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 language | English |
|---|---|
| Pages (from-to) | 45-48 |
| Number of pages | 4 |
| Journal | Journal of the Neurological Sciences |
| Volume | 385 |
| Early online date | Nov 2017 |
| DOIs | |
| Publication status | Published - Feb 15 2018 |
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Keywords
- Parkinson's disease
- Polymorphism
- SNP
- TNF-α
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
Cite this
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 journal › Article
}
TY - JOUR
T1 - TNF-α − 308 G/A and − 238 G/A promoter polymorphisms and sporadic Parkinson's disease in an Italian cohort
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
PY - 2018/2/15
Y1 - 2018/2/15
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.
AB - 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.
KW - Parkinson's disease
KW - Polymorphism
KW - SNP
KW - TNF-α
UR - http://www.scopus.com/inward/record.url?scp=85037699176&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85037699176&partnerID=8YFLogxK
U2 - 10.1016/j.jns.2017.12.011
DO - 10.1016/j.jns.2017.12.011
M3 - Article
AN - SCOPUS:85037699176
VL - 385
SP - 45
EP - 48
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
SN - 0022-510X
ER -