{
  "abstract": "Background: Autism is a lifelong neurodevelopmental condition, but the biological processes shaping aging are poorly understood. DNA methylation-based measures index physiological decline and mortality risk independently of chronological age. We tested whether biological aging differs in autistic adults, whether differences are system-specific, and which factors predict within-autism variation. Methods: Saliva DNA methylation (Illumina EPIC) was assayed in 37 autistic adults (31 male, 6 female; mean age 29.8 years), followed from early childhood, spanning a broad ability range including intellectual disability, and 188 non-autistic adults from four public datasets, processed jointly. Fifteen measures were calculated: four global (Horvath, GrimAge, DunedinPACE, SystemsAge) and 11 system-specific SystemsAge subscores. Models adjusted for age, sex, and epithelial-cell proportion. Results: Global aging measures did not differ between groups (all q > .34). However, autistic adults had higher Brain ({beta} = 0.81), Blood ({beta} = 0.65), and Liver SystemsAge ({beta} = 0.58; all q < .01), with Brain and Blood robust across sensitivity analyses. Within autism, aging measures were unrelated to symptom severity, IQ, co-occurring diagnoses, or medication use. Instead, elevations were associated with psychosocial circumstances, including a lack of structured daytime activity, greater loneliness, and lower quality of life. Conclusions: Differences in aging biology in autism appeared system-specific rather than global, with no evidence of generalized epigenetic age acceleration. This vulnerability appeared more closely tied to psychosocial factors than core clinical features. System-specific DNAm measures may therefore provide a more sensitive framework for identifying biological heterogeneity and potentially modifiable contributors to healthy aging in autistic adulthood.",
  "abstract_shown": true,
  "affiliations": [
    "UCLA"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "A. Dickinson"
    },
    {
      "name": "C. R. Lewis"
    },
    {
      "name": "D. H. Geschwind"
    },
    {
      "name": "J. E. Carroll"
    },
    {
      "name": "C. Lord"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/8tjc6rrst5y9a.bib",
  "cited_by": 1,
  "doi": "10.64898/2026.09.12.751174",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.12.751174v1.full",
  "id": "8tjc6rrst5y9a",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.09.12.751174v1",
  "language": null,
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "genomics"
    ],
    [
      "openalex",
      "2805|Autism Spectrum Disorder Research"
    ]
  ],
  "openalex": "W7213609626",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.12.751174v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-12",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/8tjc6rrst5y9a.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:23:10Z",
      "native_id": "10.64898/2026.09.12.751174",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.12.751174v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:genomics",
      "subfield": "genetics-genomics"
    }
  ],
  "title": "System-Specific Epigenetic Aging Signatures in Autistic Adults",
  "title_text": "System-Specific Epigenetic Aging Signatures in Autistic Adults",
  "type": "preprint",
  "updated_at": "2026-10-30T12:23:10Z",
  "url": "https://research.draconitic.com/paper/8tjc6rrst5y9a",
  "venue": "bioRxiv",
  "versions": []
}