Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson's disease. (6th May 2015)

• Record Type: Journal Article
• Authors: Carbutt, Sophia; Duff, Jennifer; Yarnall, Alison; Burn, David J.; Hudson, Gavin
• Is Part Of: Neuroscience letters. Volume 594(2015)
• Page Start: 66
• Page End: 69
• Publication Date: 2015-05-06
• Subjects: Parkinson's disease -- Cognitive decline; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.03.048
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Cognitive decline is a strong hallmark of PD. Genetic variation in C1Q – does not account for the cognitive decline seen in PD. Genetic variation in C1Q – is unlikely to contribute to PD aetiology. Abstract: Traditional dogma regarding the brain as an immune exempt organ has changed in recent years. New research has highlighted the role of the classical complement cascade in both synaptic elimination and function, driven largely by the role of the pathway initiating protein C1q. Given the links between C1q and cognitive function we assessed the genetic variability of the C1q encoding genes: C1QA, C1QB and C1QC between PD patients and matched controls. Despite a strong link between C1Q/cognitive decline and PD/cognitive decline we were unable to find a link between common C1Q variation and PD. We conclude that common C1Q-A/B/C genetic variation is unlikely to contribute to cognitive decline or the missing heritability in PD.