期刊
NEUROSCIENCE RESEARCH
卷 157, 期 -, 页码 44-50出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neures.2019.07.008
关键词
Docosahexaenoic acid; Traumatic brain injury; JNK; Tau; Hippocampus
Hyperphosphorylation of Tau has been found in patients with traumatic brain injury (TBI). Inhibition of c-Jun N-terminal kinases (JNKs) improves neurological function by suppressing Tau phosphorylation. By inhibiting JNK, docosahexaenoic acid (DHA) protects against cognitive decline in a mouse model of Alzheimers disease (AD). We hypothesize that DHA protects against neuronal damage and behavioral deficits by inhibition of JNK mediated Tau phosphorylation. We induced TBI in mice and examined the phosphorylation status of JNK and Tau. We treated TBI and sham operated mice with DHA, and investigated the effects of DHA on JNK and Tau phosphorylation, hippocampal long term potentiation (LTP), learning and memory, and motor function by Western blot analysis, electrophysiology recording and behavioral assessments including Morris water maze test, beam-balance test, beam-walk test and rotarod test. We found that TBI induction lead to increased phosphorylation of JNK and Tau. DHA suppressed TBI induced JNK and Tau hyperphosphorylation, rescued TBI mediated hippocampal LTP deficits and hippocampus dependent learning and memory dysfunction, and improved motor function. Inhibition of JNK and Tau phosphorylation by DHA may represent a potential therapeutic strategy for TBI induced neurological dysfunction and Tauopathy. (C) 2019 Elsevier B.V. and Japan Neuroscience Society. All rights reserved.
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