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      Inhibition of JNK phosphorylation reverses memory deficit induced by β-amyloid (1-42) associated with decrease of apoptotic factors.

      Behavioural Brain Research

      bcl-2-Associated X Protein, metabolism, Animals, Anthracenes, therapeutic use, Apoptosis, drug effects, Caspase 3, Cyclooxygenase 2, Analysis of Variance, Disease Models, Animal, Enzyme Inhibitors, Gene Expression Regulation, Enzymologic, Hippocampus, cytology, In Situ Nick-End Labeling, MAP Kinase Kinase 4, Male, Maze Learning, Memory Disorders, chemically induced, drug therapy, enzymology, Neurons, Peptide Fragments, toxicity, Phosphorylation, Proto-Oncogene Proteins c-bcl-2, Rats, Rats, Wistar, Statistics, Nonparametric, Amyloid beta-Peptides

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          Alzheimer's disease (AD) is the most common form of dementia that is degenerative and terminal disease. The main reason of the disease is still unknown. β-amyloid (Aβ) plaques are the important hallmarks of memory impairment in patients suffering from AD. Aggregation of these plaques in the hippocampus appears during the development of the disease. One of the prominent factors having crucial impact in this process is MAPK. JNK, as a member of MAPK family has a pivotal role, especially in cell survival. We hypothesized that JNK may have beneficial effect on the process of memory improvement. Hence, we performed Morris water maze to investigate the possible impact of JNK inhibitor on spatial memory in Aβ-injected rats. Our data indicated that intracerebroventricular administration of SP600125, a JNK inhibitor, could significantly decrease escape latency and increase time spent in target quadrant, in treatment group. Furthermore, we evaluated some of the apoptotic factors in the hippocampus of the treated rats. Based on our data, the inhibitor led to the significant decrease in the amount of caspase-3, TUNEL positive cells, cyclooxygenase-2 and increase in Bcl-2/Bax ratio. Given the possible neuroprotective effects of SP600125 on Aβ-induced memory impairment and apoptosis, our results may open a new avenue for the treatment of AD. Copyright © 2010 Elsevier B.V. All rights reserved.

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