty of Medicine,Guilan University of Medical Sciences, Rasht, Iran.
7- Student Research Committee, Faculty of Medicine, Kashan University of Medical Science, Kashan, Iran.
8- Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
9- Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
10- Student Research Committee, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
11- Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
12- Department of Neurology, Firoozabadi Clinical Research Development Unit (FACRDU), Iran University of Medical Sciences, Tehran, Iran. ,
Abstract: (1120 Views)
Background: Parkinson disease (PD) is a prevalent neurodegenerative disorder affecting dopaminergic neurons in the substantia nigra (SN). Neuroinflammation has a vital role in PD pathophysiology.
Objectives: This study assesses whether the neuroinflammatory molecular and signaling pathways could be associated with PD’s progression and clinical manifestations.
Materials & Methods: PubMed, Web of Science, Embase, and Scopus databases were investigated from 2006 until December 2023 to find relevant studies. All observational studies written in English and reporting qualitative or quantitative information on the relationship between neuroinflammation and PD were included in this review.
Results: Finally, 41 papers were involved in the systematic review. According to the involved studies, it is suggested that tumor necrosis factor-α, C-reactive protein, microsomal prostaglandin E synthase1, toll-like receptor-4 (TLR-4), CCL23, CCL25, TNF-receptor superfamily member 9, EV-derived cytokines, transforming growth factor alpha, vascular endothelial growth factor A, SH-SY5Y, TLR 2/4, miR-485-3p, leucine-rich repeat kinase 2, and α-synuclein may be upregulated in the PD patients. Also, the activity of astrocytes and microglial cells was reported to be increased in PD patients through different mechanisms.
Conclusion: This study demonstrated that the neurodegeneration in PD could be initiated by α-synuclein protein aggregation and the activation of astrocytes and microglial cells, which leads to neuroinflammation characterized by inflammatory responses in neurons. Finally, chronic neuroinflammation could be the cause of dopaminergic neuronal death in SN. The impact of both single and all factors involved in neuroinflammation was assessed to plan further studies in a particular pathway to intercept the onset of inflammatory pathways in favor of therapeutic purposes.
Objectives: This study assesses whether the neuroinflammatory molecular and signaling pathways could be associated with PD’s progression and clinical manifestations.
Materials & Methods: PubMed, Web of Science, Embase, and Scopus databases were investigated from 2006 until December 2023 to find relevant studies. All observational studies written in English and reporting qualitative or quantitative information on the relationship between neuroinflammation and PD were included in this review.
Results: Finally, 41 papers were involved in the systematic review. According to the involved studies, it is suggested that tumor necrosis factor-α, C-reactive protein, microsomal prostaglandin E synthase1, toll-like receptor-4 (TLR-4), CCL23, CCL25, TNF-receptor superfamily member 9, EV-derived cytokines, transforming growth factor alpha, vascular endothelial growth factor A, SH-SY5Y, TLR 2/4, miR-485-3p, leucine-rich repeat kinase 2, and α-synuclein may be upregulated in the PD patients. Also, the activity of astrocytes and microglial cells was reported to be increased in PD patients through different mechanisms.
Conclusion: This study demonstrated that the neurodegeneration in PD could be initiated by α-synuclein protein aggregation and the activation of astrocytes and microglial cells, which leads to neuroinflammation characterized by inflammatory responses in neurons. Finally, chronic neuroinflammation could be the cause of dopaminergic neuronal death in SN. The impact of both single and all factors involved in neuroinflammation was assessed to plan further studies in a particular pathway to intercept the onset of inflammatory pathways in favor of therapeutic purposes.
Keywords: C-reactive protein (CRP), Tumor necrosis factor (TNF)-α, α-Synuclein, Toll-like receptor (TLR)2, TLR9, Neuroinflammation, Parkinson disease (PD), Lipocalin-2 (LCN2)
Type of Study: Review |
Subject:
Special
Received: 2024/04/23 | Accepted: 2024/04/30 | Published: 2024/07/17
Received: 2024/04/23 | Accepted: 2024/04/30 | Published: 2024/07/17
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