Background: Life expectancy is on rise and the intriguing question is: When does cognitive decline occur among adults with intellectual disability, compared to adults with typical development? This cross-sectional study examined cognitive performance of crystallised/fluid intelligence, working and long-term memory of adults with intellectual disability of etiologies other than Down syndrome (IQ 50-68) and adults with typical development (IQ 85-114) in four age cohorts (30-39; 40-49; 50-59; 60-69).

Method: The WAIS III and the Rey-AVLT were administered to both groups.

Results: Four patterns of cognitive performance were found: (a) Vocabulary (crystallised intelligence), Spatial Span Forward and Retention yielded similar scores across all four age cohorts in participants with typical development and with intellectual disability. (b) Similarities, Raven and Digit Span Backward exhibit lower scores only in 50-59 or 60-69 compared to the 30-39 age cohort in both groups, (c) Digit Span Forward, Spatial Span Backward and Total Leaning (LTM) yielded lower scores in the 50-59 or 60-69 age cohorts in the typical group, but similar scores in participants with intellectual disability along the age cohorts, (d) Block Design (fluid intelligence) yielded a lower score in the 50-59 cohort versus lower scores only at ages 60-69 in participants with typical development.

Conclusions: Our findings suggest a possible parallel trajectory in age-related cognitive performance for individuals with and without intellectual disability in six measures, and a possible more preserved trajectory in fluid intelligence and some memory measures in adults with intellectual disability compared to their peers. Caution should be exercised regarding Digit and Spatial Span Backwards, which yielded a floor effect in participants with intellectual disability. The Cognitive Reserve Theory, the Safeguard Hypothesis and late maturation might serve as explanations for these findings.

Download full-text PDF

Source
http://dx.doi.org/10.1111/jar.13096DOI Listing

Publication Analysis

Top Keywords

intellectual disability
32
adults intellectual
16
age cohorts
16
cognitive performance
12
spatial span
12
lower scores
12
reserve theory
8
intellectual
8
disability
8
typical development?
8

Similar Publications

Unlabelled: We investigated the impact of participation in post-secondary university education (PSE) on the academic knowledge of adult students with severe intellectual disability and extensive support needs (SIDESN) vs. a similar group of controls who did not participate in PSE. We also examined whether the PSE would result in a "near transfer" to basic crystallized (facts and information) and fluid (problems involving executive functions and working memory) cognitive abilities, the contribution of background characteristics and crystallized and fluid abilities to their academic knowledge, semantic fluency and temporal relations.

View Article and Find Full Text PDF

The Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway.

Cell Rep

January 2025

Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:

Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.

View Article and Find Full Text PDF

Animal models of kabuki syndrome and their applicability to novel drug discovery.

Expert Opin Drug Discov

January 2025

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.

Introduction: Kabuki Syndrome (KS) is a rare genetic disorder characterized by distinctive facial features, intellectual disability, and multiple congenital anomalies. It is caused by pathogenic variants in the and genes. Despite its significant disease burden, there are currently no approved therapies for KS, highlighting the need for advanced research and therapeutic development.

View Article and Find Full Text PDF

Use of the Adaptive Behaviour Dementia Questionnaire in a Down Syndrome Specialty Clinic.

J Integr Neurosci

January 2025

Down Syndrome Program, Division of Medical Genetics and Metabolism, Department of Pediatrics, Massachusetts General Hospital, Boston, MA 02114, USA.

Objective: To study the use of a dementia screening tool in our clinic cohort of adults with Down syndrome.

Study Design: A retrospective chart review of patients with Down syndrome was conducted to follow the use of the Adaptive Behaviour Dementia Questionnaire (ABDQ) in a dementia screening protocol. The ABDQ results for patients aged 40 years and older at a Down syndrome specialty clinic program were assessed.

View Article and Find Full Text PDF

Purpose: Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental condition that affects approximately 5% of the pediatric population, with increased prevalence among those with type 1 diabetes (T1D). Reports suggest that unrecognized and untreated ADHD impairs T1D control and that ADHD may be underdiagnosed in the Polish population. The International Society for Pediatric and Adolescent Diabetes recommends neurodevelopmental assessments in children with T1D, but specific guidelines on procedures and implementation are lacking.

View Article and Find Full Text PDF

Want 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!