Evidence map›Paper›PMID 41826324›Full record

ArticleNature communications2026

Shared genetic and neuroimmune architecture links type 1 diabetes with neurocognitive traits.

Priscilla Saarah, Zehra A Syeda, Ziang Xu, Yikai Dong, Habei Jiang, Michelle Shanguhyia, Sourav Roy, Biqing Zhu, Le Zhang, Andrew T Dewan and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Priscilla Saarah *Yale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Zehra A Syeda *Yale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Ziang XuYale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0009-0009-0877-5488
Yikai DongYale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Habei JiangYale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-8068-4187
Michelle ShanguhyiaYale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Sourav RoyYale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Biqing ZhuProgram of Computational Biology and Bioinformatics, Yale University, New Haven, CT, 06510, USA.ORCID http://orcid.org/0000-0002-7428-6297
Le ZhangDepartment of Neurology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-4860-831X
Andrew T DewanDepartment of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-7679-8704
Samira AsgariInstitute for Genomic Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.ORCID http://orcid.org/0000-0002-2347-8985
David A AlagpulinsaYale Center for Molecular & Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA. david.alagpulinsa@yale.edu.ORCID http://orcid.org/0000-0002-8737-4907

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes, particularly with childhood onset, is associated with altered neurocognitive traits, yet the underlying biological mechanisms are unclear. Here, we integrate genome-wide association results with single-cell epigenomic profiles and show that type 1 diabetes heritability is enriched in accessible chromatin of human brain-resident cells, most notably microglia, across neurodevelopment into adulthood. Bonferroni-corrected cross-trait genetic correlation analyses reveal negative correlations of type 1 diabetes with intelligence, executive function, and bipolar disorder, and a positive correlation with myasthenia gravis. Conjunctional false discovery rate analysis identifies pleiotropic loci jointly influencing type 1 diabetes and neurocognitive traits, including the 17q21.31 neurogenomic hub. Mendelian randomization further demonstrates protective effects of educational attainment, intelligence, Alzheimer's disease, and bipolar disorder on type 1 diabetes risk, whereas liability to multiple sclerosis and myasthenia gravis increases type 1 diabetes risk. In the reverse direction, liability to type 1 diabetes is associated with increased risk of myasthenia gravis. We identify several gene expression regulatory variants in brain and immune cells that jointly influence type 1 diabetes and neurocognitive traits, some of which show concordant differential expression in disease-affected versus control tissue. Together, these findings highlight pleiotropic genetic and neuroimmune mechanisms that link type 1 diabetes with cognition and neuropsychiatric disease risk.

Indexed as

Diabetes Mellitus, Type 1Alzheimer DiseaseBipolar DisorderBrainFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIntelligenceMaleMicrogliaMultiple SclerosisMyasthenia GravisNeuroimmunomodulationPolymorphism, Single Nucleotide

Identifiers

PMID41826324
PMCPMC13139607

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.