Journal
BIOMOLECULES
Volume 10, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/biom10081177
Keywords
contactin; Lewy bodies; cerebrospinal fluid (CSF); biomarker; synaptic degeneration; Parkinson's disease (PD); dementia with Lewy bodies (DLB)
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Funding
- European Neuroscience Campus Network, an Erasmus Mundus Joint Doctoral Program [cycle 5/2014/P-04]
- Stichting Alzheimer Nederland
- Stichting VUmc funds
- Stichting Dioraphte
- Scientific Excellence Program of Amsterdam Neuroscience
- Memorabel grant programme of the Netherlands Organisation for Health Research and Development (ZonMW grant) [733050509]
- Parkinson Association
- Amsterdam Neuroscience
- Alzheimer's Association-LECMA
- ZonMW Memorabel and ZonMWDTLS
- Roche Pharma
- Lysosomal Therapeutics
- CHDR
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Synaptic degeneration is an early phenomenon in Parkinson's disease (PD) pathogenesis. We aimed to investigate whether levels of synaptic proteins contactin-1 and contactin-2 in cerebrospinal fluid (CSF) of PD patients are reduced compared to dementia with Lewy bodies (DLB) patients and controls and to evaluate their relationship with alpha-synuclein aggregation. Contactin-1 and -2 were measured in CSF from PD patients (n =58), DLB patients (n =72) and age-matched controls (n =90). Contactin concentration differences between diagnostic groups were assessed by general linear models adjusted for age and sex. Contactin immunoreactivity was characterized in postmortem substantia nigra, hippocampus and entorhinal cortex tissue of PD patients (n =4) and controls (n =4), and its relation to alpha-syn aggregation was evaluated using confocal laser scanning microscopy. Contactin-1 levels were lower in PD patients (42 (36-49) pg/mL) compared to controls (52 (44-58) pg/mL,p =0.003) and DLB patients (56 (46-67) pg/mL,p =0.001). Contactin-2 levels were similar across all diagnostic groups. Within the PD patient group, contactin-1 correlated with t-alpha-syn, tTau and pTau (r =0.30-0.50,p <0.05), whereas contactin-2 only correlated with t-alpha-syn (r =0.34,p =0.03). Contactin-1 and -2 were observed within nigral and cortical Lewy bodies and clustered within bulgy Lewy neurites in PD brains. A decrease in CSF contactin-1 may reflect synaptic degeneration underlying Lewy body pathology in PD.
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