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ABSTRACT Purpose To address the need for a standardized assessment tool for assessing cognitive-communication abilities among Indian preschoolers, the current study aimed at describing a Delphi based development and validation process for developing one such tool. The objectives of the research were to conceptualize and construct the tool, validate its content, and assess its feasibility through pilot testing. Methods The study followed a Delphi approach to develop and validate the tool across four phases i.e. conceptualization; construction; content validation; and pilot testing. The first three phases were performed with a panel of six experts including speech-language pathologists and preschool teachers while the pilot testing was done with 20 typically developing preschoolers. A literature review was also conducted with the Delphi rounds to support the developmental process. Results The first two rounds of the Delphi aided in the construction of a culturally and linguistically suitable story-based cognitive-communication assessment tool with the memory (free recall, recognition, and literary recall) and executive function (reasoning, inhibition, and switching) related tasks relevant for preschoolers. The content validation of the tool was continued with the experts till the revisions were satisfactory and yielded an optimum Content Validity Index. The pilot test of the finalized version confirmed its feasibility and appropriateness to assess developmental changes in the cognitive-communication abilities of preschoolers. Conclusion The study describes the Delphi-based conceptualization, construction, content validation, and feasibility check of a tool to assess cognitive-communication skills in preschool children.
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PURPOSE: To address the need for a standardized assessment tool for assessing cognitive-communication abilities among Indian preschoolers, the current study aimed at describing a Delphi based development and validation process for developing one such tool. The objectives of the research were to conceptualize and construct the tool, validate its content, and assess its feasibility through pilot testing. METHODS: The study followed a Delphi approach to develop and validate the tool across four phases i.e. conceptualization; construction; content validation; and pilot testing. The first three phases were performed with a panel of six experts including speech-language pathologists and preschool teachers while the pilot testing was done with 20 typically developing preschoolers. A literature review was also conducted with the Delphi rounds to support the developmental process. RESULTS: The first two rounds of the Delphi aided in the construction of a culturally and linguistically suitable story-based cognitive-communication assessment tool with the memory (free recall, recognition, and literary recall) and executive function (reasoning, inhibition, and switching) related tasks relevant for preschoolers. The content validation of the tool was continued with the experts till the revisions were satisfactory and yielded an optimum Content Validity Index. The pilot test of the finalized version confirmed its feasibility and appropriateness to assess developmental changes in the cognitive-communication abilities of preschoolers. CONCLUSION: The study describes the Delphi-based conceptualization, construction, content validation, and feasibility check of a tool to assess cognitive-communication skills in preschool children.
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Transtornos da Comunicação , Professores Escolares , Humanos , Pré-Escolar , Técnica Delphi , Comunicação , CogniçãoRESUMO
BACKGROUND: Type 2 diabetes is a risk factor for Alzheimer's disease (AD), and AD brain shows impaired insulin signalling. The role of peripheral insulin resistance on AD aetiopathogenesis in non-diabetic patients is still debated. Here we evaluated the influence of insulin resistance on brain glucose metabolism, grey matter volume and white matter lesions (WMLs) in non-diabetic AD subjects. METHODS: In total, 130 non-diabetic AD subjects underwent MRI and [18F]FDG PET scans with arterial cannula insertion for radioactivity measurement. T1 Volumetric and FLAIR sequences were acquired on a 3-T MRI scanner. These subjects also had measurement of glucose and insulin levels after a 4-h fast on the same day of the scan. Insulin resistance was calculated by the updated homeostatic model assessment (HOMA2). For [18F]FDG analysis, cerebral glucose metabolic rate (rCMRGlc) parametric images were generated using spectral analysis with arterial plasma input function. RESULTS: In this non-diabetic AD population, HOMA2 was negatively associated with hippocampal rCMRGlc, along with total grey matter volumes. No significant correlation was observed between HOMA2, hippocampal volume and WMLs. CONCLUSIONS: In non-diabetic AD, peripheral insulin resistance is independently associated with reduced hippocampal glucose metabolism and with lower grey matter volume, suggesting that peripheral insulin resistance might influence AD pathology by its action on cerebral glucose metabolism and on neurodegeneration.
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Doença de Alzheimer , Diabetes Mellitus Tipo 2 , Resistência à Insulina , Doença de Alzheimer/complicações , Doença de Alzheimer/diagnóstico por imagem , Encéfalo/diagnóstico por imagem , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/diagnóstico por imagem , Fluordesoxiglucose F18 , Glucose , Humanos , Imageamento por Ressonância Magnética , Tomografia por Emissão de PósitronsRESUMO
An amendment to this paper has been published and can be accessed via the original article.
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BACKGROUND: Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue currently approved for type 2 diabetes and obesity. Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells. The primary objective of the study is to evaluate the change in cerebral glucose metabolic rate after 12 months of treatment with liraglutide in participants with Alzheimer's disease compared to those who are receiving placebo. METHODS/DESIGN: ELAD is a 12-month, multi-centre, randomised, double-blind, placebo-controlled, phase IIb trial of liraglutide in participants with mild Alzheimer's dementia. A total of 206 participants will be randomised to receive either liraglutide or placebo as a daily injection for a year. The primary outcome will be the change in cerebral glucose metabolic rate in the cortical regions (hippocampus, medial temporal lobe, and posterior cingulate) from baseline to follow-up in the treatment group compared with the placebo group. The key secondary outcomes are the change from baseline to 12 months in z scores for clinical and cognitive measures (Alzheimer's Disease Assessment Scale-Cognitive Subscale and Executive domain scores of the Neuropsychological Test Battery, Clinical Dementia Rating Sum of Boxes, and Alzheimer's Disease Cooperative Study-Activities of Daily Living) and the incidence and severity of treatment-emergent adverse events or clinically important changes in safety assessments. Other secondary outcomes are 12-month change in magnetic resonance imaging volume, diffusion tensor imaging parameters, reduction in microglial activation in a subgroup of participants, reduction in tau formation and change in amyloid levels in a subgroup of participants measured by tau and amyloid imaging, and changes in composite scores using support machine vector analysis in the treatment group compared with the placebo group. DISCUSSION: Alzheimer's disease is a leading cause of morbidity worldwide. As available treatments are only symptomatic, the search for disease-modifying therapies is a priority. If the ELAD trial is successful, liraglutide and GLP-1 analogues will represent an important class of compounds to be further evaluated in clinical trials for Alzheimer's treatment. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01843075 . Registration 30 April 2013.
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Doença de Alzheimer/tratamento farmacológico , Encéfalo/efeitos dos fármacos , Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas , Glucose/metabolismo , Hipoglicemiantes/uso terapêutico , Liraglutida/uso terapêutico , Fármacos Neuroprotetores/uso terapêutico , Atividades Cotidianas , Doença de Alzheimer/metabolismo , Doença de Alzheimer/fisiopatologia , Doença de Alzheimer/psicologia , Encéfalo/metabolismo , Encéfalo/fisiopatologia , Ensaios Clínicos Fase II como Assunto , Cognição/efeitos dos fármacos , Método Duplo-Cego , Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo , Humanos , Hipoglicemiantes/efeitos adversos , Liraglutida/efeitos adversos , Memória/efeitos dos fármacos , Estudos Multicêntricos como Assunto , Fármacos Neuroprotetores/efeitos adversos , Ensaios Clínicos Controlados Aleatórios como Assunto , Índice de Gravidade de Doença , Fatores de Tempo , Resultado do Tratamento , Reino UnidoRESUMO
The use of antipsychotics for the treatment of behavioural and psychological symptoms of dementia (BPSD) is controversial. Antipsychotics cause harm and evidence-based guidelines advise against their use. We argue that antipsychotics may be justified using a palliative model: by reducing severe distress in those whose life expectancy is short.