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a(MESH:"Amyloid beta-Peptides")

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Entity

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

Appears in Networks 11

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

Amyloid Precursor Protein Trafficking, Processing, and Function v1.0.0

Amyloid Precursor Protein Trafficking, Processing, and Function by Thinakaran, et al., 2008

Proteolytic processing of Alzeimer's beta-amyloid precursor protein v1.0.1

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

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

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0

Caenorhabditis elegans models of tauopathy v1.0.0

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

In-Edges 19

path(MESH:"Alzheimer Disease") positiveCorrelation a(MESH:"Amyloid beta-Peptides") View Subject | View Object

The histopathological changes in the brain include the presence of extracellular amyloid plaques consisted of various peptide variants of amyloid β (Aβ) and accumulation of intracellular neurofibrillary tangles (NFTs) composed mainly of phosphorylated Tau proteins (pTau), localized predominantly in neurons (reviewed by Serrano-Pozo et al. 2011). PubMed:29196815

Appears in Networks:
Annotations
Confidence
Medium

complex(FPLX:"Gamma_secretase") increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

γ-Secretase cleaves at multiple sites within the transmembrane domain of APP, generating Aβ peptides ranging in length from 38 to 43 residues (4). PubMed:18650430

Appears in Networks:
Annotations
Confidence
Medium

a(HBP:HBP00018) association a(MESH:"Amyloid beta-Peptides") View Subject | View Object

The amyloid plaques associated with AD were first purified and found to consist of multimeric aggregates of Abeta polypeptide containing about 40 amino acid residues in the mid-1980s (Glenner and Wong 1984; Masters et al. 1985) PubMed:22122372

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:APP) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

APP undergoes post-translational proteolysis/processing to generate the hydrophobic beta-amyloid (Abeta) peptides PubMed:22122372

Appears in Networks:
Annotations
Confidence
High

path(MESH:"Alzheimer Disease") association a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Plaques consisting of beta-amyloid (Abeta) peptide (Selkoe 1998), neurofibrillary tangles consisting largely of hyperphosphorylated microtubule-associated tau protein (Buee et al. 2000; Gendron and Petrucelli 2009) and neuron loss in the hippocampus and cortex regions are the major pathological hallmarks of Alzheimer’s disease. PubMed:22122372

Appears in Networks:
Annotations
Confidence
High

rxn(reactants(a(HBP:HBP00081)), products(a(HBP:HBP00071), a(MESH:"Amyloid beta-Peptides"))) hasProduct a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Appears in Networks:

a(MESH:"Amyloid Precursor Protein Secretases") decreases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Moreover, AF267B treatment leads to an increase in alpha secretase, which is an enzyme that can prevent the production of Aβ peptide PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(a(MESH:"Amyloid beta-Peptides"), p(HGNC:ACHE)) hasComponent a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

p(HGNC:APP) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

The plaques in AD are rich in amyloid beta peptides (Abeta) that are produced by proteolytic cleavage of the amyloid precursor peptide (APP), a glycolipid located in the outer cell membrane PubMed:14556719

Appears in Networks:

path(MESH:"Plaque, Amyloid") association a(MESH:"Amyloid beta-Peptides") View Subject | View Object

The plaques in AD are rich in amyloid beta peptides (Abeta) that are produced by proteolytic cleavage of the amyloid precursor peptide (APP), a glycolipid located in the outer cell membrane PubMed:14556719

Appears in Networks:

rxn(reactants(p(HGNC:APP)), products(a(MESH:"Amyloid beta-Peptides"))) hasProduct a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Appears in Networks:

a(CHEBI:cholesterol) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Cellular cholesterol can directly impact the level of Aβ, as decreases in cholesterol levels inhibit the generation of Aβ peptides through direct modulation of γ-secretase activity [78,79]. PubMed:29758300

Appears in Networks:

p(HGNC:APP) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Aβ peptides originate from the transmembrane protein amyloid precursor protein (APP) which undergoes sequential cleavage via two distinct pathways by the enzyme complexes β- and γ-secretase [31] PubMed:29758300

Appears in Networks:

p(HGNC:BECN1) decreases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

In line with this, reduced Beclin 1 levels, as seen in AD models [16], increase the levels of intracellular and extracellular Aβ peptides, supporting the role of macroautophagy in the generation and degradation of Aβ [33,35]. PubMed:29758300

Appears in Networks:

bp(GO:"lysosomal protein catabolic process") increases deg(a(MESH:"Amyloid beta-Peptides")) View Subject | View Object

AVs are also enriched in APP substrates and secretases and, during autophagy, Ab peptide is generated from APP (Yu et al. 2005), although it is subsequently degraded in lysosomes under normal circumstances (Heinrich et al. 1999; Bahr et al. 2002; Florez-McClure et al. 2007). PubMed:22908190

Appears in Networks:

p(HGNC:TNF) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Tumor necrosis factor-α (TNFα) has been shown to induce BACE-1 expression and to contribute to brain accumulation of Aβ peptides PubMed:25331948

Appears in Networks:
Annotations
MeSH
Brain

composite(a(MESH:"Amyloid beta-Peptides"), a(PUBCHEM:160718443)) hasComponent a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Appears in Networks:

act(complex(GO:"NF-kappaB complex")) decreases act(a(MESH:"Amyloid beta-Peptides")) View Subject | View Object

NF-κB activity abrogates Amyloid-β peptide-induced toxicity in dissociated hippocampal cultures from C57Bl/6 mice PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 6

a(MESH:"Amyloid beta-Peptides") positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

The histopathological changes in the brain include the presence of extracellular amyloid plaques consisted of various peptide variants of amyloid β (Aβ) and accumulation of intracellular neurofibrillary tangles (NFTs) composed mainly of phosphorylated Tau proteins (pTau), localized predominantly in neurons (reviewed by Serrano-Pozo et al. 2011). PubMed:29196815

Appears in Networks:
Annotations
Confidence
Medium

a(MESH:"Amyloid beta-Peptides") increases bp(GO:"cell adhesion") View Subject | View Object

Interestingly, because the RHDS sequence is contained within the N terminus of Aβ, similar cell adhesion-promoting properties have also been attributed to the Aβ peptide itself. PubMed:18650430

Appears in Networks:
Annotations
Confidence
Medium

a(MESH:"Amyloid beta-Peptides") association path(MESH:"Alzheimer Disease") View Subject | View Object

Plaques consisting of beta-amyloid (Abeta) peptide (Selkoe 1998), neurofibrillary tangles consisting largely of hyperphosphorylated microtubule-associated tau protein (Buee et al. 2000; Gendron and Petrucelli 2009) and neuron loss in the hippocampus and cortex regions are the major pathological hallmarks of Alzheimer’s disease. PubMed:22122372

Appears in Networks:
Annotations
Confidence
High

a(MESH:"Amyloid beta-Peptides") association a(HBP:HBP00018) View Subject | View Object

The amyloid plaques associated with AD were first purified and found to consist of multimeric aggregates of Abeta polypeptide containing about 40 amino acid residues in the mid-1980s (Glenner and Wong 1984; Masters et al. 1985) PubMed:22122372

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(MESH:"Amyloid beta-Peptides") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

a(MESH:"Amyloid beta-Peptides") association path(MESH:"Plaque, Amyloid") View Subject | View Object

The plaques in AD are rich in amyloid beta peptides (Abeta) that are produced by proteolytic cleavage of the amyloid precursor peptide (APP), a glycolipid located in the outer cell membrane PubMed:14556719

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.