SynthesisThe Journal of clinical endocrinology and metabolism2018
A Common DIO2 Polymorphism and Alzheimer Disease Dementia in African and European Americans.
Synthesis in The Journal of clinical endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 58 citations in OpenAlex.
- The type 2 deiodinase Thr92Ala polymorphism and cognitive aging: current evidence and biological context.Therapeutic advances in endocrinology and metabolism · 2026Review
- Reply to 'Why the science on TNature reviews. Endocrinology · 2025Article
- Gene-Diet Interaction Analysis in UK Biobank Identified Genetic Loci That Modify the Association Between Fish Oil Supplementation and the Incidence of Dementia.Current developments in nutrition · 2025Article
- Gene polymorphisms and thyroid hormone signaling: implication for the treatment of hypothyroidism.Endocrine · 2024Review
- Genetics of Alzheimer's Disease in the African American Population.Journal of clinical medicine · 2023Review
- The Physiological Functions and Polymorphisms of Type II Deiodinase.Endocrinology and metabolism (Seoul, Korea) · 2023Review
- Impaired Sensitivity to Thyroid Hormones is Associated with Mild Cognitive Impairment in Euthyroid Patients with Type 2 Diabetes.Clinical interventions in aging · 2023Article
- Age Worsens the Cognitive Phenotype in Mice Carrying the Thr92Ala-DIO2 Polymorphism.Metabolites · 2022Article
- Identification of polymorphic loci in the deiodinase 2 gene and their associations with head dimensions in geese.Animal bioscience · 2022Article
- Improvement of depression in a patient with hypothyroidism and deiodinase polymorphism with LT3 Therapy.Clinical case reports · 2022Article
- An Assessment ofGenes · 2022Article
- Cell type-specific potential pathogenic genes and functional pathways in Alzheimer's Disease.BMC neurology · 2021Article
- Assessment of children in the autistic spectrum disorder that carry the Thr92Ala-DIO2 polymorphism.Journal of endocrinological investigation · 2021Article
- Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.Endocrinology · 2021Review
- Genetic Risk Factors for Alzheimer's Disease in Racial/Ethnic Minority Populations in the U.S.: A Scoping Review.Frontiers in public health · 2021Article
- Individualized Therapy for Hypothyroidism: Is T4 Enough for Everyone?The Journal of clinical endocrinology and metabolism · 2020Review
- Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury.Frontiers in neuroscience · 2020Review
- The Year in Basic Thyroidology.Thyroid : official journal of the American Thyroid Association · 2020Article
- Thyroid Hormone and Alcoholic Fatty Liver: The Developmental Input.Alcoholism, clinical and experimental research · 2019Article
- Paradigms of Dynamic Control of Thyroid Hormone Signaling.Endocrine reviews · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Context: A common single nucleotide polymorphism in DIO2, Thr92AlaD2, has been associated with a transcriptome typically found in neurodegenerative diseases in postmortem human brain tissue. Objective: To determine whether Thr92AlaD2 is associated with incident Alzheimer disease (AD). Design: Population-based study; human brain tissue microarray. Setting: Community-based cohorts from Chicago and northeastern Illinois and religious clergymen from across the United States constituted the primary population. A representative sample of the U.S. population was used for secondary analyses. Participants: 3054 African Americans (AAs) and 9304 European Americans (EAs). Main Outcome Measure: Incident AD. Results: In the primary population, AAs with Thr92AlaD2 had 1.3 times [95% confidence interval (CI), 1.02 to 1.68; P = 0.048] greater odds of developing AD. AAs from a second population with Thr92AlaD2 showed a trend toward increased odds of dementia (odds ratio, 1.33; 95% CI, 0.99 to 1.78; P = 0.06) and 1.35 times greater odds of developing cognitive impairment not demented (CIND; 95% CI, 1.09 to 1.67; P = 0.006). Meta-analysis showed that AAs with Thr92AlaD2 had 1.3 times increased odds of developing AD/dementia (95% CI, 1.07 to 1.58; P = 0.008). In EAs, no association was found between Thr92AlaD2 and AD, dementia, or CIND. Microarray of AA brain tissue identified transcriptional patterns linked to AD pathogenesis. Conclusions: Thr92AlaD2 was associated with molecular markers known to underlie AD pathogenesis in AAs, translating to an observed phenotype of increased odds of developing AD/dementia in AAs in these populations. Thr92AlaD2 might represent one factor contributing to racial discrepancies in incident AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.