Advanced paternal age effects in neurodevelopmental disorders—review of potential underlying mechanisms
Open accessAbstract
Multiple epidemiological studies suggest a relationship between advanced paternal age (APA) at conception and adverse neurodevelopmental outcomes in offspring, particularly with regard to increased risk for autism and schizophrenia. Conclusive evidence about how age-related changes in paternal gametes, or age-independent behavioral traits affect neural development is still lacking. Recent evidence suggests that the origins of APA effects are likely to be multidimensional, involving both inherited predisposition and de novo events. Here we provide a review of the epidemiological and molecular findings to date. Focusing on the latter, we present the evidence for genetic and epigenetic mechanisms underpinning the association between late fatherhood and disorder in offspring. We also discuss the limitations of the APA literature. We propose that different hypotheses relating to the origins of the APA effects are not mutually exclusive. Instead, multiple mechanisms likely contribute, reflecting the etiological complexity of neurodevelopmental disorders.
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Advanced maternal and paternal age are associated with increased risk of ASD in offspring.
“There is accumulating evidence of the relevance of older parental age in the etiology of psychiatric and neurodevelopmental conditions [43] including bipolar disorder, schizophrenia, substance use disorders, ADHD, and ASD [44].”
From The contribution of environmental exposure to the etiology of autism spectrum disorder (2019) · cites this paper as [44]
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- Authors
- Janecka, M., Mill, J., Basson, M. A., Goriely, A., Spiers, H., Reichenberg, A., Schalkwyk, L., & Fernandes, C.
- Affiliations
- King's College London (GB)
- University of Oxford (GB)
- University of Exeter (GB)
- Icahn School of Medicine at Mount Sinai (US)
- University of Essex (GB)
- Corresponding author
- Janecka, M
- Venue
- Translational Psychiatry
- Published
- 2017-01-31
- Volume
- 7
- Issue
- 1
- Pages
- e1019-e1019
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC5299396
- OpenAlex
- W2584834954
- Cited by
- 140
- References
- 147
- Citations by year
- 2026: 11 · 2025: 17 · 2024: 11 · 2023: 8 · 2022: 16 · 2021: 17 · 2020: 21 · 2019: 25 · 2018: 9 · 2017: 5
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Translational Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Open Access at Essex (University of Essex) (acceptedVersion)
- Research Portal (King's College London) (submittedVersion, cc-by)
- Royal Devon and Exeter Research Repository (Royal Devon and Exeter) (submittedVersion)
- Funders
- Simons Foundation
- Wellcome Trust (102731/Z/13/Z, 102731)
- Simons Foundation Autism Research Initiative (#344763)
- Medical Research Council (MR/K022377/1, MR/J500380/1, MR/N026063/1)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- advanced paternal age, neurodevelopmental disorders, autism spectrum disorder, schizophrenia, de novo mutations, epigenetics, genetic susceptibility, offspring neurodevelopment, paternal age effect
- MeSH terms
- Age Factors, Autistic Disorder, Humans, Paternal Age, Risk Factors, Schizophrenia, Epigenesis, Genetic, Neurodevelopmental Disorders
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