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bp(GO:behavior)

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Entity

Name
behavior
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 8

Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer's disease and schizophrenia. v1.0.0

This file encodes the article Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer’s disease and schizophrenia by Choi et al, 2014

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

The role of inflammasome in Alzheimer’s disease v1.0.3

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

The autism/neuroprotection-linked ADNP/NAP regulate the excitatory glutamatergic synapse v1.0.0

In-Edges 11

bp(GO:"synaptic transmission, cholinergic") association bp(GO:behavior) View Subject | View Object

1 Several lines of evidence suggest that impaired cholinergic signaling plays a key role in mediating both the cognitive and the behavioral impairments observed in AD patients.12 The basal forebrain cholinergic system is disproportionately affected in AD patients, with a robust loss of cholinergic neurons, including those innervating the hippocampus and cortex. PubMed:24511233

Appears in Networks:

path(MESH:Schizophrenia) association bp(GO:behavior) View Subject | View Object

Psychosis is the hallmark symptom of SZ and manifests as hallucinations, disordered thought/speech, and delusions. While these psychotic symptoms are commonly associated with SZ, it has become well documented that these patients also experience cognitive and behavioral disturbances that are not adequately addressed by currently prescribed typical and atypical psychotics. PubMed:24511233

Appears in Networks:

a(CHEBI:bexarotene) increases bp(GO:behavior) View Subject | View Object

Bexarotene is a highly specific RXR agonist and is currently FDA approved with a favorable side effect profile. Studies in our laboratory have shown that treatment of APP/ PS1 animals with bexarotene for only 3 days results in a dramatic induction of ApoE and ABCA1 and the rapid reversal of AD-associated pathological hallmarks including reduction in amyloid deposition and deficits in behavior as well as neural networks. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:pioglitazone) increases bp(GO:behavior) View Subject | View Object

Furthermore, the treatment of APP/PS1 mouse model of AD with pioglitazone (80 mg/kg/day) for 9 days lowered plaque burden by ~ 50% and reversed behavioral deficits in contextual fear conditioning assay. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:rosiglitazone) increases bp(GO:behavior) View Subject | View Object

Pedersen and Flynn examined the effects of rosiglitazone and found that activation of PPAR-g ameliorated behavioral deficits in the Tg2576 AD mouse model. However, these animals displayed no changes in plaque pathology, but had reduced brain Ab42 levels. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

p(HGNC:MAPT) association bp(GO:behavior) View Subject | View Object

While evidence has linked FTD with parkinsonism in patients to tau mutations on chromosome 17 (FTDP-17), implying that tau dysfunction alone can cause neurodegeneration (Reed et al., 2001), studies in animal models have shown that overexpression of tau can lead to cell death (Lee et al., 2001; Tanemura et al., 2001, 2002; Tatebayashi et al., 2002) and exhibit behavioral abnormalities and synaptic dysfunction without the presence of NFTs (Wittmann et al., 2001; Andorfer et al., 2003; Santacruz et al., 2005; Spires et al., 2006; Berger et al., 2007; Yoshiyama et al., 2007; Cowan et al., 2010) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex

p(HGNC:MME) increases bp(GO:behavior) View Subject | View Object

And in APP transgenic mice, long-term gene therapy of NEP ameliorates behavior by lowering the levels of Aβ (Spencer et al. 2008) PubMed:29626319

Appears in Networks:

g(HGNC:NLRP3) decreases bp(GO:behavior) View Subject | View Object

Deficiency of the NLRP3 gene reduces Aβ deposition and plays a protective role on memory and behavior (Heneka et al.,2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph

complex(GO:"NF-kappaB complex") regulates bp(GO:behavior) View Subject | View Object

Given the indispensable role of NF-κB proteins in synaptic transmission and synaptic plasticity, it is not surprising that NF-κB is plays an indispensable role in cognition and behavior as well PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:sirolimus) increases bp(GO:behavior) View Subject | View Object

This is further supported by mounting evidence obtained in rodent models, which demonstrate that rapamycin normalizes impaired social interactions and reverses behavioral defects PubMed:30061532

Appears in Networks:

a(PUBCHEM:9832404) causesNoChange bp(GO:behavior) View Subject | View Object

We have previously shown essentially no significant NAP effects on behavior in the Adnp+/+ mice PubMed:30664622

Appears in Networks:

Out-Edges 3

bp(GO:behavior) association path(MESH:Schizophrenia) View Subject | View Object

Psychosis is the hallmark symptom of SZ and manifests as hallucinations, disordered thought/speech, and delusions. While these psychotic symptoms are commonly associated with SZ, it has become well documented that these patients also experience cognitive and behavioral disturbances that are not adequately addressed by currently prescribed typical and atypical psychotics. PubMed:24511233

Appears in Networks:

bp(GO:behavior) association bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

1 Several lines of evidence suggest that impaired cholinergic signaling plays a key role in mediating both the cognitive and the behavioral impairments observed in AD patients.12 The basal forebrain cholinergic system is disproportionately affected in AD patients, with a robust loss of cholinergic neurons, including those innervating the hippocampus and cortex. PubMed:24511233

Appears in Networks:

bp(GO:behavior) association p(HGNC:MAPT) View Subject | View Object

While evidence has linked FTD with parkinsonism in patients to tau mutations on chromosome 17 (FTDP-17), implying that tau dysfunction alone can cause neurodegeneration (Reed et al., 2001), studies in animal models have shown that overexpression of tau can lead to cell death (Lee et al., 2001; Tanemura et al., 2001, 2002; Tatebayashi et al., 2002) and exhibit behavioral abnormalities and synaptic dysfunction without the presence of NFTs (Wittmann et al., 2001; Andorfer et al., 2003; Santacruz et al., 2005; Spires et al., 2006; Berger et al., 2007; Yoshiyama et al., 2007; Cowan et al., 2010) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex

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.