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a(MESHC:"pro-nerve growth factor, human")

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Entity

Name
pro-nerve growth factor, human
Namespace
MESHC
Namespace Version
20170725
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/mesh-chemicals/mesh-chemicals-20170725.belns

Appears in Networks 1

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

In-Edges 6

complex(a(MESHC:"pro-nerve growth factor, human"), p(HGNC:NGFR)) hasComponent a(MESHC:"pro-nerve growth factor, human") View Subject | View Object

Appears in Networks:

composite(a(MESHC:"pro-nerve growth factor, human"), complex(p(HGNC:NGFR), p(HGNC:SORT1))) hasComponent a(MESHC:"pro-nerve growth factor, human") View Subject | View Object

Appears in Networks:

complex(a(MESHC:"pro-nerve growth factor, human"), p(HGNC:NTRK1)) hasComponent a(MESHC:"pro-nerve growth factor, human") View Subject | View Object

Appears in Networks:

path(MESH:D000544) increases a(MESHC:"pro-nerve growth factor, human") View Subject | View Object

In this regard, immunoblotting studies demonstrated that proNGF is the predominant form of NGF present in the cortex of aged cognitively intact humans [60]. ProNGF levels are increased in the cortex of subjects diagnosed with MCI or mild AD compared to those with NCI [61]. The biological consequences of proNGF are controversial, as is the function of its accumulation in the cortex during the prodromal stages of AD. Emerging literature suggests that recombinant proNGF binds TrkA and promotes neuronal survival and neurite outgrowth similar to mature NGF, but is approximately fivefold less active than the mature NGF peptide [62,63]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Cognitive Dysfunction

path(MESH:D003072) positiveCorrelation a(MESHC:"pro-nerve growth factor, human") 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

path(MESH:D060825) increases a(MESHC:"pro-nerve growth factor, human") View Subject | View Object

In this regard, immunoblotting studies demonstrated that proNGF is the predominant form of NGF present in the cortex of aged cognitively intact humans [60]. ProNGF levels are increased in the cortex of subjects diagnosed with MCI or mild AD compared to those with NCI [61]. The biological consequences of proNGF are controversial, as is the function of its accumulation in the cortex during the prodromal stages of AD. Emerging literature suggests that recombinant proNGF binds TrkA and promotes neuronal survival and neurite outgrowth similar to mature NGF, but is approximately fivefold less active than the mature NGF peptide [62,63]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Cognitive Dysfunction

Out-Edges 2

a(MESHC:"pro-nerve growth factor, human") positiveCorrelation 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

a(MESHC:"pro-nerve growth factor, human") biomarkerFor path(MESH:D000544) View Subject | View Object

Thus, the concomitant reduction of TrkA and accumulation of proNGF in the cortex may be an early pathobiological marker for the onset of AD (Figure 1A). In fact, significantly increased cerebrospinal fluid (CSF) levels of NGF are detectable in AD [65], demonstrating the potential utility of NGF as a diagnostic biomarker. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

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.