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Development of the pupillary light reflex from 9 to 24 months: association with common autism spectrum disorder (ASD) genetic liability and 3‐year ASD diagnosis.

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Title: Development of the pupillary light reflex from 9 to 24 months: association with common autism spectrum disorder (ASD) genetic liability and 3‐year ASD diagnosis.
Authors: Fish, Laurel A., Nyström, Pär, Gliga, Teodora, Gui, Anna, Begum Ali, Jannath, Mason, Luke, Garg, Shruti, Green, Jonathan, Johnson, Mark H., Charman, Tony, Harrison, Rebecca, Meaburn, Emma, Falck‐Ytter, Terje, Jones, Emily J. H.
Source: Journal of Child Psychology & Psychiatry. Nov2021, Vol. 62 Issue 11, p1308-1319. 12p. 1 Diagram, 2 Charts, 3 Graphs.
Subjects: Diagnosis of autism, Genetics of autism, Personality, Infant development, Confidence intervals, Affect (Psychology), Reflexes, Neural development, Genotypes, Phenotypes
Abstract: Background: Although autism spectrum disorder (ASD) is heritable, the mechanisms through which genes contribute to symptom emergence remain unclear. Investigating candidate intermediate phenotypes such as the pupillary light reflex (PLR) prospectively from early in development could bridge genotype and behavioural phenotype. Methods: Using eye tracking, we longitudinally measured the PLR at 9, 14 and 24 months in a sample of infants (N = 264) enriched for a family history of ASD; 27 infants received an ASD diagnosis at 3 years. We examined the 9‐ to 24‐month developmental trajectories of PLR constriction latency (onset; ms) and amplitude (%) and explored their relation to categorical 3‐year ASD outcome, polygenic liability for ASD and dimensional 3‐year social affect (SA) and repetitive/restrictive behaviour (RRB) traits. Polygenic scores for ASD (PGSASD) were calculated for 190 infants. Results: While infants showed a decrease in latency between 9 and 14 months, higher PGSASD was associated with a smaller decrease in latency in the first year (β = −.16, 95% CI = −0.31, −0.002); infants with later ASD showed a significantly steeper decrease in latency (a putative 'catch‐up') between 14 and 24 months relative to those with other outcomes (typical: β =.54, 95% CI = 0.08, 0.99; other: β =.53, 95% CI = 0.02, 1.04). Latency development did not associate with later dimensional variation in ASD‐related traits. In contrast, change in amplitude was not related to categorical ASD or genetics, but decreasing 9‐ to 14‐month amplitude was associated with higher SA (β =.08, 95% CI = 0.01, 0.14) and RRB (β =.05, 95% CI = 0.004, 0.11) traits. Conclusions: These findings corroborate PLR development as possible intermediate phenotypes being linked to both genetic liability and phenotypic outcomes. Future work should incorporate alternative measures (e.g. functionally informed structural and genetic measures) to test whether distinct neural mechanisms underpin PLR alterations. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Child Psychology & Psychiatry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Development of the pupillary light reflex from 9 to 24 months: association with common autism spectrum disorder (ASD) genetic liability and 3‐year ASD diagnosis.
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  Data: <searchLink fieldCode="AR" term="%22Fish%2C+Laurel+A%2E%22">Fish, Laurel A.</searchLink><br /><searchLink fieldCode="AR" term="%22Nyström%2C+Pär%22">Nyström, Pär</searchLink><br /><searchLink fieldCode="AR" term="%22Gliga%2C+Teodora%22">Gliga, Teodora</searchLink><br /><searchLink fieldCode="AR" term="%22Gui%2C+Anna%22">Gui, Anna</searchLink><br /><searchLink fieldCode="AR" term="%22Begum+Ali%2C+Jannath%22">Begum Ali, Jannath</searchLink><br /><searchLink fieldCode="AR" term="%22Mason%2C+Luke%22">Mason, Luke</searchLink><br /><searchLink fieldCode="AR" term="%22Garg%2C+Shruti%22">Garg, Shruti</searchLink><br /><searchLink fieldCode="AR" term="%22Green%2C+Jonathan%22">Green, Jonathan</searchLink><br /><searchLink fieldCode="AR" term="%22Johnson%2C+Mark+H%2E%22">Johnson, Mark H.</searchLink><br /><searchLink fieldCode="AR" term="%22Charman%2C+Tony%22">Charman, Tony</searchLink><br /><searchLink fieldCode="AR" term="%22Harrison%2C+Rebecca%22">Harrison, Rebecca</searchLink><br /><searchLink fieldCode="AR" term="%22Meaburn%2C+Emma%22">Meaburn, Emma</searchLink><br /><searchLink fieldCode="AR" term="%22Falck‐Ytter%2C+Terje%22">Falck‐Ytter, Terje</searchLink><br /><searchLink fieldCode="AR" term="%22Jones%2C+Emily+J%2E+H%2E%22">Jones, Emily J. H.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Child+Psychology+%26+Psychiatry%22">Journal of Child Psychology & Psychiatry</searchLink>. Nov2021, Vol. 62 Issue 11, p1308-1319. 12p. 1 Diagram, 2 Charts, 3 Graphs.
– Name: Subject
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  Data: <searchLink fieldCode="DE" term="%22Diagnosis+of+autism%22">Diagnosis of autism</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics+of+autism%22">Genetics of autism</searchLink><br /><searchLink fieldCode="DE" term="%22Personality%22">Personality</searchLink><br /><searchLink fieldCode="DE" term="%22Infant+development%22">Infant development</searchLink><br /><searchLink fieldCode="DE" term="%22Confidence+intervals%22">Confidence intervals</searchLink><br /><searchLink fieldCode="DE" term="%22Affect+%28Psychology%29%22">Affect (Psychology)</searchLink><br /><searchLink fieldCode="DE" term="%22Reflexes%22">Reflexes</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+development%22">Neural development</searchLink><br /><searchLink fieldCode="DE" term="%22Genotypes%22">Genotypes</searchLink><br /><searchLink fieldCode="DE" term="%22Phenotypes%22">Phenotypes</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background: Although autism spectrum disorder (ASD) is heritable, the mechanisms through which genes contribute to symptom emergence remain unclear. Investigating candidate intermediate phenotypes such as the pupillary light reflex (PLR) prospectively from early in development could bridge genotype and behavioural phenotype. Methods: Using eye tracking, we longitudinally measured the PLR at 9, 14 and 24 months in a sample of infants (N = 264) enriched for a family history of ASD; 27 infants received an ASD diagnosis at 3 years. We examined the 9‐ to 24‐month developmental trajectories of PLR constriction latency (onset; ms) and amplitude (%) and explored their relation to categorical 3‐year ASD outcome, polygenic liability for ASD and dimensional 3‐year social affect (SA) and repetitive/restrictive behaviour (RRB) traits. Polygenic scores for ASD (PGSASD) were calculated for 190 infants. Results: While infants showed a decrease in latency between 9 and 14 months, higher PGSASD was associated with a smaller decrease in latency in the first year (β = −.16, 95% CI = −0.31, −0.002); infants with later ASD showed a significantly steeper decrease in latency (a putative 'catch‐up') between 14 and 24 months relative to those with other outcomes (typical: β =.54, 95% CI = 0.08, 0.99; other: β =.53, 95% CI = 0.02, 1.04). Latency development did not associate with later dimensional variation in ASD‐related traits. In contrast, change in amplitude was not related to categorical ASD or genetics, but decreasing 9‐ to 14‐month amplitude was associated with higher SA (β =.08, 95% CI = 0.01, 0.14) and RRB (β =.05, 95% CI = 0.004, 0.11) traits. Conclusions: These findings corroborate PLR development as possible intermediate phenotypes being linked to both genetic liability and phenotypic outcomes. Future work should incorporate alternative measures (e.g. functionally informed structural and genetic measures) to test whether distinct neural mechanisms underpin PLR alterations. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Journal of Child Psychology & Psychiatry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/jcpp.13518
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      – Code: eng
        Text: English
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        PageCount: 12
        StartPage: 1308
    Subjects:
      – SubjectFull: Diagnosis of autism
        Type: general
      – SubjectFull: Genetics of autism
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      – SubjectFull: Personality
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      – SubjectFull: Infant development
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      – SubjectFull: Confidence intervals
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      – SubjectFull: Affect (Psychology)
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      – SubjectFull: Reflexes
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      – SubjectFull: Neural development
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      – SubjectFull: Genotypes
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      – TitleFull: Development of the pupillary light reflex from 9 to 24 months: association with common autism spectrum disorder (ASD) genetic liability and 3‐year ASD diagnosis.
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              Text: Nov2021
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