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α-synuclein antibodies recognize a protein present at lower levels in the CSF of patients with dementia with Lewy bodies

Published online by Cambridge University Press:  14 September 2009

Clive Ballard*
Affiliation:
Wolfson Centre for Age-Related Disease, King's College London, U.K.
Emma L. Jones
Affiliation:
Wolfson Centre for Age-Related Disease, King's College London, U.K.
Elisabet Londos
Affiliation:
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden
Lennart Minthon
Affiliation:
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden
Paul Francis
Affiliation:
Wolfson Centre for Age-Related Disease, King's College London, U.K.
Dag Aarsland
Affiliation:
Wolfson Centre for Age-Related Disease, King's College London, U.K. Clinical Neuroscience Research, Stavanger University Hospital, Norway
*
Correspondence should be addressed to: Professor Clive Ballard, Wolfson Centre for Age-Related Diseases, Wolfson Building, Guy's Campus, King's College London, London Bridge, SE1 1UL, U.K. Phone: +44 207 848 6568; Fax: +44 207 848 6145. Email: [email protected].

Abstract

Background: Dementia with Lewy bodies (DLB) accounts for 15–20% of the millions of people worldwide with dementia. Accurate diagnosis is essential to avoid harm and optimize clinical management. There is therefore an urgent need to identify reliable biomarkers.

Methods: Mass spectrometry was used to determine the specificity of antibody α-synuclein (211) for α-synuclein. Using gel electrophoresis we measured protein levels detected by α-synuclein specific antibodies in the cerebrospinal fluid (CSF) of DLB patients and compared them to age matched controls.

Results: A 24 kDa band was detected using α-synuclein specific antibodies which was significantly reduced in the CSF of DLB patients compared to age matched controls (p < 0.05). Further analysis confirmed that even DLB patients with mild dementia showed significant reductions in this protein in comparison to controls.

Conclusions: The current study emphasizes the necessity for further studies of CSF α-synuclein as a biomarker of DLB and extends our previous knowledge by establishing a potential relationship between α-synuclein and the severity of cognitive impairment. The identification of this 24 kDa protein is the next important step in these studies.

Type
Research Article
Copyright
Copyright © International Psychogeriatric Association 2009

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