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C Siri,
S Duerr,
M Canesi,
M Delazer,
R Esselink,
B R Bloem,
T Gurevich,
M Balas,
N Giladi,
P Santacruz,
F Marti,
E Tolosa,
A Rubino, G Meco,
W Poewe,
G Pezzoli,
G Wenning,
A Antonini
[show abstract]
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ABSTRACT: Imaging and neuropathology studies have demonstrated significant abnormalities not only in subcortical, but also in cortical regions of patients with multiple system atrophy (MSA). This raises the possibility that cognitive dysfunction may contribute to the clinical spectrum of this disorder to a greater extent than it is currently not widely appreciated. In this cross-sectional multicenter study from the European multiple system atrophy study group ( http://www.emsa-sg.org ), we applied an extensive neuropsychological test battery in a series of 61 clinically diagnosed probable MSA patients. The results demonstrated that general cognitive decline as assessed by MMSE was uncommon (2 out of 61 patients <24). In contrast, frontal lobe-related functions (as measured by FAB) were impaired in 41 % of patients, with abstract reasoning and sustained attention less compromised. This pattern was similar to our control group of 20 patients with Parkinson's disease (matched for disease duration and age at onset). There was no difference in cognitive performance between MSA patients with the parkinsonian versus the cerebellar variant. Behaviourally, MSA patients had greater depression than PD and in the case of MSA of the cerebellar variant significantly lower anxiety. Our data show that cognitive abnormalities are relatively frequent in multiple system atrophy and this involves primarily frontal-executive functions. Their contribution to clinical disability and disease progression needs to be addressed in larger prospective studies.
Acta Neurovegetativa 03/2013; · 2.73 Impact Factor
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ABSTRACT: Pascale E, Passarelli E, Purcaro C, Vestri AR, Fakeri A, Guglielmi R, Passarelli F, Meco G. Lack of association between IL-1β, TNF-α, and IL-10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort. Acta Neurol Scand: 2011: 124: 176–181. © 2010 John Wiley & Sons A/S.Objective – There is increasing evidence suggesting that neuroinflammation and microglia activation may play important roles in the pathway leading to neuronal cell death in Parkinson’s disease (PD). Chronic activation of microglia may cause neuronal damage through the release of potentially cytotoxic molecules, such as pro-inflammatory cytokines. Different functional promoter polymorphisms within genes coding pro- or anti-inflammatory cytokines involved in the immune reactions in the brain might influence the risk of developing PD or the age of disease onset.Aim – To investigate the interleukin (IL)-1β-511, tumor necrosis factor alpha (TNF-α)-308, and interleukin (IL)-10-1082 gene polymorphisms as susceptibility factors for PD.Methods;– We analyzed genotype and allele distributions of these polymorphisms in146 Italian patients with PD and 156 healthy controls.Results – None of the polymorphisms we investigated was found to be associated with PD or with age of disease onset. No significant differences between patients with PD and controls were found as regards the concomitant presence of variant alleles in the three polymorphisms studied. We found that only the combined genotype TNF-α-308GG/IL-1β-511T(+) is associated with a decreased risk of PD.Conclusion – Our results indicate that the cytokine gene polymorphisms we investigated are not related to the development of PD in the Italian population; further studies are warranted to clarify the role of the TNF-α-308GG/IL-1β-511T(+) combined genotype.
Acta Neurologica Scandinavica 08/2011; 124(3):176 - 181. · 2.47 Impact Factor
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ABSTRACT: There is increasing evidence suggesting that neuroinflammation and microglia activation may play important roles in the pathway leading to neuronal cell death in Parkinson's disease (PD). Chronic activation of microglia may cause neuronal damage through the release of potentially cytotoxic molecules, such as pro-inflammatory cytokines. Different functional promoter polymorphisms within genes coding pro- or anti-inflammatory cytokines involved in the immune reactions in the brain might influence the risk of developing PD or the age of disease onset.
To investigate the interleukin (IL)-1β-511, tumor necrosis factor alpha (TNF-α)-308, and interleukin (IL)-10-1082 gene polymorphisms as susceptibility factors for PD.
We analyzed genotype and allele distributions of these polymorphisms in 146 Italian patients with PD and 156 healthy controls.
None of the polymorphisms we investigated was found to be associated with PD or with age of disease onset. No significant differences between patients with PD and controls were found as regards the concomitant presence of variant alleles in the three polymorphisms studied. We found that only the combined genotype TNF-α-308GG/IL-1β-511T+ is associated with a decreased risk of PD.
Our results indicate that the cytokine gene polymorphisms we investigated are not related to the development of PD in the Italian population; further studies are warranted to clarify the role of the TNF-α-308GG/IL-1β-511T+ combined genotype.
Acta Neurologica Scandinavica 09/2010; 124(3):176-81. · 2.47 Impact Factor
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C. Colosimo,
N. Vanacore,
V. Bonifati,
G. Fabbrini,
A. Rum,
G. De Michele,
M. De Mari,
U. Bonuccelli,
D. J. Nicholl, G. Meco,
European Study Group on Atypical Parkinsonism (ESGAP) Consortium
Acta Neurologica Scandinavica 06/2008; 103(4):261 - 264. · 2.47 Impact Factor
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A Di Fonzo,
H F Chien,
M Socal,
S Giraudo,
C Tassorelli,
G Iliceto,
G Fabbrini,
R Marconi,
E Fincati,
G Abbruzzese, [......],
F Stocchi,
S Goldwurm,
J J Ferreira, G Meco,
E Martignoni,
L Lopiano,
L B Jardim,
B A Oostra,
E R Barbosa,
V Bonifati
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ABSTRACT: To assess the prevalence, nature, and associated phenotypes of ATP13A2 gene mutations among patients with juvenile parkinsonism (onset <21 years) or young onset (between 21 and 40 years) Parkinson disease (YOPD).
We studied 46 patients, mostly from Italy or Brazil, including 11 with juvenile parkinsonism and 35 with YOPD. Thirty-three cases were sporadic and 13 had positive family history compatible with autosomal recessive inheritance. Forty-two had only parkinsonian signs, while four (all juvenile-onset) had multisystemic involvement. The whole ATP13A2 coding region (29 exons) and exon-intron boundaries were sequenced from genomic DNA.
A novel homozygous missense mutation (Gly504Arg) was identified in one sporadic case from Brazil with juvenile parkinsonism. This patient had symptoms onset at age 12, levodopa-responsive severe akinetic-rigid parkinsonism, levodopa-induced motor fluctuations and dyskinesias, severe visual hallucinations, and supranuclear vertical gaze paresis, but no pyramidal deficit nor dementia. Brain CT scan showed moderate diffuse atrophy. Furthermore, two Italian cases with YOPD without atypical features carried a novel missense mutation (Thr12Met, Gly533Arg) in single heterozygous state.
We confirm that ATP13A2 homozygous mutations are associated with human parkinsonism, and expand the associated genotypic and clinical spectrum, by describing a homozygous missense mutation in this gene in a patient with a phenotype milder than that initially associated with ATP13A2 mutations (Kufor-Rakeb syndrome). Our data also suggest that ATP13A2 single heterozygous mutations might be etiologically relevant for patients with YOPD and further studies of this gene in Parkinson disease are warranted.
Neurology 05/2007; 68(19):1557-62. · 8.31 Impact Factor
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F Geser,
K Seppi,
M Stampfer-Kountchev,
M Köllensperger,
A Diem,
J P Ndayisaba,
K Ostergaard,
E Dupont,
A Cardozo,
E Tolosa, [......],
N Giladi,
M Galitzky,
F Ory,
O Rascol,
C Kamm,
K Buerk,
S Maass,
T Gasser,
W Poewe,
G K Wenning
[show abstract]
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ABSTRACT: Introduction. The European Multiple System Atrophy-Study Group (EMSA-SG) is an academic network comprising 23 centers across Europe and Israel that has constituted itself already in January 1999. This international forum of established experts under the guidance of the University Hospital of Innsbruck as coordinating center is supported by the 5th framework program of the European Union since March 2001 (QLK6-CT-2000-00661). Objectives. Primary goals of the network include (1) a central Registry for European multiple system atrophy (MSA) patients, (2) a decentralized DNA Bank, (3) the development and validation of the novel Unified MSA Rating Scale (UMSARS), (4) the conduction of a Natural History Study (NHS), and (5) the planning or implementation of interventional therapeutic trials. Methods. The EMSA-SG Registry is a computerized data bank localized at the coordinating centre in Innsbruck collecting diagnostic and therapeutic data of MSA patients. Blood samples of patients and controls are recruited into the DNA Bank. The UMSARS is a novel specific rating instrument that has been developed and validated by the EMSA-SG. The NHS comprises assessments of basic anthropometric data as well as a range of scales including the UMSARS, Unified Parkinson's Disease Rating Scale (UPDRS), measures of global disability, Red Flag list, MMSE (Mini Mental State Examination), quality of live measures, i.e. EuroQoL 5D (EQ-5D) and Medical Outcome Study Short Form (SF-36) as well as the Beck Depression Inventory (BDI). In a subgroup of patients dysautonomic features are recorded in detail using the Queen Square Cardiovascular Autonomic Function Test Battery, the Composite Autonomic Symptom Scale (COMPASS) and measurements of residual urinary volume. Most of these measures are repeated at 6-monthly follow up visits for a total study period of 24 months. Surrogate markers of the disease progression are identified by the EMSA-SG using magnetic resonance and diffusion weighted imaging (MRI and DWI, respectively). Results. 412 patients have been recruited into the Registry so far. Probable MSA-P was the most common diagnosis (49% of cases). 507 patients donated DNA for research. 131 patients have been recruited into the NHS. There was a rapid deterioration of the motor disorder (in particular akinesia) by 26.1% of the UMSARS II, and - to a lesser degree - of activities of daily living by 16.8% of the UMSARS I in relation to the respective baseline scores. Motor progression was associated with low motor or global disability as well as low akinesia or cerebellar subscores at baseline. Mental function did not deteriorate during this short follow up period. Conclusion. For the first time, prospective data concerning disease progression are available. Such data about the natural history and prognosis of MSA as well as surrogate markers of disease process allow planning and implementation of multi-centre phase II/III neuroprotective intervention trials within the next years more effectively. Indeed, a trial on growth hormone in MSA has just been completed, and another on minocycline will be completed by the end of this year.
Acta Neurovegetativa 01/2006; 112(12):1677-86. · 2.73 Impact Factor
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S Goldwurm,
A Di Fonzo,
E J Simons,
C F Rohé,
M Zini,
M Canesi,
S Tesei,
A Zecchinelli,
A Antonini,
C Mariani, [......],
C Diroma,
P Lamberti,
C Sampaio, G Meco,
E Barbosa,
A M Bertoli-Avella,
G J Breedveld,
B A Oostra,
G Pezzoli,
V Bonifati
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ABSTRACT: Mutations in the gene Leucine-Rich Repeat Kinase 2 (LRRK2) were recently identified as the cause of PARK8 linked autosomal dominant Parkinson's disease.
To study recurrent LRRK2 mutations in a large sample of patients from Italy, including early (<50 years) and late onset familial and sporadic Parkinson's disease.
Among 629 probands, 13 (2.1%) were heterozygous carriers of the G2019S mutation. The mutation frequency was higher among familial (5.1%, 9/177) than among sporadic probands (0.9%, 4/452) (p<0.002), and highest among probands with one affected parent (8.7%, 6/69) (p<0.001). There was no difference in the frequency of the G2019S mutation in probands with early v late onset disease. Among 600 probands, one heterozygous R1441C but no R1441G or Y1699C mutations were detected. None of the four mutations was found in Italian controls. Haplotype analysis in families from five countries suggested that the G2019S mutation originated from a single ancient founder. The G2019S mutation was associated with the classical Parkinson's disease phenotype and a broad range of onset age (34 to 73 years).
G2019S is the most common genetic determinant of Parkinson's disease identified so far. It is especially frequent among cases with familial Parkinson's disease of both early and late onset, but less common among sporadic cases. These findings have important implications for diagnosis and genetic counselling in Parkinson's disease.
Journal of Medical Genetics 11/2005; 42(11):e65. · 6.36 Impact Factor
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V Bonifati,
C F Rohé,
G J Breedveld,
E Fabrizio,
M De Mari,
C Tassorelli,
A Tavella,
R Marconi,
D J Nicholl,
H F Chien, [......],
G Fabbrini,
S Goldwurm,
A de Klein,
E Barbosa,
L Lopiano,
E Martignoni,
P Lamberti,
N Vanacore, G Meco,
B A Oostra
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ABSTRACT: To assess the prevalence, nature, and associated phenotypes of PINK1 gene mutations in a large series of patients with early-onset (<50 years) parkinsonism.
The authors studied 134 patients (116 sporadic and 18 familial; 77% Italian) and 90 Italian controls. The whole PINK1 coding region was sequenced from genomic DNA; cDNA was analyzed in selected cases.
Homozygous pathogenic mutations were identified in 4 of 90 Italian sporadic cases, including the novel Gln456Stop mutation; single heterozygous truncating or missense mutations were found in another 4 Italian sporadic cases, including two novel mutations, Pro196Leu and Gln456Stop. Pathogenic mutations were not identified in the familial cases. Novel (Gln115Leu) and known polymorphisms were identified with similar frequency in cases and controls. In cases carrying single heterozygous mutation, cDNA analysis detected no additional mutations, and revealed a major pathogenic effect at mRNA level for the mutant C1366T/Gln456Stop allele. All patients with homozygous mutations had very early disease onset, slow progression, and excellent response to l-dopa, including, in some, symmetric onset, dystonia at onset, and sleep benefit, resembling parkin-related disease. Phenotype in patients with single heterozygous mutation was similar, but onset was later.
PINK1 homozygous mutations are a relevant cause of disease among Italian sporadic patients with early-onset parkinsonism. The role of mutations found in single heterozygous state is difficult to interpret. Our study suggests that, at least in some patients, these mutations are disease causing, in combination with additional, still unknown factors.
Neurology 08/2005; 65(1):87-95. · 8.31 Impact Factor
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M Martinez,
A Brice,
J R Vaughan,
A Zimprich,
M M B Breteler, G Meco,
A Filla,
M J Farrer,
C Bétard,
J Hardy,
G De Michele,
V Bonifati,
B Oostra,
T Gasser,
N W Wood,
A Dürr
[show abstract]
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ABSTRACT: To undertake a full genome-wide screen for Parkinson's disease susceptibility loci.
A genome-wide linkage study was undertaken in 227 affected sibling pairs from 199 pedigrees with Parkinson's disease. The pedigree sample consisted of 188 pedigrees from five European countries, and 11 from the USA. Individuals were genotyped for 391 microsatellite markers at approximately 10 cM intervals throughout the genome. Multipoint model-free affected sibling pair linkage analyses were carried out using the MLS (maximum LOD score) test.
There were six chromosomal regions with maximum MLS peaks of 1 or greater (pointwise p<0.018). Four of these chromosomal regions appear to be newly identified regions, and the highest MLS values were obtained on chromosomes 11q (MLS = 1.60, at 91 cM, D11S4175) and 7p (MLS = 1.51, at 5 cM, D7S531). The remaining two MLS peaks, on 2p11-q12 and 5q23, are consistent with excess sharing in regions reported by other studies. The highest MLS peak was observed on chromosome 2p11-q12 (MLS = 2.04, between markers D2S2216 and D2S160), within a relatively short distance (approximately 17 cM) from the PARK3 region. Although a stronger support of linkage to this region was observed in the late age of onset subgroup of families, these differences were not significant. The peak on 5q23 (MLS = 1.05, at 130 cM, D5S471) coincides with the region identified by three other genome scans. All peak locations fell within a 10 cM distance.
These stratified linkage analyses suggest linkage heterogeneity within the sample across the 2p11-q12 and 5q23 regions, with these two regions contributing independently to Parkinson's disease susceptibility.
Journal of Medical Genetics 12/2004; 41(12):900-7. · 6.36 Impact Factor
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ABSTRACT: Previous studies suggested a therapeutic action of the selective serotonin 5-HT2-antagonist ritanserin on negative symptoms of schizophrenia and on neuroleptic-induced parkinsonism. In this open trial the effect of risperidone, a combined serotonin-5-HT2-and dopamine-D2-antagonist, was studied on a sample of 31 schizophrenic outpatients with an unsatisfactory response to conventional neuroleptic treatment, predominance of negative symptoms, together with troublesome extrapyramidal side-effects. After 28 days of oral treatment (2–6 mg daily) the patients showed a significant improvement as measured by means of the Brief Psychiatric Rating Scale and the Scale for the Assessment of Negative Symptoms. It is possible that the 5-HT2 receptor antagonist properties of risperidone may improve negative symptoms. In addition, confirming previous studies, extrapyramidal symptoms showed a reduced incidence compared to previous neuroleptic treatment, suggesting a serotonin--dopamine interaction in the basal ganglia. No electrocardiographic, cardiovascular or laboratory abnormalities were observed.
Human Psychopharmacology Clinical and Experimental 10/2004; 5(3):225 - 231. · 2.48 Impact Factor
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Neurological Sciences 11/2003; 24(3):205-6. · 1.32 Impact Factor
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V Bonifati,
P Rizzu,
F Squitieri,
E Krieger,
N Vanacore,
J C van Swieten,
A Brice,
C M van Duijn,
B Oostra, G Meco,
P Heutink
[show abstract]
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ABSTRACT: Four chromosomal loci ( PARK2, PARK6, PARK7, and PARK9) associated with autosomal recessive, early onset parkinsonism are known. We mapped the PARK7 locus to chromosome 1p36 in a large family from a genetically isolated population in the Netherlands, and confirmed this linkage in an Italian family. By positional cloning within the refined PARK7 critical region we recently identified mutations in the DJ-1 gene in the two PARK7-linked families. The function of DJ-1 remains largely unknown, but evidence from genetic studies on the yeast DJ-1 homologue, and biochemical studies in murine and human cell lines, suggests a role for DJ-1 as an antioxidant and/or a molecular chaperone. Elucidating the role of DJ-1 will lead to a better understanding of the pathogenesis of DJ-1-related and common forms of Parkinson's disease.
Neurological Sciences 11/2003; 24(3):159-60. · 1.32 Impact Factor
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ABSTRACT: Excessive daytime somnolence (EDS) and quality of sleep were studied in 25 parkinsonian patients at baseline, when they had not yet received any antiparkinsonian medication, and after 1 year of treatment with dopaminergic drugs. EDS was measured by the Epworth Sleepiness Scale (ESS) and sleep quality by the Pittsburgh Sleep Quality Index (PSQI). At baseline, the ESS score was not different from that of age-matched healthy controls. The mean ESS score increased significantly after 1 year of follow-up, being more than 10 in 12 patients. The mean PSQI also increased significantly after 1 year of treatment, but there were no differences in the number of "bad sleepers" at baseline and at follow-up. In conclusion, EDS seems to emerge during the course of the illness, at least in a proportion of PD patients, and could represent another clinical correlate of the interaction between the ongoing neurodegenerative process and the side effects of drugs.
Neurological Sciences 11/2003; 24(3):178-9. · 1.32 Impact Factor
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[show abstract]
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ABSTRACT: Excessive daytime somnolence (EDS) and quality of sleep
were studied in 25 parkinsonian patients at baseline, when they
had not yet received any antiparkinsonian medication, and after
1 year of treatment with dopaminergic drugs. EDS was measured by
the Epworth Sleepiness Scale (ESS) and sleep quality by the
Pittsburgh Sleep Quality Index (PSQI). At baseline, the ESS
score was not different from that of agematched healthy
controls. The mean ESS score increased significantly after 1
year of follow-up, being more than 10 in 12 patients. The mean
PSQI also increased significantly after 1 year of treatment, but
there were no differences in the number of bad sleepers at
baseline and at follow-up. In conclusion, EDS seems to emerge
during the course of the illness, at least in a proportion of PD
patients, and could represent another clinical correlate of the
interaction between the ongoing neurodegenerative process and
the side effects of drugs.
Neurological Sciences 09/2003; 24(3):178-179. · 1.32 Impact Factor
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V. Bonifati,
P. Rizzu,
F. Squitieri,
E. Krieger,
N. Vanacore,
J.C. Swieten,
A. Brice,
C.M. Duijn,
B. Oostra, G. Meco,
P. Heutink
[show abstract]
[hide abstract]
ABSTRACT: Four chromosomal loci (PARK2, PARK6, PARK7, and PARK9) associated with autosomal
recessive, early onset parkinsonism are known. We mapped the
PARK7 locus to chromosome
1p36 in a large family from a genetically isolated population in
the Netherlands, and confirmed this linkage in an Italian
family. By positional cloning within the refined
PARK7 critical region we
recently identified mutations in the DJ-1 gene in the two PARK7-linked
families. The function of DJ-1 remains largely unknown, but
evidence from genetic studies on the yeast
DJ-1 homologue, and
biochemical studies in murine and human cell lines, suggests a
role for DJ-1 as an antioxidant and/or a molecular chaperone.
Elucidating the role of DJ-1 will lead to a better understanding
of the pathogenesis of DJ-1-related and common forms of
Parkinsons disease.
Neurological Sciences 09/2003; 24(3):159-160. · 1.32 Impact Factor
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Neurological Sciences 09/2003; 24(3):205-206. · 1.32 Impact Factor
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E M Valente,
F Brancati,
V Caputo,
E A Graham,
M B Davis,
A Ferraris,
M M B Breteler,
T Gasser,
V Bonifati,
A R Bentivoglio,
G De Michele,
A Dürr,
P Cortelli,
A Filla, G Meco,
B A Oostra,
A Brice,
A Albanese,
B Dallapiccola,
N W Wood
[show abstract]
[hide abstract]
ABSTRACT: The Parkin gene is responsible for about 50% of autosomal recessive juvenile parkinsonism (ARJP) and less than 20% of sporadic early onset cases. We recently mapped a novel ARJP locus (PARK6) on chromosome 1p. Linkage to PARK6 was confirmed in 8 families from 4 different European countries. These families share some clinical features with the European Parkin-positive cases, with a wide range of ages at onset and slow progression. However, features typical of ARJP, such as dystonia and sleep benefit, were not observed, making the clinical presentation of late-onset cases indistinguishable from that of idiopathic PD. The determination of the smallest region of homozygosity in one consanguineous family allowed reducing the candidate interval to 9 cM. PARK6 appears to be an important locus for ARJP in Europe.
Neurological Sciences 10/2002; 23 Suppl 2:S117-8. · 1.32 Impact Factor
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V Bonifati,
M C J Dekker,
N Vanacore,
G Fabbrini,
F Squitieri,
R Marconi,
A Antonini,
P Brustenghi,
A Dalla Libera,
M De Mari,
F Stocchi,
P Montagna,
V Gallai,
P Rizzu,
J C van Swieten,
B Oostra,
C M van Duijn, G Meco,
P Heutink
[show abstract]
[hide abstract]
ABSTRACT: Autosomal recessive, early onset parkinsonism (AREP) is genetically heterogeneous. Mutations in the parkin gene (PARK2 locus, chromosome 6q) account for up to 50% of AREP families. The parkin protein displays ubiquitin-ligase activity for different targets, which accumulate in the brain of patients with parkin defect and might cause neurodegeneration. Two new AREP loci (PARK6 and PARK7) have been recently mapped on chromosome 1p and confirmed in independent datasets, suggesting that both might be frequent. The three AREP forms display similar clinical phenotypes. Recruiting new families will help cloning the defective genes at PARK6 and PARK7 loci. This will contribute to unraveling the pathogenesis of AREP, and it is also expected to foster our understanding of molecular events underlying classic Parkinson's disease.
Neurological Sciences 10/2002; 23 Suppl 2:S59-60. · 1.32 Impact Factor
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N Vanacore,
A Nappo,
M Gentile,
A Brustolin,
S Palange,
A Liberati,
S Di Rezze,
G Caldora,
M Gasparini,
F Benedetti,
V Bonifati,
F Forastiere,
A Quercia, G Meco
[show abstract]
[hide abstract]
ABSTRACT: In the last two years, the environmental theory on the aetiology of Parkinson disease has acquired new data. From an experimental point of view, a new model of parkinsonism induced by rotenone, a diffuse insecticide, has been proposed, and in vitro studies have provided proof that several pesticides stimulate the formation of alpha-synuclein fibrils (one of the principal constituents of Lewy bodies). Moreover, a meta-analysis of all case-control studies so far performed showed a positive, statistically significant association between pesticide exposure and PD. In this context, we are performing a cohort study on 5575 licensed pesticide users in the province of Viterbo. After 27 years of follow-up, 4788 subjects are still alive. The aim of this study is to measure the prevalence of Parkinson's disease in a large group of workers with theoretically increased risk.
Neurological Sciences 10/2002; 23 Suppl 2:S119-20. · 1.32 Impact Factor
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ABSTRACT: Aretrospective hospital-based case-control study was performed with the aim to evaluate the association between exposure to anesthesia and Alzheimer's disease (AD). A total of 115 AD patients, 230 Parkinson's disease (PD) patients and 230 patients with non-degenerative neurological disease were studied. Each AD case was matched for sex, age (+/-3 years) and geographic area of residence with four controls (2 PD patients and 2 with other neurological disease). Information about exposure to general anesthesia and other variables was gathered through hospital records. No associations were found between the risk of AD and the exposure to anesthesia in the 1 and 5 years preceding disease onset, nor between the risk of AD and the number of surgical operations. A significant difference was observed between the mean age of AD patients and controls undergoing surgical procedures. The present study reveals a lack of association between exposure to general anesthesia and AD. Prospective epidemiological studies are needed in order to investigate levels of exposure to anesthesia, as well as any possible relationships between anesthetic exposure and genetic factors (e. g. APOEepsilon4 genotype).
Neurological Sciences 05/2002; 23(1):11-4. · 1.32 Impact Factor
