ArticleCurrent research in translational medicine2022
Fetal hemoglobin modulates neurocognitive performance in sickle cell anemia
Article in Current research in translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Genetic Variation and Sickle Cell Disease Severity: A Systematic Review and Meta-Analysis.JAMA network open · 2023Pooled it
- Early Intervention as a Way of Reducing Neurocognitive Delay in Pediatric Sickle Cell Patients.Cureus · 2025Review
- Clinical manifestations of sickle cell disease in Africa and its association with foetal haemoglobin parameters.Communications medicine · 2025Article
- Transcriptional regulators of fetal hemoglobin.Hematology, transfusion and cell therapy · 2024Review
- Empirically derived profiles of neurocognitive functioning in youth and young adults with sickle cell disease.Journal of pediatric psychology · 2024Article
- Catechol-O-methyltransferase gene (COMT) is associated with neurocognitive functioning in patients with sickle cell disease.Current research in translational medicine · 2024Article
- Intensive hydroxyurea dosing in very young children with sickle cell anemia.Blood advances · 2023Article
- Internalizing Symptoms in Adolescents With Sickle Cell Disease.Journal of pediatric psychology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
purpose of the studyFetal hemoglobin (HbF) is a modifier of the clinical and hematologic phenotype of sickle cell anemia (SCA). Three quantitative trait loci (QTL) modulate HbF expression. The neurocognitive effects of variants in these QTL have yet to be explored. We evaluated the relation between 11 SNPs in the three HbF QTL: BCL11A, MYB, the HBB gene cluster, and full-scale intelligence (IQ) in SCA. PATIENTS AND
methodsThe prospective longitudinal cohort study, Sickle Cell Clinical Research and Intervention Program, was used as a discovery cohort (n = 166). The genotypes for 11 SNPs were extracted through whole genome sequencing and were analyzed using an additive model. A polygenic score for HbF (PGS
resultsHbF was positively associated with IQ (minimum raw p = 0·0018) at pFDR<0·05. HbF mediated the relationship between two BCL11A SNPs, rs1427407 and rs7606173, HBS1L-MYB: rs9494142, and PGS
conclusionAs the major modulator of the severity of SCA, HbF also influences neurocognition, which is done through mediation of its QTL. These findings have implications for early identification of neurocognitive risk and targeted intervention.
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Registered trials
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