Association of the RAGE G82S polymorphism with Alzheimer's disease
(2010) In Journal of Neural Transmission 117(7). p.861-867- Abstract
- The receptor for advanced glycation end-products (RAGE) has been implicated in several pathophysiological processes relevant to Alzheimer's disease (AD), including transport and synaptotoxicity of AD-associated amyloid beta (A beta) peptides. A recent Chinese study (Li et al. in J Neural Transm 117:97-104, 2010) suggested an association between the 82S allele of the functional single nucleotide polymorphism (SNP) G82S (rs2070600) in the RAGE-encoding gene AGER and risk of AD. The present study aimed to investigate associations between AGER, AD diagnosis, cognitive scores and cerebrospinal fluid AD biomarkers in a European cohort of 316 neurochemically verified AD cases and 579 controls. Aside from G82S, three additional tag SNPs were... (More)
- The receptor for advanced glycation end-products (RAGE) has been implicated in several pathophysiological processes relevant to Alzheimer's disease (AD), including transport and synaptotoxicity of AD-associated amyloid beta (A beta) peptides. A recent Chinese study (Li et al. in J Neural Transm 117:97-104, 2010) suggested an association between the 82S allele of the functional single nucleotide polymorphism (SNP) G82S (rs2070600) in the RAGE-encoding gene AGER and risk of AD. The present study aimed to investigate associations between AGER, AD diagnosis, cognitive scores and cerebrospinal fluid AD biomarkers in a European cohort of 316 neurochemically verified AD cases and 579 controls. Aside from G82S, three additional tag SNPs were analyzed to cover the common genetic variation in AGER. The 82S allele was associated with increased risk of AD (P (c) = 0.04, OR = 2.0, 95% CI 1.2-3.4). There was no genetic interaction between AGER 82S and APOE epsilon 4 in producing increased risk of AD (P = 0.4), and none of the AGER SNPs showed association with A beta(42), T-tau, P-tau(181) or mini-mental state examination scores. The data speak for a weak, but significant effect of AGER on risk of AD. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1629052
- author
- Daborg, Jonny ; von Otter, Malin ; Sjolander, Annica ; Nilsson, Staffan ; Minthon, Lennart LU ; Gustafson, Deborah R. ; Skoog, Ingmar ; Blennow, Kaj and Zetterberg, Henrik
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Haplotype, SNP, product-specific receptor, Advanced glycosylation end, AGER, Alzheimer's disease, RAGE
- in
- Journal of Neural Transmission
- volume
- 117
- issue
- 7
- pages
- 861 - 867
- publisher
- Springer
- external identifiers
-
- wos:000279464300009
- scopus:77954535503
- pmid:20567859
- ISSN
- 0300-9564
- DOI
- 10.1007/s00702-010-0437-0
- language
- English
- LU publication?
- yes
- id
- 1d6d04e1-0c4b-48d2-be1b-1bc01f7d075f (old id 1629052)
- date added to LUP
- 2016-04-01 12:56:20
- date last changed
- 2022-02-26 18:22:20
@article{1d6d04e1-0c4b-48d2-be1b-1bc01f7d075f,
abstract = {{The receptor for advanced glycation end-products (RAGE) has been implicated in several pathophysiological processes relevant to Alzheimer's disease (AD), including transport and synaptotoxicity of AD-associated amyloid beta (A beta) peptides. A recent Chinese study (Li et al. in J Neural Transm 117:97-104, 2010) suggested an association between the 82S allele of the functional single nucleotide polymorphism (SNP) G82S (rs2070600) in the RAGE-encoding gene AGER and risk of AD. The present study aimed to investigate associations between AGER, AD diagnosis, cognitive scores and cerebrospinal fluid AD biomarkers in a European cohort of 316 neurochemically verified AD cases and 579 controls. Aside from G82S, three additional tag SNPs were analyzed to cover the common genetic variation in AGER. The 82S allele was associated with increased risk of AD (P (c) = 0.04, OR = 2.0, 95% CI 1.2-3.4). There was no genetic interaction between AGER 82S and APOE epsilon 4 in producing increased risk of AD (P = 0.4), and none of the AGER SNPs showed association with A beta(42), T-tau, P-tau(181) or mini-mental state examination scores. The data speak for a weak, but significant effect of AGER on risk of AD.}},
author = {{Daborg, Jonny and von Otter, Malin and Sjolander, Annica and Nilsson, Staffan and Minthon, Lennart and Gustafson, Deborah R. and Skoog, Ingmar and Blennow, Kaj and Zetterberg, Henrik}},
issn = {{0300-9564}},
keywords = {{Haplotype; SNP; product-specific receptor; Advanced glycosylation end; AGER; Alzheimer's disease; RAGE}},
language = {{eng}},
number = {{7}},
pages = {{861--867}},
publisher = {{Springer}},
series = {{Journal of Neural Transmission}},
title = {{Association of the RAGE G82S polymorphism with Alzheimer's disease}},
url = {{http://dx.doi.org/10.1007/s00702-010-0437-0}},
doi = {{10.1007/s00702-010-0437-0}},
volume = {{117}},
year = {{2010}},
}