Evidence map›Paper›PMID 42420262›Full record

ArticleTranslational psychiatry2026

The genetic relationship between ADHD and shortened telomeres points to neurodevelopmental mechanisms.

Maria E A Tavares, Eugenio H Grevet, Jaqueline B Schuch, Isabella F Temoteo, Eduardo S Vitola, Iago J Santos, Nicolas P Ciochetti, Victor F Oliveira, Cibele E Bandeira, Luis A Rohde and 3 more

Abstract read
In one paragraph

Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Maria E A TavaresADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Eugenio H GrevetADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Jaqueline B SchuchResponsabilidade Social, Hospital Moinhos de Vento, Porto Alegre, RS, Brazil.
Isabella F TemoteoLaboratory of Physiological Genomics of Mental Health (PhysioGen Lab), Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Eduardo S VitolaADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Iago J SantosLaboratory of Physiological Genomics of Mental Health (PhysioGen Lab), Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Nicolas P CiochettiADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.ORCID http://orcid.org/0000-0002-2922-1777
Victor F OliveiraLaboratory of Physiological Genomics of Mental Health (PhysioGen Lab), Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.ORCID http://orcid.org/0000-0003-3156-0249
Cibele E BandeiraADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.ORCID http://orcid.org/0000-0003-0681-1309
Luis A RohdeADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.ORCID http://orcid.org/0000-0002-4552-4188
Bruna S da SilvaADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.ORCID http://orcid.org/0000-0002-5916-4638
Diego L RovarisADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.ORCID http://orcid.org/0000-0002-8910-4927
Claiton H D BauADHD Outpatient Program & Developmental Psychiatry Program, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil. claiton.bau@ufrgs.br.ORCID http://orcid.org/0000-0001-5644-3845

Funding

Ministry of Science, Technology and Innovation | Conselho Nacional de Desenvolvimento Científico e Tecnológico (National Council for Scientific and Technological Development) 426905/2016-2Ministry of Science, Technology and Innovation | Conselho Nacional de Desenvolvimento Científico e Tecnológico (National Council for Scientific and Technological Development) 431472/2018-1Ministry of Science, Technology and Innovation | Conselho Nacional de Desenvolvimento Científico e Tecnológico (National Council for Scientific and Technological Development) 466722/2014-1
6 · The paper itself

Abstract

Attention-Deficit/Hyperactivity Disorder (ADHD) is often accompanied by other psychiatric and somatic conditions. Telomere shortening as an accelerated biological aging marker may underlie this aggregate burden. Telomere length (TL) has previously been associated with childhood inattention and hyperactivity, as well as other neuropsychiatric conditions. We hypothesize that TL and ADHD may share overlapping genetic influences, suggesting that some of the same genes could affect both cellular aging and ADHD traits. We investigated the pleiotropic and causal associations between these traits. Using the latest and largest publicly available genome-wide association study (GWAS) summary data for ADHD (38,691 cases and 186,843 controls) and TL (472,174 subjects), we tested causality, global and local genetic correlations, and joint genomic effects. Polygenic scores (PGS) were evaluated in an independent clinical sample of 665 ADHD cases and 995 controls, and TL was quantified via qPCR in a subsample of 370 subjects. The pleiotropy analysis showed global and local (a chromosome 17 locus) negative correlations. Shared genomic analysis showed loci enriched across several chromosomes, notably including the same chromosome 17 locus. This locus contains a diverse set of genes involved in many biological pathways impacting core cellular functions, tissue development, cell cycle, and apoptosis. Mendelian randomization indicated a unidirectional causal effect of ADHD on shorter TL across four methods. In our independent clinical sample, TL was shorter in individuals with ADHD. Lastly, higher PGS for longer TL was associated with reduced ADHD symptomatology. Our findings suggest that ADHD may contribute to TL, and genetic predisposition to shorter TL is associated with greater ADHD severity.

Indexed as

Attention Deficit Disorder with HyperactivityTelomere ShorteningGenetic Predisposition to DiseaseGenetic Risk ScoreGenome-Wide Association StudyHumansMultifactorial Inheritance

Identifiers

PMID42420262
PMCPMC13631302

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.