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Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease

BACKGROUND: Renin-angiotensin system (RAS) influences the central nervous system not only through its peripheral impact—the brain possesses its own local RAS. Studies showed altered RAS components in Parkinson’s disease (PD) and their association with oxidative stress which may be linked to neurodeg...

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Autores principales: Pierzchlińska, Anna, Sławek, Jarosław, Mak, Monika, Gawrońska-Szklarz, Barbara, Białecka, Monika
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8301732/
https://www.ncbi.nlm.nih.gov/pubmed/34302265
http://dx.doi.org/10.1007/s11033-021-06569-6
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author Pierzchlińska, Anna
Sławek, Jarosław
Mak, Monika
Gawrońska-Szklarz, Barbara
Białecka, Monika
author_facet Pierzchlińska, Anna
Sławek, Jarosław
Mak, Monika
Gawrońska-Szklarz, Barbara
Białecka, Monika
author_sort Pierzchlińska, Anna
collection PubMed
description BACKGROUND: Renin-angiotensin system (RAS) influences the central nervous system not only through its peripheral impact—the brain possesses its own local RAS. Studies showed altered RAS components in Parkinson’s disease (PD) and their association with oxidative stress which may be linked to neurodegeneration and dementia. Moreover, the protective functions of RAS blockade antagonists against cognitive decline and dementia have been suggested. This study aimed to examine whether genetic variability in RAS genes correlates with cognitive decline in PD. METHODS AND RESULTS: We genotyped single nucleotide polymorphisms (SNPs) in angiotensinogen (AGT: rs699, rs4762), angiotensin II receptors (AGTR1: rs5186 and AGTR2: rs5194, rs1403543) genes, as well as insertion/deletion polymorphism in the angiotensin-converting enzyme (ACE I/D) gene in 256 PD patients, divided into three groups: without cognitive decline, with mild cognitive impairment and with PD dementia. We did not find any significant differences in the frequencies of the analysed polymorphisms in any of the groups. CONCLUSIONS: Despite no direct correlation between the investigated polymorphisms in RAS genes and cognitive decline in PD, we believe the impact of those genotypes may be indirect, affecting RAS blockade treatment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11033-021-06569-6.
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spelling pubmed-83017322021-07-26 Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease Pierzchlińska, Anna Sławek, Jarosław Mak, Monika Gawrońska-Szklarz, Barbara Białecka, Monika Mol Biol Rep Original Article BACKGROUND: Renin-angiotensin system (RAS) influences the central nervous system not only through its peripheral impact—the brain possesses its own local RAS. Studies showed altered RAS components in Parkinson’s disease (PD) and their association with oxidative stress which may be linked to neurodegeneration and dementia. Moreover, the protective functions of RAS blockade antagonists against cognitive decline and dementia have been suggested. This study aimed to examine whether genetic variability in RAS genes correlates with cognitive decline in PD. METHODS AND RESULTS: We genotyped single nucleotide polymorphisms (SNPs) in angiotensinogen (AGT: rs699, rs4762), angiotensin II receptors (AGTR1: rs5186 and AGTR2: rs5194, rs1403543) genes, as well as insertion/deletion polymorphism in the angiotensin-converting enzyme (ACE I/D) gene in 256 PD patients, divided into three groups: without cognitive decline, with mild cognitive impairment and with PD dementia. We did not find any significant differences in the frequencies of the analysed polymorphisms in any of the groups. CONCLUSIONS: Despite no direct correlation between the investigated polymorphisms in RAS genes and cognitive decline in PD, we believe the impact of those genotypes may be indirect, affecting RAS blockade treatment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11033-021-06569-6. Springer Netherlands 2021-07-23 2021 /pmc/articles/PMC8301732/ /pubmed/34302265 http://dx.doi.org/10.1007/s11033-021-06569-6 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Article
Pierzchlińska, Anna
Sławek, Jarosław
Mak, Monika
Gawrońska-Szklarz, Barbara
Białecka, Monika
Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease
title Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease
title_full Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease
title_fullStr Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease
title_full_unstemmed Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease
title_short Genetic polymorphisms in the renin-angiotensin system and cognitive decline in Parkinson’s disease
title_sort genetic polymorphisms in the renin-angiotensin system and cognitive decline in parkinson’s disease
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8301732/
https://www.ncbi.nlm.nih.gov/pubmed/34302265
http://dx.doi.org/10.1007/s11033-021-06569-6
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