bp(GO:"neuron cellular homeostasis")
Extracellular deposition of amyloid-β aggregates, the main constituent of senile plaques, is considered to be a pathological hallmark of Alzheimer’s disease that contributes to neuronal dysfunction and behavioural changes PubMed:30046111
It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383
Whilst the spatial memory deficit was restored by 4OH-GTS-21 treatment, this molecule had no effect on neuronal density (Ren et al., 2007) PubMed:25514383
alpha7 nAChR on presynaptic terminals mediate release of others neurotransmitters (Wonnacott et al., 2006), while a postsynaptic or somatic localization elicits important changes in intracellular Ca++ concentration, that can activate second messenger pathways mediating cellular processes such as neuronal survival and gene expression (Berg and Conroy, 2002; Messi et al., 1997; Morley and Happe, 2000) PubMed:25514383
It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383
Accumulation of misfolded proteins and damaged organelles is highly detrimental for neuronal homeostasis and survival. PubMed:29758300
It is becoming increasingly evident that the autophagy-lysosomal system is essential to neuronal homeostasis, and may in some settings be neuroprotective PubMed:18930136
It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383
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.