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The Role of Creb and Bdnf in Neurobiology and Treatment of Alzheimer's Disease Publisher Pubmed



Amidfar M1 ; De Oliveira J2 ; Kucharska E3 ; Budni J4 ; Kim YK5
Authors
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Authors Affiliations
  1. 1. Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Programa de Pos-Graduacao em Ciencias Biologicas: Bioquimica, Departamento de Bioquimica, Instituto de Ciencias Basicas da Saude, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil
  3. 3. Jesuit University Ignatianum in Krakow, Faculty of Education, Institute of Educational Sciences, Poland
  4. 4. Laboratorio de Neurologia Experimental, Programa de Pos-Graduacao em Ciencias da Saude, Universidade do Extremo Sul Catarinense (UNESC), Criciuma, SC, Brazil
  5. 5. Departments of Psychiatry, College of Medicine, Korea University, Seoul, South Korea

Source: Life Sciences Published:2020


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. © 2020 Elsevier Inc.
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