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CSF amyloid-beta and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study.
J Neurol Neurosurg Psychiatry. 2010 Oct; 81(10):1080-6.JN

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.

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Authors+Show Affiliations

Alves G
The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway. algu@sus.no
Brønnick K
No affiliation info available
Aarsland D
No affiliation info available
Blennow K
No affiliation info available
Zetterberg H
No affiliation info available
Ballard C
No affiliation info available
Kurz MW
No affiliation info available
Andreasson U
No affiliation info available
Tysnes OB
No affiliation info available
Larsen JP
No affiliation info available
Mulugeta E
No affiliation info available

MeSH

AgedAlzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EBiomarkersCognition DisordersFemaleGenotypeHumansMaleNeuropsychological TestsNorwayParkinson DiseasePeptide Fragmentstau Proteins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20547614

Citation

Alves, Guido, et al. "CSF Amyloid-beta and Tau Proteins, and Cognitive Performance, in Early and Untreated Parkinson's Disease: the Norwegian ParkWest Study." Journal of Neurology, Neurosurgery, and Psychiatry, vol. 81, no. 10, 2010, pp. 1080-6.
Alves G, Brønnick K, Aarsland D, et al. CSF amyloid-beta and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study. J Neurol Neurosurg Psychiatry. 2010;81(10):1080-6.
Alves, G., Brønnick, K., Aarsland, D., Blennow, K., Zetterberg, H., Ballard, C., Kurz, M. W., Andreasson, U., Tysnes, O. B., Larsen, J. P., & Mulugeta, E. (2010). CSF amyloid-beta and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study. Journal of Neurology, Neurosurgery, and Psychiatry, 81(10), 1080-6. https://doi.org/10.1136/jnnp.2009.199950
Alves G, et al. CSF Amyloid-beta and Tau Proteins, and Cognitive Performance, in Early and Untreated Parkinson's Disease: the Norwegian ParkWest Study. J Neurol Neurosurg Psychiatry. 2010;81(10):1080-6. PubMed PMID: 20547614.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CSF amyloid-beta and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study. AU - Alves,Guido, AU - Brønnick,Kolbjørn, AU - Aarsland,Dag, AU - Blennow,Kaj, AU - Zetterberg,Henrik, AU - Ballard,Clive, AU - Kurz,Martin Wilhelm, AU - Andreasson,Ulf, AU - Tysnes,Ole-Bjørn, AU - Larsen,Jan Petter, AU - Mulugeta,Ezra, Y1 - 2010/06/14/ PY - 2010/6/16/entrez PY - 2010/6/16/pubmed PY - 2010/10/20/medline SP - 1080 EP - 6 JF - Journal of neurology, neurosurgery, and psychiatry JO - J Neurol Neurosurg Psychiatry VL - 81 IS - 10 N2 - 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. SN - 1468-330X UR - https://www.unboundmedicine.com/medline/citation/20547614/CSF_amyloid_beta_and_tau_proteins_and_cognitive_performance_in_early_and_untreated_Parkinson's_disease:_the_Norwegian_ParkWest_study_ L2 - https://jnnp.bmj.com/lookup/pmidlookup?view=long&amp;pmid=20547614 DB - PRIME DP - Unbound Medicine ER -