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Appears in Networks 1

In-Edges 5

path(MESH:D000544) decreases p(HGNC:NTRK1) 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

path(MESH:D003072) negativeCorrelation p(HGNC:NTRK1) 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

Out-Edges 4

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

p(HGNC:NTRK1) 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

p(HGNC:NTRK1) decreases act(p(HGNC:BACE1)) View Subject | View Object

It is also important to note that TrkA reduces and p75NTR activates β-secretase strike (BACE) cleavage of the amyloid precursor protein (APP), which requires NGF binding and activation of the second messenger ceramide [66]. Aging may activate beta-amyloid (Ab) generation in the brain by ‘switching’ from TrkA to p75NTR, suggesting that NGF receptor balance is a molecular link between normal aging of the brain and AD in relation to amyloid processing. PubMed:18986241

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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.