Background: Cognitive inhibition is one of the executive functions; this process over memory plays a fundamental role in recalling relevant information. The aims of this study were to understand the effects of maintenance load and stimuli on the operation of cognitive inhibition over memory in working memory tasks in adults with Down syndrome.

Method: The study included 36 individuals with Down syndrome (mean age = 33.44 years, standard deviation = 7.54 years, 50% women) and 36 individuals with neurotypical development (mean age = 33.55 years, standard deviation = 7.52 years, 50% women). The participants performed a working memory task in which they had to solve an interference problem during the maintenance phase.

Results: The Down syndrome group performed worse on cognitive inhibition over memory than the neurotypical development group. Both groups had lower recall with interference and under high-load conditions. In the neurotypical development group, memory was similar with both materials. The Down syndrome group performed better with non-social stimuli than with social stimuli.

Conclusions: Understanding the variables that influence cognitive inhibition over memory will help in planning effective interventions for people with Down syndrome. Considering the results, special importance should be placed on work with social stimuli, at least in individuals with Down syndrome.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6855476PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0225009PLOS

Publication Analysis

Top Keywords

cognitive inhibition
16
inhibition memory
12
neurotypical development
12
operation cognitive
8
memory
8
effects maintenance
8
maintenance load
8
working memory
8
individuals syndrome
8
years standard
8

Similar Publications

Quinoa, rich in pharmacologically active ingredients, possesses the potential benefit in preventing cognitive impairments induced by hypoxia. In this study, the efficacy of quinoa ethanol extracts (QEE) consumption (200 and 500 mg/kg/d, respectively) against hypobaric hypoxia (HH)-induced cognitive deficits in mice was investigated. QEE significantly ameliorated hypoxic stress induced by HH, as evidenced by improvements in baseline indices and reductions in hypoxia-inducible factor 1α levels.

View Article and Find Full Text PDF

Physical exercise is known to slow synaptic neurodegeneration and cognitive aging in Alzheimer's disease (AD). The benefits of physical exercise are related to reduced amyloid beta (Aβ) deposition and increased synaptic plasticity. Yet little is known about the mechanisms that mediate these effects.

View Article and Find Full Text PDF

Tau oligomers impair memory and synaptic plasticity through the cellular prion protein.

Acta Neuropathol Commun

January 2025

Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.

Deposition of abnormally phosphorylated tau aggregates is a central event leading to neuronal dysfunction and death in Alzheimer's disease (AD) and other tauopathies. Among tau aggregates, oligomers (TauOs) are considered the most toxic. AD brains show significant increase in TauOs compared to healthy controls, their concentration correlating with the severity of cognitive deficits and disease progression.

View Article and Find Full Text PDF

Background: Recent research has highlighted the role of fronto-parietal brain networks and cognitive control in mood disorders. Transcranial direct current stimulation (tDCS) and computer-based cognitive training are used in post-stroke rehabilitation. This study examined the combined effects ofof computer-based inhibitory control training (ICCT) and anodal tDCS on post-stroke depression and anxiety.

View Article and Find Full Text PDF

Age-related p53 SUMOylation accelerates senescence and tau pathology in Alzheimer's disease.

Cell Death Differ

January 2025

Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Aging is a major risk factor for Alzheimer's disease (AD). With the prevalence of AD increased, a mechanistic linkage between aging and the pathogenesis of AD needs to be further addressed. Here, we report that a small ubiquitin-related modifier (SUMO) modification of p53 is implicated in the process which remarkably increased in AD patient's brain.

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!