ArticleJournal of neural transmission (Vienna, Austria : 1996)2008
Two polymorphisms of presenilin-2 gene (PSEN2) 5' regulatory region are not associated with Alzheimer's disease (AD) in the Polish population.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Pharmacogenetic Study on the Effect of Rivastigmine on PS2 and APOE Genes in Iranian Alzheimer Patients.Dementia and geriatric cognitive disorders extra · 2011Article
- Current status on Alzheimer disease molecular genetics: from past, to present, to future.Human molecular genetics · 2010Review
- Genetic Association between Presenilin 2 Polymorphisms and Alzheimer's Disease and Dementia of Lewy Body Type in a Japanese Population.Dementia and geriatric cognitive disorders extraArticle
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Authors and funding
10 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Presenilin 2 gene (PSEN2) is one of the causative genes for familial Alzheimer's disease. A delA polymorphism located in PSEN2 promoter was proposed to be a risk factor for early-onset AD. We examined association between AD and PSEN2 polymorphisms located in two 5'UTR regions in group of 217 late-onset AD patients, 109 mild cognitive impairment patients, and 225 non-demented control subjects. No significant differences for genotype and allele distributions of a delA and a novel insAC polymorphisms in the studied groups as compared to controls were observed. Univariate and multivariate risk estimation shows that neither delA, insAC alleles nor the genotypes are risk factors for AD. No significant interaction between the APOE4 and PSEN2 polymorphisms was found. A bioinformatic analysis showed that delA polymorphism influences binding sites of transcription factors involved in the cellular processes related to AD. The rare variants identified in exon 3 of the PSEN2 could have a potential influence on PSEN2 transcript splicing.
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