Activation of ERK1/2-CREB pathway during potentiating synaptic transmission of ( − )clausenamide in rat dentate gyrus

Hu, Jin; Niu, Fei; Na, Ning; Duan, Wen; Chu, Shi Feng; Xue, Wei; Yuan, Yu He; Chen, Nai Hong; Zhang, Jun Tian

doi:10.1080/10286020.2011.650885

Cited by 13 publications

(5 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MAPK activation also upregulates cytokine production by direct phosphorylation of transcription factors such as CREB (cAMP response element binding). CREB has direct effect on structural changes associated with memory formation [136].…”

Section: Mapk Signaling In Diabetes and Admentioning

confidence: 99%

Overlapped Metabolic and Therapeutic Links between Alzheimer and Diabetes

Ahmad

2012

Mol Neurobiol

View full text Add to dashboard Cite

Alzheimer's disease (AD) and diabetes are among the most common diseases associated with ageing. The pathology of AD is strongly associated with accumulated misfolding proteins that results in neuronal dysfunction within the brain. Diabetes, on the contrary, is characterised by altered insulin signaling that results in reduced glucose uptake, metabolic suppression of energy consuming cells and conversion of glucose to fat in the liver. Despite distinguishing features, these diseases share common elements and may in fact be viewed as fundamentally similar disorders that differ in magnitude of specific traits, primarily affected tissues and time of onset. In this review, we outline the fundamental basis of each of the two diseases and highlight similarities in their pathophysiology. Further ahead we will discuss these features in relation to the development of drugs to treat these two diseases, particularly AD, for which the development of therapeutic chemicals has proven to be particularly difficult. We conclude with comments on efforts to develop a simple organism, Caenorhabditis elegans, as a genetic model to be used to study the systems biology of diabetes and AD.

show abstract

Section: Mapk Signaling In Diabetes and Admentioning

confidence: 99%

Overlapped Metabolic and Therapeutic Links between Alzheimer and Diabetes

Ahmad

2012

Mol Neurobiol

View full text Add to dashboard Cite

show abstract

“…Therefore, synaptic loss was considered as a main cause of dementia, and even some scientists proposed that ‘synaptic loss=AD’. For this reason, the new strategy for treatment of AD is limiting synaptic loss and increasing synaptogenesis 14 , 15 .…”

Section: Nootropic Mechanism Of (–)Claumentioning

confidence: 99%

Recent advances in the study of (–)clausenamide: chemistry, biological activities and mechanism of action

Chu

Zhang

2014

Acta Pharmaceutica Sinica B

Self Cite

View full text Add to dashboard Cite

Clausenamide (clau) is one of seven novel compounds isolated from Clausena lansium (Lour) skeels. Clau is unusual in that it contains 4 chiral centers yielding 8 pairs of enantiomers. After identification of the configuration of these enantiomers, the synthesis of 16 enantiomers, including optically active clau and (+) and (–)clau was carried out. During this study, many stereochemical and synthetic difficulties were solved and the Baldwin principle was updated. Production scale is now sufficient to meet the needs of clinical practice. In a pharmacological study numerous models and indicators showed that (–)clau is the active enantiomer, while (+)clau is inactive and elicits greater toxicity than (–)clau. The principal pharmacological effects of (–)clau are to increase cognition, demonstrated in ten models of memory impairment, as well as to inhibit β-amyloid (Aβ) toxicity, blocking neurofibrillary tangle formation by inhibiting the phosphorylation of tau protein. This anti-dementia effect is characterized by increased synaptic plasticity both in efficacy and in structure and provides new support for the theory that synaptic loss is the main cause of dementia. (–)Clau is considered to be a promising drug candidate for treatment of Alzheimer׳s disease and other neurodegenerative disorders.

show abstract

“…ERK1/2 (or MAPK) pathway forms a parallel branch in insulin signaling and is implicated in multiple forms of synaptic plasticity and cell death (70). Studies on cell cultures observed that MAPK activation led to expression of iNOS, TNFα, IL-1β genes and upregulation of cytokine production (71,72). Kumar et al (73) observed induction of apoptosis in glial cells exposed to high glucose through activation of MAPKs, down regulation of 8-oxoG-DNA glycosylase and increase in 8-hydroxydeoxyguanosine.…”

Section: Introductionmentioning

confidence: 98%

Inside the Diabetic Brain

Chomova

2014

Acta Medica Martiniana

View full text Add to dashboard Cite

A b s t r a c t CNS complications resulting from diabetes mellitus (DM) are a problem gaining more acceptance and attention in the recent years. Both types 1 and 2 DM represent an significant risk factor for decreased cognitive functions, memory and learning deficits as well as development of Alzheimer's disease. Chronic hyperglycemia through protein glycation and increased oxidative stress contributes to brain dysfunction, however increasing evidences suggest that the pathology of DM in the brain involves a progressive and coordinated disruption of insulin signaling, with profound consequences for brain function and plasticity. Since many of the CNS changes observed in diabetic patients and animal models of DM are reminiscent of the changes seen in aging, the theory of advanced brain aging in DM has been proposed. This review summarizes the findings of the literature regarding the effects of DM on the brain in the terms of diabetes-related metabolic derangements and intracellular signaling.

show abstract

Activation of ERK1/2-CREB pathway during potentiating synaptic transmission of ( − )clausenamide in rat dentate gyrus

Cited by 13 publications

References 16 publications

Overlapped Metabolic and Therapeutic Links between Alzheimer and Diabetes

Overlapped Metabolic and Therapeutic Links between Alzheimer and Diabetes

Recent advances in the study of (–)clausenamide: chemistry, biological activities and mechanism of action

Inside the Diabetic Brain

Contact Info

Product

Resources

About