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Cultural influences on face scanning are consistent across infancy and adulthood.

ABSTRACT: The emergence of cultural differences in face scanning is thought to be shaped by social experience. However, previous studies mainly investigated eye movements of adults and little is known about early development. The current study recorded eye movements of British and Japanese infants (aged 10 and 16 months) and adults, who were presented with static and dynamic faces on screen. Cultural differences were observed across all age groups, with British participants exhibiting more mouth scanning, and Japanese individuals showing increased central face (nose) scanning for dynamic stimuli. Age-related influences independent of culture were also revealed, with a shift from eye to mouth scanning between 10 and 16 months, while adults distributed their gaze more flexibly. Against our prediction, no age-related increases in cultural differences were observed, suggesting the possibility that cultural differences are largely manifest by 10 months of age. Overall, the findings suggest that individuals adopt visual strategies in line with their cultural background from early in infancy, pointing to the development of a highly adaptive face processing system that is shaped by early sociocultural experience.

SUBMITTER: Haensel JX

PROVIDER: S-EPMC7768814 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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Cultural influences on face scanning are consistent across infancy and adulthood.

Haensel Jennifer X JX Ishikawa Mitsuhiko M Itakura Shoji S Smith Tim J TJ Senju Atsushi A

Infant behavior & development 20201112

The emergence of cultural differences in face scanning is thought to be shaped by social experience. However, previous studies mainly investigated eye movements of adults and little is known about early development. The current study recorded eye movements of British and Japanese infants (aged 10 and 16 months) and adults, who were presented with static and dynamic faces on screen. Cultural differences were observed across all age groups, with British participants exhibiting more mouth scanning, ...[more]

PMID: 33190091

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Project description:Dopamine transporter deficiency syndrome due to SLC6A3 mutations is the first inherited dopamine 'transportopathy' to be described, with a classical presentation of early infantile-onset progressive parkinsonism dystonia. In this study we have identified a new cohort of patients with dopamine transporter deficiency syndrome, including, most significantly, atypical presentation later in childhood with a milder disease course. We report the detailed clinical features, molecular genetic findings and in vitro functional investigations undertaken for adult and paediatric cases. Patients presenting with parkinsonism dystonia or a neurotransmitter profile characteristic of dopamine transporter deficiency syndrome were recruited for study. SLC6A3 mutational analysis was undertaken in all patients. The functional consequences of missense variants on the dopamine transporter were evaluated by determining the effect of mutant dopamine transporter on dopamine uptake, protein expression and amphetamine-mediated dopamine efflux using an in vitro cellular heterologous expression system. We identified eight new patients from five unrelated families with dopamine transporter deficiency syndrome. The median age at diagnosis was 13 years (range 1.5-34 years). Most significantly, the case series included three adolescent males with atypical dopamine transporter deficiency syndrome of juvenile onset (outside infancy) and progressive parkinsonism dystonia. The other five patients in the cohort presented with classical infantile-onset parkinsonism dystonia, with one surviving into adulthood (currently aged 34 years) and labelled as having 'juvenile parkinsonism'. All eight patients harboured homozygous or compound heterozygous mutations in SLC6A3, of which the majority are previously unreported variants. In vitro studies of mutant dopamine transporter demonstrated multifaceted loss of dopamine transporter function. Impaired dopamine uptake was universally present, and more severely impacted in dopamine transporter mutants causing infantile-onset rather than juvenile-onset disease. Dopamine transporter mutants also showed diminished dopamine binding affinity, reduced cell surface transporter, loss of post-translational dopamine transporter glycosylation and failure of amphetamine-mediated dopamine efflux. Our data series expands the clinical phenotypic continuum of dopamine transporter deficiency syndrome and indicates that there is a phenotypic spectrum from infancy (early onset, rapidly progressive disease) to childhood/adolescence and adulthood (later onset, slower disease progression). Genotype-phenotype analysis in this cohort suggests that higher residual dopamine transporter activity is likely to contribute to postponing disease presentation in these later-onset adult cases. Dopamine transporter deficiency syndrome remains under-recognized and our data highlights that dopamine transporter deficiency syndrome should be considered as a differential diagnosis for both infantile- and juvenile-onset movement disorders, including cerebral palsy and juvenile parkinsonism.

Dataset Information

Cultural influences on face scanning are consistent across infancy and adulthood.

Publications

Cultural influences on face scanning are consistent across infancy and adulthood.

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