a(HBP:AβOs)
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
a4b2-nAChRs have been implicated in nicotine self-administration, reward, and depen- dence, and in diseases such as Alzheimer’s and epilepsy [1–5,27–33]. PubMed:21787755
Among the various molecular species of Abeta present in the brain, soluble oligomeric forms of Abeta are arguably the most plausible candidates to impair synaptic function (reviewed in Walsh and Selkoe 2004). PubMed:22908190
Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190
Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190
Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190
They also facilitate long-term depression by, among other effects, disrupting synaptic glutamate uptake (Li et al. 2009). PubMed:22908190
They also facilitate long-term depression by, among other effects, disrupting synaptic glutamate uptake (Li et al. 2009). PubMed:22908190
Recently, it has been shown that soluble Ab oligomers isolated from AD cortex can induce tau hyperphosphorylation at AD-relevant epitopes and subsequent neuritic degeneration (Jin et al. 2011). PubMed:22908190
Recently, it has been shown that soluble Ab oligomers isolated from AD cortex can induce tau hyperphosphorylation at AD-relevant epitopes and subsequent neuritic degeneration (Jin et al. 2011). PubMed:22908190
Moreover, soluble Ab oligomers themselves can inhibit proteasomal activity (Tseng et al. 2008). PubMed:22908190
For comparison, in the case of Ab oligomers, only higher concentrations (w1 mM) cause an appreciable spine reduction of w30% (Fig. 4C, bar 3) (Zempel et al., 2010 [30]). PubMed:28528849
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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.