scholarly journals cAMP Response Element-Binding Protein 1 Feedback Loop Is Necessary for Consolidation of Long-Term Synaptic Facilitation in Aplysia

2008 ◽  
Vol 28 (8) ◽  
pp. 1970-1976 ◽  
Author(s):  
R.-Y. Liu ◽  
D. Fioravante ◽  
S. Shah ◽  
J. H. Byrne
Keyword(s):  
Feedback Loop ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Synaptic Facilitation ◽  
Element Binding Protein

scholarly journals Long-Term Memory Is Facilitated by cAMP Response Element-Binding Protein Overexpression in the Amygdala

2001 ◽  
Vol 21 (7) ◽  
pp. 2404-2412 ◽  
Author(s):  
Sheena A. Josselyn ◽  
Chanjun Shi ◽  
William A. Carlezon ◽  
Rachael L. Neve ◽  
Eric J. Nestler ◽  
...  
Keyword(s):  
Binding Protein ◽  
Camp Response Element Binding ◽  
Long Term Memory ◽  
Protein Overexpression ◽  
Camp Response Element ◽  
Response Element ◽  
Term Memory ◽  
Element Binding Protein

CREB: A Multifaceted Target for Alzheimer’s Disease

2021 ◽  
Vol 18 ◽  
Author(s):  
Vivek Kumar Sharma ◽  
Thakur Gurjeet Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Signaling ◽  
Camp Response Element ◽  
Response Element ◽  
Term Memory ◽  
Element Binding Protein

: Alzheimer’s disease (AD) is a persistent neuropathological stipulation manifested in the form of neuronal/synapse demise, the formation of senile plaques, hyperphosphorylated tau tangles, neuroinflammation, and apoptotic cell death. The absence of a therapeutic breakthrough for AD has continued the quest to find a suitable intervention. Apart from various candidates, the cyclic AMP-protein kinase A-cAMP response element-binding protein (cAMP/PKA/CREB) pathway is the most sought-after drug target AD as the bulk of quality literature documents that there is downregulation of cAMP signaling and CREB mediated transcriptional cascade in AD. cAMP signaling is evolutionarily conserved and can be found in all species. cAMP response element-binding protein (CREB) is a ubiquitous and integrally articulated transcription aspect that regulates neuronal growth, neuronal differentiation/proliferation, synaptic plasticity, neurogenesis, maturation of neurons, spatial memory, long-term memory formation as well as ensures neuronal survival. CREB is a central part of the molecular machinery that has a role in transforming short-term memory to long-term. Besides AD, impairment of CREB signaling has been well documented in addiction, Parkinsonism, schizophrenia, Huntington’s disease, hypoxia, preconditioning effects, ischemia, alcoholism, anxiety, and depression. The current work highlights the role and influence of CREB mediated transcriptional signaling on major pathological markers of AD (amyloid β, neuronal loss, inflammation, apoptosis, etc.). The present work justifies the continuous efforts being made to explore the multidimensional role of CREB and related downstream signaling pathways in cognitive deficits and neurodegenerative complications in general and AD particularly. Moreover, it is reaffirmed that cyclic nucleotide signaling may have vast potential to treat neurodegenerative complications like AD.

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