Affiliations: Department of Experimental Medical Science, Brain Disease Biomarker Unit, Wallenberg Neuroscience Center, Lund University, Lund, Sweden | Department of Measurement Technology and Industrial Electrical Engineering, Division Nanobiotechnology, Lund University, Lund, Sweden | Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK | Department of Clinical Neurosciences, UCL Institute of Neurology, London, UK
Note:  Correspondence to: Edina Silajdžić, Department of Experimental Medical Science, Brain Disease Biomarker Unit, Wallenberg Neuroscience Center, Lund University, SE-221 84 Lund, Sweden. Tel.: +46 46 222 8516; E-mail: [email protected]
Abstract: Background: Huntington's Disease (HD) is a hereditary, progressive neurodegenerative disorder characterised by both neurological and systemic symptoms. In HD, immune changes can be observed before the onset of overt clinical features raising the possibility that inflammatory markers in plasma could be used to track disease progression. It has previously been demonstrated that a widespread, progressive innate immune response is detectable in plasma throughout the course of HD. Objective: The aim of the present study was to investigate the potential of several components of inflammation and innate immunity as plasma biomarkers in HD. Methods: We utilised antibody-based detection technologies as well as mass spectrometric quantification, multiple reaction monitoring (MRM-MS). Results: Levels of several markers previously described as altered in HD, such as clusterin, complement component 4, complement component 9 and α-2 macroglobulin did not differ between healthy controls and HD subjects as measured by Luminex, ELISA or MRM-MS. C-reactive protein was decreased in early HD, while the other immune markers tested were unaltered. Conclusions: Although only C-reactive protein was found to be reduced in early HD, some of the inflammatory markers measured correlated with clinical measures.