ArticleBMC geriatrics2022
An antisense Alu transposon insertion/deletion polymorphism of ALDH1A1 may functionally associate with Parkinson's disease.
Article in BMC geriatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 5 citations in OpenAlex.
- Multiple roles of ALDH1 in health and disease.Frontiers in physiology · 2025Review
- DOPAL initiates αSynuclein-dependent impaired proteostasis and degeneration of neuronal projections in Parkinson's disease.NPJ Parkinson's disease · 2023Article
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Authors and funding
9 authors at 3 institutions in 1 country.
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Abstract
backgroundAldehyde dehydrogenase 1 (encoded by ALDH1A1) has been shown to protect against Parkinson's disease (PD) by reducing toxic metabolites of dopamine. We herein revealed an antisense Alu element insertion/deletion polymorphism in intron 4 of ALDH1A1, and hypothesized that it might play a role in PD.
methodsA Han Chinese cohort comprising 488 PD patients and 515 controls was recruited to validate the Alu insertion/deletion polymorphism following a previous study of tag-single nucleotide polymorphisms, where rs7043217 was shown to be significantly associated with PD. Functional analyses of the Alu element insertion were performed.
resultsThe Alu element of ALDH1A1 was identified to be a variant of Yb8 subfamily and termed as Yb8c4. The antisense Yb8c4 insertion/deletion polymorphism (named asYb8c4
conclusionsOur results consolidate an involvement of ALDH1 in PD pathogenesis. The asYb8c4 polymorphism may be a functional output of its linkage disequilibrium-linked single nucleotide polymorphisms.
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