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Parkinson Disease: HELP
Articles by Martin Wilhelm Kurz
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, Martin W. Kurz wrote the following 4 articles about Parkinson Disease.
+ Citations + Abstracts
1 Review The epidemiology of dementia associated with Parkinson's disease. 2010

Aarsland, Dag / Kurz, Martin Wilhelm. ·Department of Psychiatry, Stavanger University Hospital, Postboks 8100, 4068 Stavanger, Norway. daarsland@gmail.com ·Brain Pathol · Pubmed #20522088.

ABSTRACT: Parkinson's disease (PD) is the second most common neurodegenerative illness after Alzheimer's disease (AD). Cognitive impairment and dementia are common features in PD and characterized by a wide range of cognitive deficits distinct from those seen in AD. Mild cognitive impairment occurs even early in PD and is associated with shorter time to dementia. The purpose of this review is to present recent findings on clinical aspects of dementia in PD and to elucidate underlying clinical and neurobiological risk factors.

2 Article Cerebrospinal fluid Aβ levels correlate with structural brain changes in Parkinson's disease. 2013

Beyer, Mona K / Alves, Guido / Hwang, Kristy S / Babakchanian, Sona / Bronnick, Kolbjorn S / Chou, Yi-Yu / Dalaker, Turi O / Kurz, Martin W / Larsen, Jan P / Somme, Johanne H / Thompson, Paul M / Tysnes, Ole-Bjørn / Apostolova, Liana G. ·The Norwegian Center for Movement Disorders, Stavanger University Hospital, Stavanger, Norway. mona.beyer@lyse.net ·Mov Disord · Pubmed #23408705.

ABSTRACT: ParkWest is a large Norwegian multicenter study of newly diagnosed drug-naïve subjects with Parkinson's disease (PD). Cognitively normal PD subjects (PDCN) and PD subjects with mild cognitive impairment (PDMCI) from this cohort have significant hippocampal atrophy and ventricular enlargement, compared to normal controls. Here, we aimed to investigate whether the same structural changes are associated with cerebrospinal fluid (CSF) levels of amyloid beta (Aβ)38 , Aβ40 , Aβ42 , total tau (t-tau), and phosphorylated tau (p-tau). We performed three-dimensional radial distance analyses of the hippocampi and lateral ventricles using the MRI data from ParkWest subjects who provided CSF at baseline. Our sample consisted of 73 PDCN and 18 PDMCI subjects. We found significant associations between levels of all three CSF Aβ analytes and t-tau and lateral ventricular enlargement in the pooled sample. In the PDCN sample, all three amyloid analytes showed significant associations with the radial distance of the occipital and frontal horns of the lateral ventricles. CSF Aβ38 and Aβ42 showed negative associations, with enlargement in occipital and frontal horns of the lateral ventricles in the pooled sample, and a negative association with the occipital horns in PDMCI. CSF Aβ levels in early PD correlate with ventricular enlargement, previously associated with PD dementia. Therefore, CSF and MRI markers may help identify PD patients at high risk for developing cognitive decline and dementia in the course of their illness. Contrary to Alzheimer's disease, we found no associations between CSF t-tau and p-tau and hippocampal atrophy.

3 Article CSF amyloid-beta and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study. 2010

Alves, Guido / Brønnick, Kolbjørn / Aarsland, Dag / Blennow, Kaj / Zetterberg, Henrik / Ballard, Clive / Kurz, Martin Wilhelm / Andreasson, Ulf / Tysnes, Ole-Bjørn / Larsen, Jan Petter / Mulugeta, Ezra. ·The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway. algu@sus.no ·J Neurol Neurosurg Psychiatry · Pubmed #20547614.

ABSTRACT: BACKGROUND: Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. METHODS: CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. RESULTS: PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p<0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. CONCLUSION: CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.

4 Article The role of APOE alleles in incident Parkinson's disease. The Norwegian ParkWest Study. 2010

Vefring, H / Haugarvoll, K / Tysnes, O-B / Larsen, J P / Kurz, Martin W / Anonymous2870660. ·The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway. kuma@sus.no ·Acta Neurol Scand · Pubmed #20456244.

ABSTRACT: OBJECTIVES: Apolipoprotein E (APOE) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between APOE alleles and Parkinson's disease (PD) and age at onset in PD. There exist no data on APOE alleles in an unselected cohort of patients with incident PD. PATIENTS AND METHODS: To determine the role of APOE alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their APOE allele status. RESULTS: No association was observed between any APOE alleles and susceptibility to PD or age at onset in PD. CONCLUSION: In our cohort of unselected, incident PD patients APOE alleles do not seem to play a role for development of PD. Prospective, long-term follow-up may still reveal associations between APOE alleles and clinical and neuropsychological progression in PD.