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Cognitive tutoring induces widespread neuroplasticity and remediates brain function in children with mathematical learning disabilities.

ABSTRACT: Competency with numbers is essential in today's society; yet, up to 20% of children exhibit moderate to severe mathematical learning disabilities (MLD). Behavioural intervention can be effective, but the neurobiological mechanisms underlying successful intervention are unknown. Here we demonstrate that eight weeks of 1:1 cognitive tutoring not only remediates poor performance in children with MLD, but also induces widespread changes in brain activity. Neuroplasticity manifests as normalization of aberrant functional responses in a distributed network of parietal, prefrontal and ventral temporal-occipital areas that support successful numerical problem solving, and is correlated with performance gains. Remarkably, machine learning algorithms show that brain activity patterns in children with MLD are significantly discriminable from neurotypical peers before, but not after, tutoring, suggesting that behavioural gains are not due to compensatory mechanisms. Our study identifies functional brain mechanisms underlying effective intervention in children with MLD and provides novel metrics for assessing response to intervention.

SUBMITTER: Iuculano T

PROVIDER: S-EPMC4598717 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Cognitive tutoring induces widespread neuroplasticity and remediates brain function in children with mathematical learning disabilities.

Iuculano Teresa T Rosenberg-Lee Miriam M Richardson Jennifer J Tenison Caitlin C Fuchs Lynn L Supekar Kaustubh K Menon Vinod V

Nature communications 20150930

Competency with numbers is essential in today's society; yet, up to 20% of children exhibit moderate to severe mathematical learning disabilities (MLD). Behavioural intervention can be effective, but the neurobiological mechanisms underlying successful intervention are unknown. Here we demonstrate that eight weeks of 1:1 cognitive tutoring not only remediates poor performance in children with MLD, but also induces widespread changes in brain activity. Neuroplasticity manifests as normalization o ...[more]

PMID: 26419418

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Project description:BackgroundChildren with learning disabilities (CLD) have worse health outcomes than children with no learning disabilities (CNLD). This systematic review compared caries experience and met dental care need for CLD to CNLD using Decayed, Missing, Filled Permanent Teeth (DMFT) and decayed, missing/extracted, filled primary teeth (dmft/deft), care index (CI), and restorative index (RI) values.MethodsWithout date or language restrictions four databases were searched for; cross-sectional studies comparing caries experience and CI/ RI in CLD matched to groups of CNLD. Screening and data extraction were carried out independently and in duplicate. Risk of bias was assessed using the Newcastle-Ottawa Scale. Meta-analyses were carried out (random effects model).ResultsThere were 25 articles with 3976 children (1 to 18?years old), from 18 countries, fitting the inclusion criteria. Children with; Down syndrome were investigated in 11 studies, autism in 8 and mixed learning disabilities in 6. The overall mean DMFT for CLD was 2.31 (standard deviation±1.97; range 0.22 to 7.2) and for CNLD was 2.51 (±2.14; 0.37 to 4.76). Using standardised mean difference (SMD), meta-analysis showed no evidence of a difference between CLD and CNLD (n =?16 studies) for caries experience (SMD?=?-0.43; 95%CI?=?-0.91 to 0.05). This was similar for sub-groups of children with autism (SMD?=?-0.28; 95%CI?=?1.31 to 0.75) and mixed disabilities (SMD?=?0.26; 95%CI?=?-0.94 to 1.47). However, for children with Down syndrome, caries experience was lower for CLD than CNLD (SMD?=?-0.73; 95%CI?=?-1.28 to -?0.18). For primary teeth, mean dmft/deft was 2.24 for CLD and 2.48 for CNLD (n =?8 studies). Meta-analyses showed no evidence of a difference between CLD and CNLD for caries experience across all disability groups (SMD?=?0.41; 95% CI?=?-0.14 to 0.96), or in sub-groups: Down syndrome (SMD?=?0.55; 95%CI-?=?-?0.40 to 1.52), autism (SMD?=?0.43; 95%CI?=?-0.53 to 2.39) and mixed disabilities (SMD?=?-0.10; 95%CI?=?-0.34 to 0.14). The studies' risk of bias were medium to high.ConclusionThere was no evidence of a difference in caries levels in primary or permanent dentitions for CLD and CNLD. This was similar for learning disability sub-groups, except for Down syndrome where dental caries levels in permanent teeth was lower. Data on met need for dental caries was inconclusive.Trial registrationThe protocol was published in PROSPERO: CRD42017068964 (June 8th, 2017).

Project description:We are searching for common gene expression alteration in the hippocampus of animal models of learning disabilities and in post-mortem human tissues derived from patients with cognitive deficits. Our study has three phases. In phase I, we want to investigate the changes in gene expression in a transgenic mouse line that shows impairments in hippocampal-dependent learning. These animals are overexpressing the RNA-binding protein HuD in the forebrain under the control of the alpha CAMKinII promoter. For phase II, we plan to characterize the hippocampus of another animal model of learning disabilities: fetal alcohol exposed (FAE) rats. Last, for phase III, we would like to examine gene expression changes in the hippocampus and other tissues from patients with schizophrenia. To test our hypothesis, in phase 2 of our project, we propose to compare the pattern of gene expression in our mouse model with that in the hippocampus of rats prenatally exposed to alcohol (FAE model). Our hypothesis is that learning disabilities have common neural substrates regardless of the origin of the disability being genetic, environmental of a combination of these two. To test this hypothesis, we plan to examine the pattern of gene expression in the hippocampus of animals and humans with cognitive deficits and use bioinformatics tools to identify common changes in gene expression in three of such conditions: a genetic model (HuD transgenic mice), an environmental model (FAE rats) and a model for combined environmental and genetic effects (patients with schizophrenia). All the animals are adult male Sprague-Dawley rats (age 90-100 days). Animals were divided in three diet groups and three experimental treatment conditions (9 conditions altogether). Three groups of pregnant rat dams were placed on different diet regimens: a liquid diet containing 5% alcohol (A) groups, a control group fed an isocaloric liquid diet without alcohol (B) and a group of rats fed lab chow ad libitum (C). Offspring from each of these groups were allowed to grow until adulthood and placed into each of three training groups: a contextual fear conditioned group (1), a non-learning stress control group (2) and a naive/unhandled group (3). Hippocampi were dissected and used to isolate total RNA from each rat diet and training condition. Initially, we will submit 18 samples as follows: 10 samples from training group 1 and 8 samples from training group 3 (training group 2 will be analyzed at a later date). The diet assignment for the 18 samples is: 8 samples from group A, 6 samples of group B and 4 samples of group C. Please note that I was able to enter only the first 8 samples, as the sample list does not hold 18 samples altogether. Keywords: dose response

Dataset Information

Cognitive tutoring induces widespread neuroplasticity and remediates brain function in children with mathematical learning disabilities.

Publications

Cognitive tutoring induces widespread neuroplasticity and remediates brain function in children with mathematical learning disabilities.

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