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Dive into the research topics where Marjolijn Bornebroek is active.

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Featured researches published by Marjolijn Bornebroek.


Neurology | 2005

Dietary fatty acids and the risk of Parkinson disease: The Rotterdam Study

L.M.L. de Lau; Marjolijn Bornebroek; J. C. M. Witteman; A. Hofman; Peter J. Koudstaal; Monique M.B. Breteler

Background: Unsaturated fatty acids are important constituents of neuronal cell membranes and have neuroprotective, antioxidant, and anti-inflammatory properties. Objective: To determine if a high intake of unsaturated fatty acids might be associated with a lower risk of Parkinson disease (PD). Methods: In the Rotterdam Study, a prospective population-based cohort study of people ages ≥55, the association between intake of unsaturated fatty acids and the risk of incident PD was evaluated among 5,289 subjects who were free of dementia and parkinsonism and underwent complete dietary assessment at baseline. PD was assessed through repeated in-person examination, and the cohort was continuously monitored by computer linkage to medical records. The data were analyzed using Cox proportional hazards regression models. Results: After a mean follow-up of 6.0 years, 51 participants with incident PD were identified. Intakes of total fat, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) were significantly associated with a lower risk of PD, with an adjusted hazard ratio per SD increase of energy-adjusted intake of 0.69 (95% CI 0.52 to 0.91) for total fat, of 0.68 (95% CI 0.50 to 0.94) for MUFAs, and 0.66 (95% CI 0.46 to 0.96) for PUFAs. No associations were found for dietary saturated fat, cholesterol, or trans-fat. Conclusion: These findings suggest that high intake of unsaturated fatty acids might protect against Parkinson disease.


Neuroepidemiology | 2007

Nonsteroidal Anti-Inflammatory Drugs and the Risk of Parkinson Disease

Marjolijn Bornebroek; Lonneke M. L. de Lau; Mendel D.M. Haag; Peter J. Koudstaal; Albert Hofman; Bruno H. Stricker; Monique M.B. Breteler

Background: Several lines of evidence suggest a role of inflammatory processes in Parkinson disease, although it is still unclear whether inflammation is a cause or rather a consequence of neurodegeneration. Methods: In a prospective population-based cohort study among 6,512 participants aged ≧55 years, with repeated in-person examination, we evaluated the association between cumulative use of nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of Parkinson disease. Complete information on filled prescriptions was available from automated pharmacy records. Data were analyzed by means of Cox proportional hazards regression analysis, adjusted for age, sex, smoking habits and coffee consumption. Results: After an average 9.4 years of follow-up, 88 new cases of Parkinson disease were detected. No association was found between use of NSAIDs and the risk of Parkinson disease (adjusted hazard ratio for any NSAID use, 1.50; 95% confidence interval, 0.95–2.37). Conclusion: Our findings do not support the hypothesis that NSAIDs might decrease the risk of Parkinson disease.


Clinical Neuroscience Research | 2004

Epidemiology of non-AD dementias

Marjolijn Bornebroek; Monique M.B. Breteler

Abstract Dementia is a common neurodegenerative disorder that affects about 10% of the population over 65 years of age. A distinction can be made between primary degenerative dementias and dementia secondary to other diseases. This review focuses on the primary non-Alzheimers disease (AD) dementias: vascular dementia (VaD), dementia with Lewy bodies (DLB) and frontotemporal dementia (FTD). VaD is after AD most frequent subtype of dementia with a prevalence of about 1%, ranging from 0 to 10% mainly depending on the age group investigated and the criteria used. Its incidence rate is between 1.5 and 4.1 per 1000 person-years, with no clear difference between men and women and with possibly a higher incidence in East Asia compared to Canada and Europe. Most of the VaD cases are sporadic although there are some rare familial forms of VaD as cerebral autosomal dominant arteriopathy with subcortical infarctions and leukoencephalopathy and familial cerebral amyloid angiopathy. Important risk factors for sporadic VaD are cerebrovascular pathology (brain infarction, white matter lesions and brain atrophy), midlife hypertension, and diabetes leading to increasing risk ratios. A protective effect is often found for education and moderate use of alcohol. The association between VaD and amyloid β, cholesterol, and statin use remains unclear yet. DLB and FTD are less frequent forms of dementia with prevalence rates of, respectively, 0.1–0.6 and 0.002–0.015%. FTD affects people in their middle age, accounting for up to 10–20% of the presenile dementia cases. About 14% of the FTD cases are caused by an autosomal dominant tau-mutation. However, since the prevalence of sporadic FTD is relatively low, population-based epidemiological studies are hard to perform and no non-genetic risk factors are known yet. DLB is a relative common form of dementia in old age accounting for 15–20% of cases in hospital autopsy case-series. The only known possible risk factor for DLB is the presence of an apolipoprotein E e4 allele.


European Journal of Epidemiology | 2002

Studying risk factors for Parkinson's disease.

Marjolijn Bornebroek; Monique M.B. Breteler

Epidemiological studies in Parkinson’s disease (PD) are of great importance to contribute to the unraveling of the causes of this disease. PD is after Alzheimer’s disease the most frequent neurodegenerative disease in the elderly. Due to a growing proportion of elderly in the population this disabling disease will affect an increasing number of persons. Despite numerous research efforts the etiology of the disease is still largely unknown. It is known that excessive dopaminergic cell loss leads to the disease but the cause of the cell loss is poorly understood. During the last decades it became more and more clear that PD is a multifactorial disease in which genetic and environmental factors contribute to the pathogenesis. In this issue Pals et al. report on a retrospective case–control study about potential risk factors for PD in the Flemish part of Belgium [1]. The study was designed to investigate complex genetic and environmental factors in PD. Here they report on the role of the environmental factors. The 438 PD patients were recruited from a patients support group and from the three Flemish University Hospitals and the 231 controls were spouses of the patients. During a 3year period data were collected through self-reporting questionnaires. Sufficient data were available for 423


Radiology | 2002

Subcortical lacunar lesions: an MR imaging finding in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Rivka van den Boom; Saskia A. J. Lesnik Oberstein; Sjoerd G. van Duinen; Marjolijn Bornebroek; Michel D. Ferrari; Joost Haan; Mark A. van Buchem


Stroke | 1998

Microvasculopathy Is Associated With the Number of Cerebrovascular Lesions in Hereditary Cerebral Hemorrhage With Amyloidosis, Dutch Type

Remco Natté; Harry V. Vinters; Marion L. C. Maat-Schieman; Marjolijn Bornebroek; Joost Haan; Raymund A.C. Roos; Sjoerd G. van Duinen


Neurobiology of Disease | 2003

Hereditary cerebral hemorrhage with amyloidosis dutch type (AβPP 693): decreased plasma amyloid-β 42 concentration

Marjolijn Bornebroek; Chris De Jonghe; Joost Haan; Samir Kumar-Singh; Steve Younkin; Raymund A.C. Roos; Christine Van Broeckhoven


JAMA Neurology | 1996

White Matter Lesions and Cognitive Deterioration in Presymptomatic Carriers of the Amyloid Precursor Protein Gene Codon 693 Mutation

Marjolijn Bornebroek; Joost Haan; Mark A. van Buchem; Jan B. K. Lanser; M. A. C. Simone de Vries-vd Weerd; Moniek Zoeteweij; Raymund A.C. Roos


The Lancet | 2004

A novel drug target in Alzheimer's disease

Marjolijn Bornebroek; Samir Kumar-Singh


Neuroepidemiology | 2007

Contents Vol. 28, 2007

Marjolijn Bornebroek; Lonneke M. L. de Lau; Mendel D.M. Haag; Peter J. Koudstaal; Albert Hofman; Bruno H. Stricker; Monique M.B. Breteler; Martin Röösli; Manfred Lörtscher; Matthias Egger; Dominik Pfluger; Nadja Schreier; Emanuel Lörtscher; Peter Locher; Adrian Spoerri; Christoph E. Minder; Pirjo Komulainen; Miia Kivipelto; Timo A. Lakka; Maija Hassinen; Eeva-Liisa Helkala; Kristiina Patja; Aulikki Nissinen; Rainer Rauramaa; J. Massa; K.L. Munger; E.J. O’Reilly; K.I. Falk; A. Ascherio; Mustapha Danesi

Collaboration


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Monique M.B. Breteler

German Center for Neurodegenerative Diseases

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Peter J. Koudstaal

Erasmus University Rotterdam

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Albert Hofman

Erasmus University Rotterdam

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Bruno H. Stricker

Erasmus University Rotterdam

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Lonneke M. L. de Lau

Erasmus University Rotterdam

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Mendel D.M. Haag

Erasmus University Rotterdam

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Mark A. van Buchem

Leiden University Medical Center

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Sjoerd G. van Duinen

Leiden University Medical Center

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