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J Neurol Neurosurg Psychiatry 81:1080-1086 doi:10.1136/jnnp.2009.199950
  • Research paper

CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study

  1. Ezra Mulugeta1,5
  1. 1The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway
  2. 2Department of Neurology, Stavanger University Hospital, Stavanger, Norway
  3. 3Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway
  4. 4Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden
  5. 5Wolfson Centre for Age Related Diseases, King's College, London, UK
  6. 6Institute of Clinical Medicine, University of Bergen, Bergen, Norway
  7. 7Department of Neurology, Haukeland University Hospital, Bergen, Norway
  1. Correspondence to Dr Guido Alves, The Norwegian Centre for Movement Disorders, Stavanger University Hospital, PO Box 8100 N-4068 Stavanger, Norway; algu{at}sus.no
  • Received 11 November 2009
  • Revised 11 January 2010
  • Accepted 20 January 2010
  • Published Online First 14 June 2010

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.

Footnotes

  • Funding The Norwegian ParkWest study is funded by the Western Norway Regional Health Authority (grant no 911218), the Research Council of Norway (grant no 177966) and the Norwegian Parkinson's Disease Association.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval Ethics approval was provided by the Regional Committee for Medical Research Ethics, University of Bergen, Norway.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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