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Ahmadi, Ahmad
Publications (10 of 16) Show all publications
Ran, C., Willows, T., Sydow, O., Johansson, A., Söderkvist, P., Dizdar (Dizdar Segrell), N., . . . Belin, C. (2013). The HLA-DRA variation rs3129882 is not associated with Parkinsons disease in Sweden [Letter to the editor]. Parkinsonism & Related Disorders, 19(7), 701-702
Open this publication in new window or tab >>The HLA-DRA variation rs3129882 is not associated with Parkinsons disease in Sweden
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2013 (English)In: Parkinsonism & Related Disorders, ISSN 1353-8020, E-ISSN 1873-5126, Vol. 19, no 7, p. 701-702Article in journal, Letter (Other academic) Published
Place, publisher, year, edition, pages
Elsevier, 2013
Keywords
Parkinsons disease; HLA-DRA; PARK18; Association study; SNP
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-96455 (URN)10.1016/j.parkreldis.2013.03.001 (DOI)000320750300012 ()23579001 (PubMedID)
Available from: 2013-08-23 Created: 2013-08-20 Last updated: 2018-01-12Bibliographically approved
Belin, A. C., Ran, C., Anvret, A., Paddock, S., Westerlund, M., Håkansson, A., . . . Galter, D. (2012). Association of a protective paraoxonase 1 (PON1) polymorphism in Parkinson's disease. Neuroscience Letters, 522(1), 30-5
Open this publication in new window or tab >>Association of a protective paraoxonase 1 (PON1) polymorphism in Parkinson's disease
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2012 (English)In: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 522, no 1, p. 30-5Article in journal (Refereed) Published
Abstract [en]

Pesticide exposure has been suggested to increase the risk to develop Parkinson's disease (PD). The arylesterase paraoxonase 1 (PON1) is mainly expressed in the liver and hydrolyzes organophosphates such as pesticides. The polymorphism Leu54Met (rs854560) in PON1, impairing enzyme activity and leading to decreased PON1 expression levels, has been reported to be associated with Parkinson's disease (PD). PON1 is part of a cluster on chromosome 7q21.3 together with PON2 and PON3. We investigated the occurrence of four additional polymorphisms in PON1 and two in PON2 in a Swedish PD case-control material. We found a significant association (p=0.007) with a PON1 promoter polymorphism, rs854571. The minor allele was more common among controls than PD cases which suggest a protective effect. This is strengthened by the fact that rs854571 is in strong linkage disequilibrium with another PON1 promoter polymorphism, rs854572, reported to increase PON1 gene expression. Our findings support the hypothesis that PON1 is involved in the etiology of PD and that higher PON1 levels are reducing the risk for PD.

Place, publisher, year, edition, pages
Elsevier, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-80804 (URN)10.1016/j.neulet.2012.06.007 (DOI)000307035700007 ()22704918 (PubMedID)
Note

funding agencies|Swedish Research Council||Magnus Bergvall Foundation||Swedish Parkinson Foundation||Swedish Brain Foundation||Swedish Brain Power||Ake Wiberg Foundation||Karolinska Institutet Funds||

Available from: 2012-08-30 Created: 2012-08-30 Last updated: 2018-01-12
Dick, F., De Palma, G., Ahmadi, A., Scott, N., Prescott, G., Bennett, J., . . . Felice, A. (2007). Environmental risk factors for Parkinson's disease and parkinsonism: The Geoparkinson study. Occupational and Environmental Medicine, 64(10), 666-672
Open this publication in new window or tab >>Environmental risk factors for Parkinson's disease and parkinsonism: The Geoparkinson study
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2007 (English)In: Occupational and Environmental Medicine, ISSN 1351-0711, E-ISSN 1470-7926, Vol. 64, no 10, p. 666-672Article in journal (Refereed) Published
Abstract [en]

Objective: To investigate the associations between Parkinson's disease and other degenerative parkinsonian syndromes and environmental factors in five European countries. Methods: A case-control study of 959 prevalent cases of parkinsonism (767 with Parkinson's disease) and 1989 controls in Scotland, Italy, Sweden, Romania and Malta was carried out. Cases were defined using the United Kingdom Parkinson's Disease Society Brain Bank criteria, and those with drug-induced or vascular parkinsonism or dementia were excluded. Subjects completed an interviewer-administered questionnaire about lifetime occupational and hobby exposure to solvents, pesticides, iron, copper and manganese. Lifetime and average annual exposures were estimated blind to disease status using a job-exposure matrix modified by subjective exposure modelling. Results were analysed using multiple logistic regression, adjusting for age, sex, country, tobacco use, ever knocked unconscious and family history of Parkinson's disease. Results: Adjusted logistic regression analyses showed significantly increased odds ratios for Parkinson's disease/parkinsonism with an exposure-response relationship for pesticides (low vs no exposure, odds ratio (OR) =1.13, 95% Cl 0.82 to 1.57, high vs no exposure, OR =1.41, 95% Cl 1.06 to 1.88) and ever knocked unconscious (once vs never, OR= 1.35, 95% Cl 1.09 to 1.68, more than once vs never, OR = 2.53, 95% Cl 1.78 to 3.59). Hypnotic, anxiolytic or antidepressant drug use for more than 1 year and a family history of Parkinson's disease showed significantly increased odds ratios. Tobacco use was protective (OR = 0.50, 95% Cl 0.42 to 0.60). Analyses confined to subjects with Parkinson's disease gave similar results. Conclusions: The association of pesticide exposure with Parkinson's disease suggests a causative role. Repeated traumatic loss of consciousness is associated with increased risk.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-39588 (URN)10.1136/oem.2006.027003 (DOI)49967 (Local ID)49967 (Archive number)49967 (OAI)
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13
Dick, F., De Palma, G., Ahmadi, A., Osborne, A., Scott, N., Prescott, G., . . . Tondel, M. (2007). Gene-environment interactions in parkinsonism and Parkinson's disease: The Geoparkinson study. Occupational and Environmental Medicine, 64(10), 673-680
Open this publication in new window or tab >>Gene-environment interactions in parkinsonism and Parkinson's disease: The Geoparkinson study
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2007 (English)In: Occupational and Environmental Medicine, ISSN 1351-0711, E-ISSN 1470-7926, Vol. 64, no 10, p. 673-680Article in journal (Refereed) Published
Abstract [en]

Objectives: To investigate associations of Parkinson's disease (PD) and parkinsonian syndromes with polymorphic genes that influence metabolism of either foreign chemical substances or dopamine and to seek evidence of gene-environment interaction effects that modify risk. Methods: A case-control study of 959 prevalent cases of parkinsonism (767 with PD) and 1989 controls across five European centres. Occupational hygienists estimated the average annual intensity of exposure to solvents, pesticides and metals, (iron, copper, manganese), blind to disease status. CYP2D6, PON1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, CYP1B1, MAO-A, MAO-B, SOD 2, EPHX, DATl, DRD2 and NAT2 were genotyped. Results were analysed using multiple logistic regression adjusting for key confounders. Results: There was a modest but significant association between MAO-A polymorphism in males and disease risk (G vs T, OR 1.30, 95% C1 1.02 to 1.66, adjusted). The majority of gene-environment analyses did not show significant interaction effects. There were possible interaction effects between GSTM1 null genotype and solvent exposure (which were stronger when limited to PD cases only). Conclusions: Many small studies have reported associations between genetic polymorphisms and PD. Fewer have examined gene-environment interactions. This large study was sufficiently powered to examine these aspects. GSTM1 null subjects heavily exposed to solvents appear to be at increased risk of PD. There was insufficient evidence that the other gene-environment combinations investigated modified disease risk, suggesting they contribute little to the burden of PD.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-39589 (URN)10.1136/oem.2006.032078 (DOI)49969 (Local ID)49969 (Archive number)49969 (OAI)
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13
Garcia, J., Ahmadi, A., Wonnacott, A., Sutcliffe, W., Nagga, K., Söderkvist, P. & Marcusson, J. (2006). Association of insulin-like growth factor-1 receptor polymorphism in dementia. Dementia and Geriatric Cognitive Disorders, 22(5-6), 439-444
Open this publication in new window or tab >>Association of insulin-like growth factor-1 receptor polymorphism in dementia
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2006 (English)In: Dementia and Geriatric Cognitive Disorders, ISSN 1420-8008, E-ISSN 1421-9824, Vol. 22, no 5-6, p. 439-444Article in journal (Refereed) Published
Abstract [en]

There is an increasing interest in how oxidative stress can cause cells to go into apoptosis in both normal ageing and in neurodegenerative disorders. Previous research has implicated insulin-like growth factor-1 (IGF-1) as being involved in the pathogenesis in Alzheimer's disease (AD) by protecting the neurons through reducing neuronal susceptibility to oxidative stress. IGF-1 receptor (IGF-1R) polymorphisms alter cerebral and systemic levels of IGF-1 and may alter the function of the receptor. We genotyped the IGF-1R gene by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) to assess whether this gene polymorphism can be linked to dementia. We used leukocyte DNA from 72 patients with AD, 75 patients with vascular dementia (VaD), 14 patients with mixed dementia (AD+VaD), and a control group consisting of 209 individuals without a history of progressive neurological disorders. Analysis of gene frequency for gender revealed a significant difference between female VaD patients and female controls carrying at least one A allele (OR = 1.8, CI 95% 1.1-2.9, p = 0.02), but not for male patients. In addition, we found a strong tendency to a difference between all cases of female dementia patients and controls carrying the A allele (OR = 1.5, CI 95% 0.99-2.2, p = 0.054). Our results suggest that the A allele of IGF-1R may be involved in the pathogenesis of VaD in females. Copyright © 2006 S. Karger AG.

Keywords
Alzheimer's disease, Dementia, Insulin-like growth factor-1 receptor, Mixed dementia, Vascular dementia
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-50094 (URN)10.1159/000095803 (DOI)
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2017-12-12
Sun, X.-F., Ahmadi, A., Arbman, G., Wallin, Å., Asklid, D. & Zhang, H. (2005). Polymorphisms in sulfotransferase 1A1 and glutathione S-transferase P1 genes in relation to colorectal cancer risk and patients' survival. World Journal of Gastroenterology, 11(43), 6875-6879
Open this publication in new window or tab >>Polymorphisms in sulfotransferase 1A1 and glutathione S-transferase P1 genes in relation to colorectal cancer risk and patients' survival
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2005 (English)In: World Journal of Gastroenterology, ISSN 1007-9327, E-ISSN 2219-2840, Vol. 11, no 43, p. 6875-6879Article in journal (Refereed) Published
Abstract [en]

Aim: To examine whether polymorphisms in SULT1A1 and GSTP1 genes contribute to colorectal cancer development and whether they are associated with clinicopathological variables are not well identified. Methods: We examined the genotypes of 125 colorectal cancer patients and 666 healthy controls in a Swedish population by using PCR restriction fragment length polymorphism (RFLP). Results: SULT1A1 *2/*2 genotype (OR = 2.49, 95%CI = 1.48-4.19, P = 0.0002) and *2 allele (OR = 1.56, 95%CI = 1.16-2.10, P = 0.002) had an effect on colorectal cancer susceptibility, while GSTP1 genotype was without effect. However, GSTP1 G-type predicted a worse prognosis in the patients independently of gender, age, Dukes' stage, growth pattern, and differentiation (P = 0.03). Conclusion: Polymorphism in SULT1A1 may predispose to colorectal cancer and GSTP1 may be a biological indicator of prognosis in the patients. © 2005 The WJG Press and Elsevier Inc. All rights reserved.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-31173 (URN)16912 (Local ID)16912 (Archive number)16912 (OAI)
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2017-12-13
Jerevall, P.-L., Ahmadi, A., Bergman, M., Stål, O. & Wingren, S. (2005). Sulfotransferase1A1 and risk of postmenopausal breast cancer. Anticancer Research, 25(3 C), 2515-2517
Open this publication in new window or tab >>Sulfotransferase1A1 and risk of postmenopausal breast cancer
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2005 (English)In: Anticancer Research, ISSN 0250-7005, E-ISSN 1791-7530, Vol. 25, no 3 C, p. 2515-2517Article in journal (Refereed) Published
Abstract [en]

The detoxification enzyme sulfotransferase1A1 (SULT1A1) is implicated in the inactivation of estrogens and the activation of promutagens andprocarcinogens. SULT1A1 activity varies among individuals, and this difference in phenotype is, in part, controlled by genetic polymorphism (Arg→His in codon 213). It is hypothesized that the His allele contributes to the risk of postmenopausal breast cancer. Frequencies of the Arg/His alleles were estimated in 229 postmenopausal breast cancer patients and 227 age-matched controls using a PCR-RFLP assay. Allele frequencies and genotype distributions were not statistically different between postmenopausal breast cancer patients and the population-based controls, i.e. neither of the alleles is associated with an increased risk of breast cancer in the present study.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-31348 (URN)17114 (Local ID)17114 (Archive number)17114 (OAI)
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2017-12-13Bibliographically approved
Kastbom, A., Ahmadi, A., Söderkvist, P. & Skogh, T. (2005). The 158V polymorphism of Fc gamma receptor type IIIA in early rheumatoid arthritis: increased susceptibility and severity in male patients (the Swedish TIRA project). Rheumatology, 44(10), 1294-1298
Open this publication in new window or tab >>The 158V polymorphism of Fc gamma receptor type IIIA in early rheumatoid arthritis: increased susceptibility and severity in male patients (the Swedish TIRA project)
2005 (English)In: Rheumatology, ISSN 1462-0324, Vol. 44, no 10, p. 1294-1298Article in journal (Refereed) Published
Abstract [en]

Objectives. To evaluate the influence of Fc receptor IIIA (FcRIIIA) 158V/F polymorphism on susceptibility and disease severity in early rheumatoid arthritis (RA).

Methods. In 181 Swedish patients (128 women, 53 men) with RA of recent onset, disease and disability variables such as erythrocyte sedimentation rate, 28-joint disease activity score (DAS28) and health assessment questionnaire (HAQ) scores were monitored regularly during 3 yr. Three hundred and sixty-two controls were recruited from the same geographical area as the patients. FcRIIIA genotyping was performed using denaturing high-performance liquid chromatography.

Results. In all RA patients, FcRIIIA-158VV was significantly over-represented compared with controls [odds ratio (OR) 1.9, 95% confidence interval (CI) 1.01–3.5, P<0.05]. After stratifying for sex, the difference remained in the male population (OR 3.2, 95%CI 1.03–11, P<0.05) but disappeared among women (OR 1.4, 95%CI 0.7–3.1, P=0.4). In addition, 158VV patients were more likely to exhibit early joint erosions (OR 6.1, 95%CI 1.4–28, P<0.01). At baseline, patients with different FcRIIIA genotypes did not differ with respect to measures of disease activity or functional ability. Thereafter, in male patients with at least one V allele the mean DAS28 and HAQ scores were higher compared with 158FF. In contrast, female patients with at least one 158V allele displayed lower mean DAS28 and HAQ scores compared with those with 158FF.

Conclusions. In a male population, the FcRIIIA-158VV genotype is associated with an increased risk of developing RA, and the 158V allele with more severe disease in early RA.

Keywords
Disease course, Early rheumatoid arthritis, Fc receptor, Single-nucleotide polymorphism
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-14378 (URN)10.1093/rheumatology/kei010 (DOI)
Available from: 2007-04-20 Created: 2007-04-20 Last updated: 2015-08-31
Ahmadi, A. (2004). Genetic predisposition and risk factors for neurodegenerative diseases. (Doctoral dissertation). Linköping: Linköpings universitet
Open this publication in new window or tab >>Genetic predisposition and risk factors for neurodegenerative diseases
2004 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The inter-individual variability in biotransformation, may lead to differences in activation and detoxification of both endogenous and exogenous compounds. Polymorphism studies in such genes were applied for Parkinson's disease (PD) and Chronic toxic encephalopathy (CTE), two diseases influenced by both genetic and enviromnental factors.

An elevated median age for the onset of PD was found among GS1M1 gene carriers compared to PD patients being GS1M1 null genotypes (68 years versus 57 years). No similar difference was found for GSTT1. mEPHX (113HH) isoform, which has been suggested as a low activity variant, is over represented in PD patients (OR=3.8, CI 95%, 1.2-11.8).

Monoamine oxidases (MAO-A and -B) are important in the dopamine metabolism and in the detoxification of neurotoxins and genetic variants in these genes have earlier been assigned to PD. However, no difference was revealed between any of the polymorphisms studied in the MAO-A and -B genes and PD. Smoking displayed an enviromnental exposure with a strong decreased risk for PD in this study (OR=0.40 for men and OR=0.48 for women) but no obvious interaction with the MAO genotypes could be observed.

Mitochondrial dysfunction and oxidative stress have been hypothesized to contribute to the pathogenesis of PD. The superoxide dismutases (SOD) potentially play an important role in PD by detoxifying superoxide radicals in mitochondria. Polymorphisms neither in superoxide dismutase 2 (SOD2) nor mitochondrial complex I subunit, NDUFV2, were associated with PD.

An increased risk ratio for CTE was found in smokers with the GSTM1 null genotype (RR=2.5, Cl 95%, 1.4-4.2) or the GSTT1 null genotype (RR=1.4, Ci 95%, 1.02-2.0). In non-smokers GS1M1 null genotype did not confer any risk for CTE. Polymorphisms in mEPHX were not associated with an increased risk for CTE.

Thus, various genetic and enviromnental factors most likely influence both PD and solvent-induced CTE. Detoxification pathways may represent important protective mechanisms against reactive intermediates, thus genetic predisposition in these pathways could modify the susceptibility and onset of PD and solvent-induced CTE.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2004. p. 63
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 844
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-24042 (URN)3598 (Local ID)91-7373-817-4 (ISBN)3598 (Archive number)3598 (OAI)
Public defence
2004-04-16, Elsa Brändström-Salen, Hälsouniversitetet, Linköping, 09:00 (Swedish)
Opponent
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2012-10-22Bibliographically approved
Landtblom, A.-M., Wasteson, M., Ahmadi, A. & Söderkvist, P. (2003). Multiple sclerosis and exposure to organic solvents, investigated by genetic polymorphisms of the GSTM1 and CYP2D6 enzyme systems. Neurological Sciences, 24(4), 248-251
Open this publication in new window or tab >>Multiple sclerosis and exposure to organic solvents, investigated by genetic polymorphisms of the GSTM1 and CYP2D6 enzyme systems
2003 (English)In: Neurological Sciences, ISSN 1590-1874, E-ISSN 1590-3478, Vol. 24, no 4, p. 248-251Article in journal (Refereed) Published
Abstract [en]

An association between multiple sclerosis (MS) and exposure to organic solvents has been discussed. Organic solvents are metabolised by enzyme systems like glutathione S-transferase M1 (GSTM1) and CYP2D6, which express polymorphisms in the general poulation. GSTM1 null genotype has been associated with solvent-induced chronic toxic encephalopathy. Our aim was to see if a defect in one of these enzyme systems could explain the association between MS and exposure to organic solvents. In our study, 50 patients with MS were investigated, including 24 who had been significantly exposed to organic solvents and 26 who were not exposed. Polymerase chain reaction-based methods were used for genotyping GSTM1 and CYP2D6 polymorphisms in leukocyte DNA. No differences in genetic predisposition were found between MS patients exposed and those not exposed to organic solvents regarding GSTM1 null or CYP2D6 poor metaboliser genotypes. The possible association between multiple sclerosis and solvents may not, as for chronic toxic encephalopathy, be explained by defects in these systems.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-24839 (URN)10.1007/s10072-003-0148-5 (DOI)9237 (Local ID)9237 (Archive number)9237 (OAI)
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2017-12-13
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