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a(HBP:AβOs)

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Entity

Name
AβOs
Namespace
HBP
Namespace Version
20181128
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/7e4be528f12abd28be768b62402fba6e083eaf9e/export/hbp-names.belns

Appears in Networks 3

Naturally-expressed nicotinic acetylcholine receptor subtypes v1.0.0

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

In-Edges 3

path(MESH:"Alzheimer Disease") association a(HBP:AβOs) View Subject | View Object

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

Appears in Networks:

path(MESH:"Tobacco Use Disorder") association a(HBP:AβOs) View Subject | View Object

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

Appears in Networks:

path(MESH:Epilepsy) association a(HBP:AβOs) View Subject | View Object

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

Appears in Networks:

Out-Edges 13

a(HBP:AβOs) association path(MESH:"Tobacco Use Disorder") View Subject | View Object

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

Appears in Networks:

a(HBP:AβOs) association path(MESH:"Alzheimer Disease") View Subject | View Object

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

Appears in Networks:

a(HBP:AβOs) association path(MESH:Epilepsy) View Subject | View Object

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

Appears in Networks:

a(HBP:AβOs) decreases act(a(GO:synapse)) View Subject | View Object

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

Appears in Networks:

a(HBP:AβOs) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190

Appears in Networks:

a(HBP:AβOs) decreases bp(GO:learning) View Subject | View Object

Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190

Appears in Networks:

a(HBP:AβOs) decreases bp(GO:memory) View Subject | View Object

Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190

Appears in Networks:

a(HBP:AβOs) increases bp(GO:"long-term synaptic depression") View Subject | View Object

They also facilitate long-term depression by, among other effects, disrupting synaptic glutamate uptake (Li et al. 2009). PubMed:22908190

Appears in Networks:

a(HBP:AβOs) decreases bp(GO:"L-glutamate import") View Subject | View Object

They also facilitate long-term depression by, among other effects, disrupting synaptic glutamate uptake (Li et al. 2009). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Synapses

a(HBP:AβOs) increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

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

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(HBP:AβOs) increases deg(a(MESH:Neurites)) View Subject | View Object

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

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(HBP:AβOs) decreases act(complex(GO:"proteasome complex")) View Subject | View Object

Moreover, soluble Ab oligomers themselves can inhibit proteasomal activity (Tseng et al. 2008). PubMed:22908190

Appears in Networks:

a(HBP:AβOs) decreases a(MESH:"Dendritic Spines") View Subject | View Object

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

Appears in Networks:

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.