Early and late neurodegeneration and memory disruption after intracerebroventricular streptozotocin
Autor: | Andréa da Silva Torrão, Caio Henrique Mazucanti, Taisa de Oliveira Santos, Gilberto Fernando Xavier |
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Rok vydání: | 2012 |
Předmět: |
Blood Glucose
Male Aging Time Factors endocrine system diseases Tau protein Learning/memory Hippocampus tau Proteins Experimental and Cognitive Psychology Water maze Motor Activity Carbohydrate metabolism Streptozocin Glucose/energy metabolism Choline O-Acetyltransferase Behavioral Neuroscience Cognitive dysfunction Glial Fibrillary Acidic Protein Reaction Time medicine Animals Neurodegeneration Rats Wistar Maze Learning Injections Intraventricular Analysis of Variance Memory Disorders Amyloid beta-Peptides biology Streptozotocin Working memory Neurodegenerative Diseases Alzheimer's disease Fluoresceins medicine.disease Rats FISIOLOGIA Insulin receptor Memory Short-Term Gene Expression Regulation biology.protein Psychology Neuroscience medicine.drug |
Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
Popis: | Glucose metabolism and insulin signaling disruptions in the brain have been proposed as a likely etiology of Alzheimer's disease. The aim of the present study was to investigate the time course of cognitive impairments induced by intracerebroventricular injection of streptozotocin (STZ) in rats and correlate them with the ensuing neurodegenerative process. Early and late effects of STZ were evaluated by using the reference and working memory versions of the Morris' water maze task and the evaluation of neurodegenerative markers by immunoblotting and the Fluoro-Jade C histochemistry. The results revealed different types of behavioral and neurodegenerative responses, with distinct time courses. We observed an early disruption on the working memory as early as 3h after STZ injections, which was followed by degenerative processes in the hippocampus at 1 and 15days after STZ injections. Memory disruption increases over time and culminates with significant changes in amyloid-beta peptide and hyperphosphorylated Tau protein levels in distinct brain structures. These findings add information on the Alzheimer's disease-like STZ animal model and on the mechanisms underlying neurodegenerative processes. |
Databáze: | OpenAIRE |
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