ArticleMolecular biology reports2014
The alternative splicing of the apolipoprotein E gene is unperturbed in the brains of Alzheimer's disease patients.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Identification of a specific APOE transcript and functional elements associated with Alzheimer's disease.Molecular neurodegeneration · 2024Article
- Alternative splicing in neurodegenerative disease and the promise of RNA therapies.Nature reviews. Neuroscience · 2023Review
- Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice.NPJ aging and mechanisms of disease · 2021Article
- Review
- Defining early changes in Alzheimer's disease from RNA sequencing of brain regions differentially affected by pathology.Scientific reports · 2021Article
- Epigenome-wide association study of Alzheimer's disease replicates 22 differentially methylated positions and 30 differentially methylated regions.Clinical epigenetics · 2020Article
- The relationship between the morphological subtypes of microglia and Alzheimer's disease neuropathology.Brain pathology (Zurich, Switzerland) · 2019Article
- Evidence supporting oxidative stress in a moderately affected area of the brain in Alzheimer's disease.Scientific reports · 2018Article
- Alternative splicing isoforms in health and disease.Pflugers Archiv : European journal of physiology · 2018Review
- Genetic variation affecting exon skipping contributes to brain structural atrophy in Alzheimer's disease.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science · 2018Article
- Article
- Alternative Splicing in Alzheimer's Disease.Journal of Parkinson's disease and Alzheimer's disease · 2015Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The prevalence of Alzheimer's disease (AD) is increasing rapidly worldwide due to an ageing population and a lack of disease modifying therapeutics. In monogenic forms of AD mutations lead to the accumulation of neurotoxic peptides called beta-amyloid. Beta-amyloid accumulation is also postulated to precipitate sporadic AD although the pathogenesis of this common form remains largely unknown. The two leading risk factors for sporadic AD are ageing and the possession of the APOE epsilon 4 allele. Changes in APOE expression that are independent of the epsilon genotype have also been described in the AD brain including a recent RNA-Seq analysis that showed upregulation of a rare alternative splice isoform (APOE-005). To replicate these RNA-Seq findings we used quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) to compare APOE-005 and total APOE expression in the superior temporal gyrus of 14 AD cases and 16 neurologically normal controls. In AD, this area shows prominent beta-amyloid deposition but few neurofibrillary tangles and only moderate neuronal loss. As poorer RNA quality among the AD cases was a likely confounder in this study, the analysis was repeated in a RIN-matched sub-cohort of 17 individuals. Contrary to the original RNA-Seq study, we found no difference in total APOE, APOE-005 or the common isoform, APOE-001, between AD cases and controls. Our findings are consistent with ApoE acting largely at the protein level to increase the risk for sporadic AD.
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Registered trials
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