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Kainic Acid Impairs the Memory Behavior of APP23 Mice by Increasing Brain Amyloid Load through a Tumor Necrosis Factor-α-Dependent Mechanism.
Ruan, Yang; Guo, Shi-Jie; Wang, Xu; Dong, Dong; Shen, Dong-Hui; Zhu, Jie; Zheng, Xiang-Yu.
Afiliación
  • Ruan Y; Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, China.
  • Guo SJ; Department of Neonatology, The First Hospital of Jilin University, Changchun, China.
  • Wang X; Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
  • Dong D; Department of Radiology, The First Hospital of Jilin University, Changchun, China.
  • Shen DH; Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
  • Zhu J; Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
  • Zheng XY; Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden.
J Alzheimers Dis ; 64(1): 103-116, 2018.
Article en En | MEDLINE | ID: mdl-29782313
Kainic acid (KA) was recently identified as an epileptogenic and neuroexcitotoxic agent that is responsible for inducing learning and memory deficits in various neurodegenerative diseases, such as Alzheimer's disease (AD). However, the mechanism by which KA acts upon AD remains unclear. To this end, we presently investigated the roles of KA in processing amyloid-ß protein precursor (AßPP) and amyloid-ß protein (Aß) loads during the course of AD development and progression. Specifically, KA treatment clearly caused the upregulation of tumor necrosis factor α (TNF-α) via activation of the PI3-K/AKT, ERK1/2, and p65 pathways in glial cells. TNF-α secreted from glial cells was then found to be responsible for stimulating the expression of BACE-1 and PS1/2, which resulted in the production and deposition of Aß in neurons. Finally, the accumulation and aggregation of Aß lead to the cognitive decline of APP23 mice. These results indicate that KA accelerates the progression of AD by inducing the crosstalk between glial cells and neurons.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Encéfalo / Péptidos beta-Amiloides / Factor de Necrosis Tumoral alfa / Agonistas de Aminoácidos Excitadores / Ácido Kaínico / Trastornos de la Memoria Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Alzheimers Dis Asunto de la revista: GERIATRIA / NEUROLOGIA Año: 2018 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Encéfalo / Péptidos beta-Amiloides / Factor de Necrosis Tumoral alfa / Agonistas de Aminoácidos Excitadores / Ácido Kaínico / Trastornos de la Memoria Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Alzheimers Dis Asunto de la revista: GERIATRIA / NEUROLOGIA Año: 2018 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos