ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2025
The Role of SLC39A8.p.(Ala391Thr) in Schizophrenia Symptom Severity and Cognitive Ability: Cross-Sectional Studies of Schizophrenia and the General UK Population.
Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- Analysis of rare coding variants in schizophrenia-associated genes and generalised cognition in the UK Biobank.Molecular psychiatry · 2026Article
- The relationship between schizophrenia polygenic scores, blood-based proteins and psychosis diagnosis in the UK Biobank.Schizophrenia (Heidelberg, Germany) · 2026Article
- Neurotoxic mechanisms of cadmium in neurodegenerative diseases.Frontiers in cell and developmental biology · 2026Review
- Genetics to Improve Outcomes in Schizophrenia (GENios): A within-case molecular genetic study protocol.PloS one · 2026Article
- Current situation and future prospect of biobank.CytoJournal · 2026Review
- Effects of Long-Term Institutionalization on the Linguistic-Communicative Performance of Patients with Schizophrenia.Healthcare (Basel, Switzerland) · 2025Article
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Abstract
The missense SNP NC_000004.12:g.102267552C>T (also known as SLC39A8.p.(Ala391Thr), rs13107325) in SLC39A8 encodes a zinc transporter. This SNP has been linked to schizophrenia and is the likely causal variant for one of the genome-wide association loci associated with the disorder. Using regression analyses, we tested whether the schizophrenia-risk allele at p.(Ala391Thr) was associated with schizophrenia-related phenotypes, including positive, negative, and disorganized symptoms, cognitive ability, educational attainment, and age of psychosis onset, within three schizophrenia cohorts (combined N = 1232) and, with equivalent phenotypes, in a sample of population controls (UK Biobank, N = 355,069). We also used the population controls to test for associations with rare protein-truncating and deleterious missense variants within SLC39A8. Within the schizophrenia cohorts, after correction for multiple testing, p.(Ala391Thr) was not significantly associated with any schizophrenia-related phenotypes. In the unaffected participants from the UK Biobank, the schizophrenia-risk allele at p.(Ala391Thr) was associated with significantly poorer cognitive ability and fluid intelligence, a lower probability of obtaining GCSEs or a degree-level qualification, and fewer years in education. There was no association between p.(Ala391Thr) and self-reported psychotic experiences in this cohort. Rare variants in SLC39A8 were nominally associated with poorer cognitive ability, but these associations did not survive correction for multiple testing. The schizophrenia-risk allele was associated with poorer cognitive ability, but not psychotic experiences, in a volunteer sample drawn from the general population. We found no evidence that p.(Ala391Thr) was associated with symptom severity in schizophrenia. To understand the impact of rare variants in SLC39A8 on cognitive impairment, larger independent samples are required.
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