AI Article Synopsis
- The study evaluated empathy in 28 adults with autism spectrum disorder (ASD) and 24 matched non-ASD controls, revealing that ASD participants demonstrated significantly lower empathy measures, particularly in perspective taking and cognitive empathy.
- Within the ASD group, higher Autism-Spectrum Quotient (AQ) scores correlated with better perspective taking and cognitive empathy, indicating specific links between autistic traits and empathy abilities.
- Additionally, the ASD group showed higher neuroticism and lower extraversion than controls, with perspective taking and extraversion identified as strong predictors of autistic traits.
Article Abstract
Reported empathy deficits in autism spectrum disorder (ASD) could be attributable to other ASD-related features. We evaluated 28 ASD adults with no intellectual disability and 24 age-matched non-ASD control subjects using the Autism-Spectrum Quotient (AQ), Questionnaire of Cognitive and Affective Empathy (QCAE), Interpersonal Reactivity Index (IRI), and NEO Personality Inventory-Revised (NEO). Compared to the controls, ASD participants showed lower scores for perspective taking, online simulation, cognitive empathy, and peripheral responsivity on the QCAE, and lower scores for perspective taking and empathic concern on the IRI. Within the ASD group, the AQ scores showed significant relationships with perspective taking, online simulation and cognitive empathy on the QCAE, and perspective taking on the IRI. The ASD group also showed higher scores for neuroticism and lower scores for extraversion on the NEO compared to the controls. However, there were no relationships between AQ scores and NEO factors within the ASD group. Multiple regression analysis with stepwise linear regression demonstrated that perspective taking score on the QCAE and extraversion score on the NEO were good predictor variables to autistic traits on the AQ. These findings help us to understand empathy and personality traits in ASD adults with no intellectual disability.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8873508 | PMC |
| http://dx.doi.org/10.1038/s41598-022-07101-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Rightward brain structural asymmetry in young children with autism.
Mol Psychiatry
January 2025
Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China.
To understand the neural mechanism of autism spectrum disorder (ASD) and developmental delay/intellectual disability (DD/ID) that can be associated with ASD, it is important to investigate individuals at an early stage with brain, behavioural and also genetic measures, but such research is still lacking. Here, using the cross-sectional sMRI data of 1030 children under 8 years old, we employed developmental normative models to investigate the atypical development of gray matter volume (GMV) asymmetry in individuals with ASD without DD/ID, ASD with DD/ID and individuals with only DD/ID, and their associations with behavioral and clinical measures and transcription profiles. By extracting the individual deviations of patients from the typical controls with normative models, we found a commonly abnormal pattern of GMV asymmetry across all ASD children: more rightward laterality in the inferior parietal lobe and precentral gyrus, and higher individual variability in the temporal pole.
View Article and Find Full Text PDFThe microcephaly-associated transcriptional regulator AUTS2 cooperates with Polycomb complex PRC2 to produce upper-layer neurons in mice.
EMBO J
January 2025
Department of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, 187-8502, Japan.
AUTS2 syndrome is characterized by intellectual disability and microcephaly, and is often associated with autism spectrum disorder, but the underlying mechanisms, particularly concerning microcephaly, remain incompletely understood. Here, we analyze mice mutated for the transcriptional regulator AUTS2, which recapitulate microcephaly. Their brains exhibit reduced division of intermediate progenitor cells (IPCs), leading to fewer neurons and decreased thickness in the upper-layer cortex.
View Article and Find Full Text PDFA randomised controlled trial of eye movement desensitisation and re-processing (EMDR) in forensic services and in prison.
Med Sci Law
January 2025
Department of Psychological Medicine, University of Otago, Wellington, New Zealand.
Cenobamate as add-on treatment for SCN8A developmental and epileptic encephalopathy.
Epilepsia
January 2025
Department of Epilepsy Genetics and Personalized Medicine, Danish Epilepsy Center, Dianalund, Denmark.
Objectives: Developmental and epileptic encephalopathies (DEEs) caused by pathogenic variants in SCN8A are associated with difficult-to-treat and early-onset seizures, developmental delay/intellectual disability, impaired quality of life, and increased risk of early mortality. High doses of sodium channel blockers are typically used to treat SCN8A-DEE caused by gain-of-function (GoF) variants. However, seizures are often drug resistant, and only a few patients achieve seizure freedom.
View Article and Find Full Text PDFThe integral role of in brain function: from neurogenesis to synaptic plasticity and social behavior.
Acta Neurobiol Exp (Wars)
January 2025
Laboratory of Animal Models, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene is a critical tumor suppressor that plays an essential role in the development and functionality of the central nervous system. Located on chromosome 10 in humans and chromosome 19 in mice, PTEN encodes a protein that regulates cellular processes such as division, proliferation, growth, and survival by antagonizing the PI3K‑Akt‑mTOR signaling pathway. In neurons, PTEN dephosphorylates phosphatidylinositol‑3,4,5‑trisphosphate (PIP3) to PIP2, thereby modulating key signaling cascades involved in neurogenesis, neuronal migration, and synaptic plasticity.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!