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Potential genetic markers of sporadic Alzheimerʼs dementia
Abstract
Polymorphisms within the genes encoding apolipoprotein E (ApoE), apolipoprotein CI (ApoCI), alpha1-antichymotrypsin (ACT), the low-density lipoprotein (LDL) receptor and lipoprotein lipase were investigated in patients suffering from Alzheimer's dementia and non-demented psychiatric patients as control subjects. The ApoE allele 4, well known as a risk factor in Alzheimer's disease, and the ApoCI allele A2, which is closely linked to the ApoE allele 4, were found elevated in the index group. Concerning the polymorphism within exon 8 of the LDL receptor (alanin/threonin), there was also a predominance of the allele carrying threonin in the index group, which barely missed significance. Distribution of the polymorphisms of ACT and lipoprotein lipase were similar in both groups investigated. We conclude that, apart from the ApoE allele 4, other genetically regulated factors like ApoCI and the LDL receptor modulate the individual risk for Alzheimer's disease.
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In the citing paper
“Several studies reported that a few single-nucleotide polymorphisms (SNPs) in LDLR gene are associated with the risk of developing AD in case-control studies (Cheng et al., 2005; Gopalraj et al., 2005; Retz et al., 2001).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Retz et al., 2001
In the citing paper
“Several groups identified a potential contribution of LDLR to AD and investigated potential links, for example by crossing AD transgenic mice with the LDLR−/− mouse model of hypercholesterolemia to investigate the effects of LDLR deficiency [30]–[40]. Some apparently opposing results were obtained.”
From LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer's Disease (2010) · cites this paper as [39]
In the citing paper
“Furthermore, the risk associated with a certain LDLR polymorphism differs dramatically depending on the patients’ APOE genotype, implying that a functional interaction between apoE and LDLR determines AD risk (Cheng et al., 2004, Retz et al., 2001).”
From Apolipoprotein E–low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner (2014) · cites this paper as Retz et al., 2001
In the citing paper
“Furthermore, the risk associated with a certain LDLR polymorphism differs dramatically depending on the patients’ APOE genotype, implying that a functional interaction between apoE and LDLR determines AD risk (Cheng et al., 2004, Retz et al., 2001).”
From Apolipoprotein E–low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner (2014) · cites this paper as Retz et al., 2001
In the citing paper
“Furthermore, studies by Retz et al. (2001) and Cheng et al. (2005) demonstrated an increase in AD risk when polymorphisms in LDLR exon 8 and exon 13 were present in conjunction with an ε4 allele.”
From Apolipoprotein E–low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner (2014) · cites this paper as Retz et al. (2001)
In the citing paper
“Still, several important genetic studies have implicated the LDLR – and the apoE-LDLR interaction – as a disease modifying mechanism in AD.”
From Apolipoprotein E–low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner (2014) · cites this paper as Retz et al. (2001)
In the citing paper
“Together with epidemiological studies (Cheng et al., 2005, Gopalraj et al., 2005, Retz et al., 2001, Vermissen et al., 2011, Zou et al., 2008), these data point toward a functional interaction between apoE and LDLR as a potential mechanism to explain the apoE isoform-dependent disease risks associated with both CVD and AD.”
From Apolipoprotein E–low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner (2014) · cites this paper as Retz et al., 2001
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Metadata
- Authors
- Retz, W., Thome, J., Durany, N., Harsányi, A., Retz-Junginger, P., Kornhuber, J., Riederer, P., & Rösler, M.
- Affiliations
- Saarland University (DE)
- Central Institute of Mental Health (DE)
- University of Würzburg (DE)
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- Corresponding author
- Retz, W.
- Venue
- Psychiatric Genetics
- Published
- 2001-09
- Volume
- 11
- Issue
- 3
- Pages
- 115-122
- ISSN
- 0955-8829 (ISSN-L)
- OpenAlex
- W2004082555
- Cited by
- 48
- References
- 2
- Citations by year
- 2019: 3 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 4 · 2012: 4
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychiatric Genetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- sporadic Alzheimer's disease, Alzheimer's dementia, genetic polymorphism, apolipoprotein E, APOC1, alpha-1-antichymotrypsin, LDL receptor, lipoprotein lipase, genetic risk factors
- MeSH terms
- Aged, alpha 1-Antichymotrypsin, Alzheimer Disease, Apolipoproteins C, Apolipoproteins E, Exons, Female, Genetic Markers, Genotype, Humans, Introns, Lipoprotein Lipase, Male, Receptors, LDL, Reference Values, DNA Primers, Apolipoprotein C-I
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