Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease

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...

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Autores principales: Carbutt, Sophia, Duff, Jennifer, Yarnall, Alison, Burn, David J., Hudson, Gavin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Scientific Publishers Ireland 2015
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407898/
https://www.ncbi.nlm.nih.gov/pubmed/25817358
http://dx.doi.org/10.1016/j.neulet.2015.03.048
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author Carbutt, Sophia
Duff, Jennifer
Yarnall, Alison
Burn, David J.
Hudson, Gavin
author_facet Carbutt, Sophia
Duff, Jennifer
Yarnall, Alison
Burn, David J.
Hudson, Gavin
author_sort Carbutt, Sophia
collection PubMed
description 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.
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spelling pubmed-44078982015-05-06 Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease Carbutt, Sophia Duff, Jennifer Yarnall, Alison Burn, David J. Hudson, Gavin Neurosci Lett Research Article 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. Elsevier Scientific Publishers Ireland 2015-05-06 /pmc/articles/PMC4407898/ /pubmed/25817358 http://dx.doi.org/10.1016/j.neulet.2015.03.048 Text en © 2015 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Carbutt, Sophia
Duff, Jennifer
Yarnall, Alison
Burn, David J.
Hudson, Gavin
Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease
title Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease
title_full Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease
title_fullStr Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease
title_full_unstemmed Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease
title_short Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson’s disease
title_sort variation in complement protein c1q is not a major contributor to cognitive impairment in parkinson’s disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407898/
https://www.ncbi.nlm.nih.gov/pubmed/25817358
http://dx.doi.org/10.1016/j.neulet.2015.03.048
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