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Valproic Acid Modifies Synaptic Structure and Accelerates Neurite Outgrowth Via the Glycogen Synthase Kinase‐3β Signaling Pathway in an Alzheimer's Disease Model
AIM: Tau hyperphosphorylation and amyloid β‐peptide overproduction, caused by altered localization or abnormal activation of glycogen synthase kinase‐3β (GSK‐3β), is a pathogenic mechanism in Alzheimer's disease (AD). Valproic acid (VPA) attenuates senile plaques and neuronal loss. Here, we con...
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| 出版年: | CNS Neurosci Ther |
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| 主要な著者: | , , , , , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
John Wiley and Sons Inc.
2015
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC6493017/ https://ncbi.nlm.nih.gov/pubmed/26385876 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/cns.12445 |
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