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  4. Cognitive Dysfunction

Cognitive Dysfunction

Name
Cognitive Dysfunction
Namespace Keyword
MeSHDisease
Namespace
MeSH
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/mesh-diseases/mesh-diseases-20170511.belanno

Sample Annotated Edges 5

bp(GO:"GO:0000165") increases act(p(FPLX:P90RSK)) View Subject | View Object

The classic MAPK cascade involves activation of the small GTPase Ras, and the kinases Raf and MEK [86,87]. Downstream consequences of MAPK activation include activation of the ribosomal S6 kinases (Rsk) and the MAPK-activated protein kinase 2 (MAPKAP2), which phosphorylates several transcription factors including Elk-1 and cAMP-regulated response element binding protein (CREB) [85]. The physiological significance of this elaborate NGF-induced network remains unclear, but the sustained activation of MAPK is linked to neurotrophin-mediated neurite outgrowth [88,89] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

path(MESH:D003967) association a(MESH:D002800) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

p(HGNC:ACHE) association path(MESH:D058225) View Subject | View Object

In this regard, AChE has been localized to SPs in the vicinity of cholinergic synapses, and experimental evidence suggests that AChE promotes Ab fibrillization [164], suggesting that a further benefit from AChE inhibitor therapy may be to prevent continued Ab deposition in cholinergic projection sites. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NTRK1) negativeCorrelation path(MESH:D003072) View Subject | View Object

Significantly, while we have shown that reduced TrkA levels in the cortex were positively associated with lower cognitive performance as assessed by Mini-Mental State Exam (MMSE) test scores [64], increased cortical proNGF levels were negatively correlated with MMSE performance [61]. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cerebral Cortex
MeSH
Cognitive Dysfunction

p(HGNC:GAB1) association bp(GO:"GO:0043491") View Subject | View Object

A second downstream pathway is the PI3K/Akt pathway that regulates neurotrophin-mediated survival responses in PC12 cells [90,91]. Regulation of this pathway involves upstream elements including Ras/Gab1/IRS1 [92,93]. PubMed:18986241

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
PC12
MeSH
Cognitive Dysfunction

Showing 5 of 207 edges

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.