TNF-α -308 G/A and -238 G/A promoter polymorphisms and sporadic Parkinson's disease in an Italian cohort

Cristina Agliardi, Franca Rosa Guerini, Milena Zanzottera, Giulio Riboldazzi, Roberta Zangaglia, Giorgio Bono, Carlo Casali, Cherubino Di Lorenzo, Claudio Pacchetti, Raffaello Nemni, Mario Clerici

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Abstract

The etiology of sporadic Parkinson's disease is (PD) still not understood but it is believed that a complex interplay between environmental and genetic factors could trigger the pathology. Pro-inflammatory TNF-α is released by activated microglia and is up-regulated in the brain and cerebrospinal fluid of PD patients; TNF-α modulates neuroinflammation and can activate the molecular mechanisms that lead to neurotoxicity and neuronal death. We analyzed two functional SNPs within the TNF-α gene promoter (rs361525 and rs1800629) in 354 Italian PD patients and 443 healthy controls (HC). In our cohort of patients, no significant associations could be observed between rs361525 and rs1800629 SNPs and either PD onset risk or PD-associated clinical parameters including age at onset of fluctuations, UPDRS-ME (Unified Parkinson Disease Rating Scale-Motor Examination), Schwab & England, Hohen & Yahr stage scale, and MMSE (Mini-Mental State Examination) score. Conflicting results on the role played by TNF-α rs1800629 SNP on PD onset risk are present in the literature. We could not find any association between TNF-α rs361525 and rs1800629 and PD.

Original languageEnglish
Pages (from-to)45-48
Number of pages4
JournalJournal of the Neurological Sciences
Volume385
DOIs
Publication statusPublished - Feb 15 2018

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Parkinson Disease
Single Nucleotide Polymorphism
Microglia
Age of Onset
England
Cerebrospinal Fluid
Pathology
Brain
Genes

Keywords

  • Journal Article

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TNF-α -308 G/A and -238 G/A promoter polymorphisms and sporadic Parkinson's disease in an Italian cohort. / Agliardi, Cristina; Guerini, Franca Rosa; Zanzottera, Milena; Riboldazzi, Giulio; Zangaglia, Roberta; Bono, Giorgio; Casali, Carlo; Di Lorenzo, Cherubino; Pacchetti, Claudio; Nemni, Raffaello; Clerici, Mario.

In: Journal of the Neurological Sciences, Vol. 385, 15.02.2018, p. 45-48.

Research output: Contribution to journalArticle

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AU - Agliardi, Cristina

AU - Guerini, Franca Rosa

AU - Zanzottera, Milena

AU - Riboldazzi, Giulio

AU - Zangaglia, Roberta

AU - Bono, Giorgio

AU - Casali, Carlo

AU - Di Lorenzo, Cherubino

AU - Pacchetti, Claudio

AU - Nemni, Raffaello

AU - Clerici, Mario

N1 - Copyright © 2017 Elsevier B.V. All rights reserved.

PY - 2018/2/15

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N2 - The etiology of sporadic Parkinson's disease is (PD) still not understood but it is believed that a complex interplay between environmental and genetic factors could trigger the pathology. Pro-inflammatory TNF-α is released by activated microglia and is up-regulated in the brain and cerebrospinal fluid of PD patients; TNF-α modulates neuroinflammation and can activate the molecular mechanisms that lead to neurotoxicity and neuronal death. We analyzed two functional SNPs within the TNF-α gene promoter (rs361525 and rs1800629) in 354 Italian PD patients and 443 healthy controls (HC). In our cohort of patients, no significant associations could be observed between rs361525 and rs1800629 SNPs and either PD onset risk or PD-associated clinical parameters including age at onset of fluctuations, UPDRS-ME (Unified Parkinson Disease Rating Scale-Motor Examination), Schwab & England, Hohen & Yahr stage scale, and MMSE (Mini-Mental State Examination) score. Conflicting results on the role played by TNF-α rs1800629 SNP on PD onset risk are present in the literature. We could not find any association between TNF-α rs361525 and rs1800629 and PD.

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