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- W3037752736 endingPage "118020" @default.
- W3037752736 startingPage "118020" @default.
- W3037752736 abstract "Alzheimer's disease (AD) is the most common form of dementia worldwide. β-amyloid peptide (Aβ) is currently assumed to be the main cause of synaptic dysfunction and cognitive impairments in AD, but the molecular signaling pathways underlying its neurotoxic consequences have not yet been completely explored. Additional investigations regarding these pathways will contribute to development of new therapeutic targets. In context, developing evidence suggest that Aβ decreases brain-derived neurotrophic factor (BDNF) mostly by lowering phosphorylated cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) protein. In fact, it has been observed that brain or serum levels of BDNF appear to be beneficial markers for cognitive condition. In addition, the participation of transcription mediated by CREB has been widely analyzed in the memory process and AD development. Designing pharmacologic or genetic therapeutic approaches based on the targeting of CREB-BDNF signaling could be a promising treatment potential for AD. In this review, we summarize data demonstrating the role of CREB-BDNF signaling pathway in cognitive status and mediation of Aβ toxicity in AD. Finally, we also focus on the developing intervention methods for improvement of cognitive decline in AD based on targeting of CREB-BDNF pathway." @default.
- W3037752736 created "2020-07-02" @default.
- W3037752736 creator A5046065442 @default.
- W3037752736 creator A5046171115 @default.
- W3037752736 creator A5086727096 @default.
- W3037752736 creator A5088301232 @default.
- W3037752736 creator A5088645194 @default.
- W3037752736 date "2020-09-01" @default.
- W3037752736 modified "2023-10-12" @default.
- W3037752736 title "The role of CREB and BDNF in neurobiology and treatment of Alzheimer's disease" @default.
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