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a(MESH:Synapses)

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Entity

Name
Synapses
Namespace
mesh
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/mesh-names.belns

Appears in Networks 3

Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

In-Edges 7

a(HBP:HBP00074) decreases a(MESH:Synapses) View Subject | View Object

Moreover, it was postulated that AβOs may trigger a harmful cascade damaging neurons and synapses (Morris et al. 2014). PubMed:29196815

Appears in Networks:
Annotations
Confidence
High

a(HBP:HBP00074) decreases a(MESH:Synapses) View Subject | View Object

In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High

a(HBP:HBP00074) decreases a(MESH:Synapses) View Subject | View Object

These results are in line with findings of Koffie et al. (2009), who revealed that AβOs surrounding plaques contribute to synapse loss in a mouse model of AD. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High

act(p(HGNC:GRIN1)) decreases a(MESH:Synapses) View Subject | View Object

Excessive activation of NMDAR by soluble AβOs triggers disproportionate influx of Ca2+ into neurons, which leads to excitotoxicity, mitochondrial dysfunction, and loss of synapses (Zhao et al. 2004). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
Medium

a(CHEBI:"amyloid-beta") decreases a(MESH:Synapses) View Subject | View Object

Although excessive Abeta causes synaptic dysfunction and synapse loss [142], low levels of Abeta increase hippocampal longterm potentiation and enhances memory, indicating a novel positive, modulatory role on neurotransmission and memory [158,159] PubMed:21214928

Appears in Networks:
Annotations
MeSH
Endosomes
Confidence
High
MeSH
Neurons
MeSH
Down Syndrome

a(CHEBI:"amyloid-beta") decreases a(MESH:Synapses) View Subject | View Object

It has long been known that cognitive decline in AD correlates well with synaptic loss (Lue et al., 1999), and it has been shown directly that soluble Abeta inhibits synaptic plasticity (Rowan et al., 2004). PubMed:19293145

Appears in Networks:

p(FPLX:PI3K) increases act(a(MESH:Synapses)) View Subject | View Object

For instance, over-expressing PI3K in Drosophila melanogaster neurons in situ results in an increase in functional synapses as well as synaptic sprouting (Martín-Pen˜ a et al., 2006). Thus it is possible that nicotine’s activation of the PI3K pathway results in increased synaptic stability, and it would be of interest to explore this further in vertebrates. Thus, the evidence suggests that activation of nAChRs activates the PI3K/AKT pathway to favor antiapoptotic pathways and possibly induce synaptogenesis. PubMed:19293145

Appears in Networks:

Out-Edges 1

a(MESH:Synapses) increases bp(GO:cognition) View Subject | View Object

It has long been known that cognitive decline in AD correlates well with synaptic loss (Lue et al., 1999), and it has been shown directly that soluble Abeta inhibits synaptic plasticity (Rowan et al., 2004). PubMed:19293145

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.