Serum Levels of Plasminogen Activator Inhibitor-1 in Patients with Parkinson’s Disease
Abstract Objectives: The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson’s disease (PD) and their relationship with clinical findings and treatment of disease. Methods: The study included 125 PD patients and 48 healthy controls. P...
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| Published in | Medical principles and practice Vol. 33; no. 6; pp. 562 - 568 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
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Basel, Switzerland
S. Karger AG
01.12.2024
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| Abstract | Abstract
Objectives: The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson’s disease (PD) and their relationship with clinical findings and treatment of disease. Methods: The study included 125 PD patients and 48 healthy controls. Patients have been taking effective dopaminergic treatment regularly. The clinical severity of parkinsonism was assessed using the Hoehn and Yahr (HY) staging scale and the Unified PD Rating Scale (UPDRS). PAI-1 level analysis was performed by enzyme-linked immunosorbent assay. Results: Patients with PD had significantly lower serum PAI-1 levels than healthy controls (p < 0.001). Correlations with clinical findings showed only a marginally positive correlation between serum PAI-1 and HY score (r = 0.170, p = 0.05). In contrast, no significant correlation was demonstrated with the UPDRS score or other clinical parameters. Conclusion: This is the first comprehensive analysis of serum PAI-1 levels in patients with PD. The distribution of PAI-1 in PD appears to be complex. The study results implicate that the paradoxical effects of tissue plasminogen activator on the brain parenchyma can be important in the pathophysiology of PD. Future studies are needed to elucidate the role of fibrinolytic system components in PD. |
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| AbstractList | Studies have revealed that genetic mutations, mitochondrial dysfunction, oxidative stress, immunological dysfunction, neuroinflammation, and protein aggregation contribute to the pathogenesis of PD. Recent studies have focused on candidate molecules that can serve as surrogate biomarkers in PD [4‒6]. [...]vascular risk factors have been implicated in the onset of AD but not in PD. In contrast, cellular death and neuroinflammation are involved in the pathophysiology of PD [4, 5, 8]. [...]PAI-1 levels in PD are of clinical interest. Materials and Methods Subjects This study included 125 consecutive patients with PD who attended the Movement Disorders Clinic of Istanbul Medeniyet University, Goztepe Training and Research Hospital, and 48 consecutive healthy subjects who were the spouses of the patients or individuals who volunteered. Exclusion criteria were as follows: the presence of dementia and/or having scores less than 24 on the mini-mental state test; a psychiatric disorder diagnosed with a structured clinical interview and/or on the Geriatric Depression Inventory, a score of 17 or higher measuring moderate to severe depression; history of comorbidities including diabetes mellitus, cardiovascular disease, cerebrovascular disorder, hyperlipidemia, infectious disease, neoplasm, endocrine disorder, autoimmune, renal, hepatic, and hematologic disorders; use of an anti-inflammatory or immunosuppressive drug; and a history of alcohol and/or substance abuse. Objectives: The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson’s disease (PD) and their relationship with clinical findings and treatment of disease. Methods: The study included 125 PD patients and 48 healthy controls. Patients have been taking effective dopaminergic treatment regularly. The clinical severity of parkinsonism was assessed using the Hoehn and Yahr (HY) staging scale and the Unified PD Rating Scale (UPDRS). PAI-1 level analysis was performed by enzyme-linked immunosorbent assay. Results: Patients with PD had significantly lower serum PAI-1 levels than healthy controls (p < 0.001). Correlations with clinical findings showed only a marginally positive correlation between serum PAI-1 and HY score (r = 0.170, p = 0.05). In contrast, no significant correlation was demonstrated with the UPDRS score or other clinical parameters. Conclusion: This is the first comprehensive analysis of serum PAI-1 levels in patients with PD. The distribution of PAI-1 in PD appears to be complex. The study results implicate that the paradoxical effects of tissue plasminogen activator on the brain parenchyma can be important in the pathophysiology of PD. Future studies are needed to elucidate the role of fibrinolytic system components in PD. Abstract Objectives: The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson’s disease (PD) and their relationship with clinical findings and treatment of disease. Methods: The study included 125 PD patients and 48 healthy controls. Patients have been taking effective dopaminergic treatment regularly. The clinical severity of parkinsonism was assessed using the Hoehn and Yahr (HY) staging scale and the Unified PD Rating Scale (UPDRS). PAI-1 level analysis was performed by enzyme-linked immunosorbent assay. Results: Patients with PD had significantly lower serum PAI-1 levels than healthy controls (p < 0.001). Correlations with clinical findings showed only a marginally positive correlation between serum PAI-1 and HY score (r = 0.170, p = 0.05). In contrast, no significant correlation was demonstrated with the UPDRS score or other clinical parameters. Conclusion: This is the first comprehensive analysis of serum PAI-1 levels in patients with PD. The distribution of PAI-1 in PD appears to be complex. The study results implicate that the paradoxical effects of tissue plasminogen activator on the brain parenchyma can be important in the pathophysiology of PD. Future studies are needed to elucidate the role of fibrinolytic system components in PD. The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson's disease (PD) and their relationship with clinical findings and treatment of disease.OBJECTIVESThe aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson's disease (PD) and their relationship with clinical findings and treatment of disease.The study included 125 PD patients and 48 healthy controls. Patients have been taking effective dopaminergic treatment regularly. The clinical severity of parkinsonism was assessed using the Hoehn and Yahr (HY) staging scale and the Unified PD Rating Scale (UPDRS). PAI-1 level analysis was performed by enzyme-linked immunosorbent assay.METHODSThe study included 125 PD patients and 48 healthy controls. Patients have been taking effective dopaminergic treatment regularly. The clinical severity of parkinsonism was assessed using the Hoehn and Yahr (HY) staging scale and the Unified PD Rating Scale (UPDRS). PAI-1 level analysis was performed by enzyme-linked immunosorbent assay.Patients with PD had significantly lower serum PAI-1 levels than healthy controls (p < 0.001). Correlations with clinical findings showed only a marginally positive correlation between serum PAI-1 and HY score (r = 0.170, p = 0.05). In contrast, no significant correlation was demonstrated with the UPDRS score or other clinical parameters.RESULTSPatients with PD had significantly lower serum PAI-1 levels than healthy controls (p < 0.001). Correlations with clinical findings showed only a marginally positive correlation between serum PAI-1 and HY score (r = 0.170, p = 0.05). In contrast, no significant correlation was demonstrated with the UPDRS score or other clinical parameters.This is the first comprehensive analysis of serum PAI-1 levels in patients with PD. The distribution of PAI-1 in PD appears to be complex. The study results implicate that the paradoxical effects of tissue plasminogen activator on the brain parenchyma can be important in the pathophysiology of PD. Future studies are needed to elucidate the role of fibrinolytic system components in PD.CONCLUSIONThis is the first comprehensive analysis of serum PAI-1 levels in patients with PD. The distribution of PAI-1 in PD appears to be complex. The study results implicate that the paradoxical effects of tissue plasminogen activator on the brain parenchyma can be important in the pathophysiology of PD. Future studies are needed to elucidate the role of fibrinolytic system components in PD. The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson's disease (PD) and their relationship with clinical findings and treatment of disease. The study included 125 PD patients and 48 healthy controls. Patients have been taking effective dopaminergic treatment regularly. The clinical severity of parkinsonism was assessed using the Hoehn and Yahr (HY) staging scale and the Unified PD Rating Scale (UPDRS). PAI-1 level analysis was performed by enzyme-linked immunosorbent assay. Patients with PD had significantly lower serum PAI-1 levels than healthy controls (p < 0.001). Correlations with clinical findings showed only a marginally positive correlation between serum PAI-1 and HY score (r = 0.170, p = 0.05). In contrast, no significant correlation was demonstrated with the UPDRS score or other clinical parameters. This is the first comprehensive analysis of serum PAI-1 levels in patients with PD. The distribution of PAI-1 in PD appears to be complex. The study results implicate that the paradoxical effects of tissue plasminogen activator on the brain parenchyma can be important in the pathophysiology of PD. Future studies are needed to elucidate the role of fibrinolytic system components in PD. |
| Author | Agirbasli, Mehmet Tanrikulu, Azra Meryem Ozdilek, Betul |
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| References | Guo C, Wang T, Zhang D, Ge X, Li J. Plasminogen decreases Aβ42 and Tau deposition, and shows multi-beneficial effects on Alzheimer’s disease in mice and humans. Biochem Biophys Res Commun. 2023;654:102–11. Liu R-M, Van Groen T, Katre A, Cao D, Kadisha I, Ballinger C, . Knockout of plasminogen activator inhibitor 1 gene reduces amyloid beta peptide burden in a mouse model of Alzheimer’s disease. Neurobiol Aging. 2011;32(6):1079–89. Johnson ME, Stecher B, Labrie V, Brundin L, Brundin P. Triggers, facilitators, and aggravators: redefining Parkinson’s disease pathogenesis. Trends Neurosci. 2019;42(1):4–13. Agirbasli M. Pivotal role of plasminogen-activator inhibitor 1 in vascular disease. Int J Clin Pract. 2005;59(1):102–6. Pan H, Zhao Y, Zhai Z, Zheng J, Zhou Y, Zhai Q, . Role of plasminogen activator inhibitor-1 in the diagnosis and prognosis of patients with Parkinson’s disease. Exp Ther Med. 2018;15(6):5517–22. Poewe W, Seppi K, Tanner CM, Halliday GM, Brundin P, Volkmann J, . Parkinson disease. Nat Rev Dis Primers. 2017;3:17013. Simon DK, Tanner CM, Brundin P. Parkinson disease epidemiology, pathology, genetics, and pathophysiology. Clin Geriatr Med. 2020;36(1):1–12. Dupont DM, Madsen JB, Kristensen T, Bodker JS, Blouse GE, Wind T, . Biochemical properties of plasminogen activator inhibitor-1. Front Biosci. 2009;14(4):1337–61. Vaughan DE, Rai R, Khan SS, Eren M, Ghosh AK. Plasminogen activator inhibitor-1 is a marker and a mediator of senescence. Arterioscler Thromb Vasc Biol. 2017;37(8):1446–52. Yarns BC, Holiday KA, Carlson DM, Cosgrove CK, Melrose RJ. Pathophysiology of Alzheimer's disease. Psychiatr Clin North Am. 2022;45(4):663–76. Viswanathan A, Rocca WA, Tzourio C. Vascular risk factors and dementia: how to move forward. Neurology. 2009;72(4):368–74. Angelucci F, Čechová K, Průša R, Hort J. Amyloid beta soluble forms and plasminogen activation system in Alzheimer’s disease: consequences on extracellular maturation of brain-derived neurotrophic factor and therapeutic implications. CNS Neurosci Ther. 2019;25(3):303–13. Nolan YM, Sullivan AM, Toulouse A. Parkinson’s disease in the nuclear age of neuroinflammation. Trends Mol Med. 2013;19(3):187–96. Fahn S, Elton RL. UPDRS program members. Unified Parkinsons disease rating scale. In: Fahn S, Marsden CD, Goldstein M, Calne DB, editors. Recent developments in Parkinsons disease. Florham Park NJ: Macmillan Healthcare Information; 1987. Vol. 2; p. 153–63. Grünblatt E. Parkinson’s disease: molecular risk factors. Parkinsonism Relat Disord. 2012;18(Suppl 1):S45–8. Yepes M. Fibrinolytic and non-fibrinolytic roles of tissue-type plasminogen activator in the ischemic brain. Neuroscience. 2024;542:69–80. Rein-Smith CM, Church FC. Emerging pathophysiological roles for fibrinolysis. Curr Opin Hematol. 2014;21(5):438–44. Yamamoto K, Takeshita K, Saito H. Plasminogen activator inhibitor-1 in aging. Semin Thromb Hemost. 2014;40(6):652–9. Tomlinson CL, Stowe R, Patel S, Rick C, Gray R, Clarke CE. Systematic review of levodopa dose equivalency reporting in Parkinson’s disease. Mov Disord. 2010;25(15):2649–53. Goetz CG, Poewe W, Rascol O, Sampaio C, Stebbins GT, Counsell C, . Movement disorder society task force report on the hoehn and yahr staging scale: status and recommendations. Mov Disord. 2004;19(9):1020–8. Michel PP, Hirsch EC, Hunot S. Understanding dopaminergic cell death pathways in Parkinson disease. Neuron. 2016;90(4):675–91. Postuma RB, Berg D, Stern M, Poewe W, Olanow CW, Oertel W, . MDS clinical diagnostic criteria for Parkinson’s disease. Mov Disord. 2015;30(12):1591–601. Angelucci F, Veverova K, Katonová A, Vyhnalek M, Hort J. Serum PAI-1/BDNF ratio is increased in Alzheimer’s disease and correlates with disease severity. ACS Omega. 2023;8(39):36025–31. Mehra A, Ali C, Parcq J, Vivien D, Docagne F. The plasminogen activation system in neuroinflammation. Biochim Biophys Acta. 2016;1862(3):395–402. Angelucci F, Veverova K, Katonová A, Piendel L, Vyhnalek M, Hort J. Alzheimer’s disease severity is associated with an imbalance in serum levels of enzymes regulating plasmin synthesis. Pharmaceuticals. 2022;15(9):1074. Barker R, Kehoe PG, Love S. Activators and inhibitors of the plasminogen system in Alzheimer’s disease. J Cel Mol Med. 2012;16(4):865–76. Xu Q, Lai Q, Wang J, Zhuang L, Cheng L, Mo Y, . Association between plasminogen activator inhibitor-1 gene polymorphisms and susceptibility to Parkinson’s disease in Chinese patients. Acta Neurol Belg. 2022;122(6):1557–66. Reuland CJ, Church FC. Synergy between plasminogen activator inhibitor-1, α-synuclein, and neuroinflammation in Parkinson’s disease. Med Hypotheses. 2020;138:109602. ref13 ref12 ref15 ref14 ref11 ref10 ref2 ref1 ref17 ref16 ref19 ref18 ref24 ref23 ref26 ref25 ref20 ref22 ref21 ref27 ref8 ref7 ref9 ref4 ref3 ref6 ref5 |
| References_xml | – reference: Dupont DM, Madsen JB, Kristensen T, Bodker JS, Blouse GE, Wind T, . Biochemical properties of plasminogen activator inhibitor-1. Front Biosci. 2009;14(4):1337–61. – reference: Yepes M. Fibrinolytic and non-fibrinolytic roles of tissue-type plasminogen activator in the ischemic brain. Neuroscience. 2024;542:69–80. – reference: Angelucci F, Veverova K, Katonová A, Vyhnalek M, Hort J. Serum PAI-1/BDNF ratio is increased in Alzheimer’s disease and correlates with disease severity. ACS Omega. 2023;8(39):36025–31. – reference: Tomlinson CL, Stowe R, Patel S, Rick C, Gray R, Clarke CE. Systematic review of levodopa dose equivalency reporting in Parkinson’s disease. Mov Disord. 2010;25(15):2649–53. – reference: Angelucci F, Čechová K, Průša R, Hort J. Amyloid beta soluble forms and plasminogen activation system in Alzheimer’s disease: consequences on extracellular maturation of brain-derived neurotrophic factor and therapeutic implications. CNS Neurosci Ther. 2019;25(3):303–13. – reference: Goetz CG, Poewe W, Rascol O, Sampaio C, Stebbins GT, Counsell C, . Movement disorder society task force report on the hoehn and yahr staging scale: status and recommendations. Mov Disord. 2004;19(9):1020–8. – reference: Simon DK, Tanner CM, Brundin P. Parkinson disease epidemiology, pathology, genetics, and pathophysiology. Clin Geriatr Med. 2020;36(1):1–12. – reference: Liu R-M, Van Groen T, Katre A, Cao D, Kadisha I, Ballinger C, . Knockout of plasminogen activator inhibitor 1 gene reduces amyloid beta peptide burden in a mouse model of Alzheimer’s disease. Neurobiol Aging. 2011;32(6):1079–89. – reference: Vaughan DE, Rai R, Khan SS, Eren M, Ghosh AK. Plasminogen activator inhibitor-1 is a marker and a mediator of senescence. Arterioscler Thromb Vasc Biol. 2017;37(8):1446–52. – reference: Yarns BC, Holiday KA, Carlson DM, Cosgrove CK, Melrose RJ. Pathophysiology of Alzheimer's disease. 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Objectives: The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson’s disease (PD)... Objectives: The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson’s disease (PD) and their... The aim of the study was to investigate serum plasminogen activator inhibitor-1 (PAI-1) levels of patients with Parkinson's disease (PD) and their relationship... Studies have revealed that genetic mutations, mitochondrial dysfunction, oxidative stress, immunological dysfunction, neuroinflammation, and protein... |
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| SubjectTerms | Aged Alzheimer's disease Biomarkers Case-Control Studies Dopamine Dyskinesia Education Enzyme-Linked Immunosorbent Assay Family medical history Female Humans Hypertension Male Males Middle Aged Original Paper Outpatient care facilities Parkinson Disease - blood Pathogenesis Pathophysiology Plasminogen Activator Inhibitor 1 - blood Posture Severity of Illness Index Tremor (Muscular contraction) |
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| Title | Serum Levels of Plasminogen Activator Inhibitor-1 in Patients with Parkinson’s Disease |
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