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bp(GO:aging)

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Entity

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

Appears in Networks 24

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

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

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus 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

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Interplay of pathogenic forms of human tau with different autophagic pathways v1.0.1

Molecular chaperones and regulation of tau quality control: strategies for drug discovery in tauopathies v1.0.0

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

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

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

Phosphatase: PP2A structural importance, regulation and its aberrant expression in cancer v1.0.0

Tau interactome mapping based identification of Otub1 as Tau deubiquitinase involved in accumulation of pathological Tau forms in vitro and in vivo v1.0.0

Model systems of protein-misfolding diseases reveal chaperone modifiers of proteotoxicity v1.0.0

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

Molecular Chaperone Functions in Protein Folding and Proteostasis v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.0

Caenorhabditis elegans models of tauopathy v1.0.0

Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0

Tau in physiology and pathology v1.0.0

Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 27

act(a(MESH:"Lymphatic Vessels")) negativeCorrelation bp(GO:aging) View Subject | View Object

The reported findings that ageing is also associated with peripheral lymphatic dysfunction led us to hypothesize that the deterioration of meningeal lymphatic vessels underlies some aspects of age-associated cognitive decline PubMed:30046111

Appears in Networks:
Annotations
Confidence
High

bp(GO:"extracellular matrix organization") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:"cell adhesion") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:"endothelial tube morphogenesis") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:"immune response") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:"inflammatory response") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:"phospholipid metabolic process") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

path(MESH:Dementia) association bp(GO:aging) View Subject | View Object

Dementia is a debilitating condition frequent in ageing populations, and Alzheimer's Disease (AD) accounts for 70% of all dementia cases. AD is characterized by neuropathological hallmarks consisting of an accumulation of Amyloid beta peptide (Ab) in extracellular plaques, intracellular deposits of tau protein, neuronal loss and, more recently, a prominent synaptic loss was identified (Braak and Braak,1991; Masliah et al., 2001; Selkoe,1991; Spires-Jones and Hyman, 2014) PubMed:25514383

Appears in Networks:

p(MGI:Chrna7) association bp(GO:aging) View Subject | View Object

However, we identify a possible role of the alpha7 subunit in the normal aging process that should be further investigated PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

a(HBP:"alpha-4-containing nAChR") negativeCorrelation bp(GO:aging) View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Brain

a(HBP:"alpha-7-containing nAChR") negativeCorrelation bp(GO:aging) View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Brain

complex(a(CHEBI:epibatidine), p(FPLX:CHRN)) negativeCorrelation bp(GO:aging) View Subject | View Object

A significant decrease in [3H]epibatidine binding has been observed with aging in the human cortical brain regions and cerebellum (Marutle et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebellum
MeSH
Cerebral Cortex

complex(a(CHEBI:epibatidine), p(FPLX:CHRN)) negativeCorrelation bp(GO:aging) View Subject | View Object

In addition, a marked reduction in the laminar distribution of [3H]epibatidine binding was observed in control cortical tissue with aging (Figure 1) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") negativeCorrelation bp(GO:aging) View Subject | View Object

Lindquist and colleagues proposed that inhibition of UPS, which can be caused by ageing or following a pharmacological treatment, can lead to accumulation of PrPc in the cytoplasm where it is spontaneously converted into a PrPsc-like species because it is not rapidly degraded by the UPS (Hooper, 2003; Ma and Lindquist,2002;Ma et al., 2002). PubMed:14556719

Appears in Networks:

act(complex(GO:"proteasome complex")) negativeCorrelation bp(GO:aging) View Subject | View Object

The proteasome activity in the mammalian brain decreases with increasing age (Keller et al., 2002), suggesting that the aged brain is less able to handle the aberrantly folded Abeta PubMed:14556719

Appears in Networks:
Annotations
MeSH
Brain

deg(p(HGNC:MAPT)) negativeCorrelation bp(GO:aging) View Subject | View Object

Interestingly, tau clearance is known to be impaired in the aging brain [45], supporting the idea that diminished quality control might be conducive to certain tauopathies, such as AD, which are linked to aging PubMed:21882945

Appears in Networks:

p(HGNC:FKBP5) positiveCorrelation bp(GO:aging) View Subject | View Object

In relation to tau biology, FKBP51 enhances the association of Hsp90 with tau, co-localizes with tau in murine neurons, coimmunoprecipitates with tau in AD tissue samples and increases with age in an AD mouse model [136]. PubMed:21882945

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") positiveCorrelation bp(GO:aging) View Subject | View Object

Meanwhile, an animal experiment showed that IDE expression will descend with age and diabetes, then resulting in Aβ deposition (Kochkina et al. 2015) PubMed:29626319

Appears in Networks:

p(HGNC:IDE) negativeCorrelation bp(GO:aging) View Subject | View Object

Meanwhile, an animal experiment showed that IDE expression will descend with age and diabetes, then resulting in Aβ deposition (Kochkina et al. 2015) PubMed:29626319

Appears in Networks:

p(HGNC:AGER) negativeCorrelation bp(GO:aging) View Subject | View Object

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

Appears in Networks:
Annotations
Uberon
blood plasma

path(MESH:"Alzheimer Disease") positiveCorrelation bp(GO:aging) View Subject | View Object

Aging, another risk factor of AD, has been found to activate the NLRP1 inflammasome and upregulate IL-18 and IL-1β levels in the hippocampus of aged mice (Mawhinney et al., 2011) PubMed:24561250

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Hippocampus
NeuroMMSigDB
Interleukin signaling subgraph

act(complex(GO:"proteasome complex")) negativeCorrelation bp(GO:aging) View Subject | View Object

AD is the most common of numerous age-associated brain diseases, and the activity of brain proteasomes appears to decline with age (Keller et al. 2002). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(complex(GO:"proteasome complex")) negativeCorrelation bp(GO:aging) View Subject | View Object

Beyond an age-related reduction (Keller et al. 2002), proteasome activities decrease in AD in a brain region–specific manner, particularly in hippocampus, parahippocampal gyrus, superior and middle temporal gyri, and the inferior parietal lobule (Keller et al. 2000), areas that are especially critical for long-term memory formation. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Parahippocampal Gyrus
MeSH
Parietal Lobe
MeSH
Temporal Lobe
MeSH
Alzheimer Disease

bp(GO:"protein oxidation") association bp(GO:aging) View Subject | View Object

Proteome oxidation and instability has been associated with ageing and the progression of several age-related diseases, including cardiovascular disorders, neu- rodegeneration, and cancer [7,95,96]. PubMed:24563850

Appears in Networks:

bp(HBP:"non-enzymatic protein modification") positiveCorrelation bp(GO:aging) View Subject | View Object

Proteome is modified post-translationally by either numerous highly regulated enzymatic protein modifications (EPMs) (e.g. phosphorylation, acetylation, ubiquitination, methylation, etc.) or by non-enzymatic protein modifications (NEPMs), which are mostly stochastic and increase with ageing or in age-related diseases (Fig. 1). PubMed:24563850

Appears in Networks:

a(HBP:"Tau aggregates") positiveCorrelation bp(GO:aging) View Subject | View Object

However, tau aggregates are also observed in the brains of some aged individuals with a condition known as primary age-related tauopathy (PART) PubMed:26631930

Appears in Networks:
Annotations
MeSH
Brain

path(MESH:"Osteoarthritis, Knee") positiveCorrelation bp(GO:aging) View Subject | View Object

Obesity, genetic factors, and aging are some of the most prominent risk factors (Sharma et al., 2006), and in the younger population, previous knee injury is an important contributor to increased prevalence of knee OA – as much as half of those sustaining a knee injury in their 20s had developed posttraumatic knee OA in the following 12 to 14 years (Lohmander et al., 2004, 2007; von Porat et al., 2004). PubMed:30505280

Appears in Networks:
Annotations
Text Location
Introduction

Out-Edges 61

bp(GO:aging) decreases bp(GO:"cerebrospinal fluid circulation") View Subject | View Object

The ageing-associated decrease in paravascular recirculation of CSF and ISF is thought to be responsible, at least in part, for the accumulation of amyloid-β in the brain parenchyma PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Parenchymal Tissue

bp(GO:aging) decreases act(a(HP:"interstitial fluid")) View Subject | View Object

The ageing-associated decrease in paravascular recirculation of CSF and ISF is thought to be responsible, at least in part, for the accumulation of amyloid-β in the brain parenchyma PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Parenchymal Tissue

bp(GO:aging) increases a(CHEBI:"amyloid-beta") View Subject | View Object

The ageing-associated decrease in paravascular recirculation of CSF and ISF is thought to be responsible, at least in part, for the accumulation of amyloid-β in the brain parenchyma PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Parenchymal Tissue

bp(GO:aging) decreases act(a(MESH:"Lymphatic Vessels")) View Subject | View Object

Ageing also leads to progressive lymphatic vessel dysfunction in peripheral tissues PubMed:30046111

Appears in Networks:
Annotations
Confidence
High

bp(GO:aging) negativeCorrelation act(a(MESH:"Lymphatic Vessels")) View Subject | View Object

The reported findings that ageing is also associated with peripheral lymphatic dysfunction led us to hypothesize that the deterioration of meningeal lymphatic vessels underlies some aspects of age-associated cognitive decline PubMed:30046111

Appears in Networks:
Annotations
Confidence
High

bp(GO:aging) decreases tloc(a(CHEBI:macromolecule), fromLoc(GO:"extracellular space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

Indeed, and in agreement with a previous study, old mice demonstrate reduced brain perfusion by CSF macromolecules compared to young counterparts (Extended Data Fig. 6a, b) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebrospinal Fluid

bp(GO:aging) association bp(GO:"immune response") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) association bp(GO:"inflammatory response") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) association bp(GO:"phospholipid metabolic process") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) association bp(GO:"extracellular matrix organization") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) association bp(GO:"cell adhesion") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) association bp(GO:"endothelial tube morphogenesis") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) decreases p(MGI:Cdk5r1) View Subject | View Object

The altered expression of genes involved in the transmembrane receptor protein tyrosine kinase signalling pathway in old mice, namely the downregulation of Cdk5r1, Adamts3 and Fgfr3, indicated possible changes in signalling by lymphangiogenic growth factors in old meningeal LECs (Fig. 2d) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) decreases p(MGI:Adamts3) View Subject | View Object

The altered expression of genes involved in the transmembrane receptor protein tyrosine kinase signalling pathway in old mice, namely the downregulation of Cdk5r1, Adamts3 and Fgfr3, indicated possible changes in signalling by lymphangiogenic growth factors in old meningeal LECs (Fig. 2d) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) decreases p(MGI:Fgfr3) View Subject | View Object

The altered expression of genes involved in the transmembrane receptor protein tyrosine kinase signalling pathway in old mice, namely the downregulation of Cdk5r1, Adamts3 and Fgfr3, indicated possible changes in signalling by lymphangiogenic growth factors in old meningeal LECs (Fig. 2d) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:aging) increases a(HBP:HBP00074) View Subject | View Object

An exponential increase of brain levels of AβOs in aging mice was observed. PubMed:29196815

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

bp(GO:aging) increases path(MESH:"Alzheimer Disease") View Subject | View Object

The risk factors of AD include: increasing age, vascular factors such as smoking, obesity, and diabetes (Reitz and Mayeux 2014) as well as genetic mutations. PubMed:29196815

Appears in Networks:
Annotations
Confidence
High

bp(GO:aging) association path(MESH:Dementia) View Subject | View Object

Dementia is a debilitating condition frequent in ageing populations, and Alzheimer's Disease (AD) accounts for 70% of all dementia cases. AD is characterized by neuropathological hallmarks consisting of an accumulation of Amyloid beta peptide (Ab) in extracellular plaques, intracellular deposits of tau protein, neuronal loss and, more recently, a prominent synaptic loss was identified (Braak and Braak,1991; Masliah et al., 2001; Selkoe,1991; Spires-Jones and Hyman, 2014) PubMed:25514383

Appears in Networks:

bp(GO:aging) association p(MGI:Chrna7) View Subject | View Object

However, we identify a possible role of the alpha7 subunit in the normal aging process that should be further investigated PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

bp(GO:aging) causesNoChange r(HGNC:CHRNA3) View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Brain

bp(GO:aging) negativeCorrelation a(HBP:"alpha-4-containing nAChR") View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Brain

bp(GO:aging) negativeCorrelation complex(a(CHEBI:epibatidine), p(FPLX:CHRN)) View Subject | View Object

In addition, a marked reduction in the laminar distribution of [3H]epibatidine binding was observed in control cortical tissue with aging (Figure 1) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

bp(GO:aging) negativeCorrelation complex(a(CHEBI:epibatidine), p(FPLX:CHRN)) View Subject | View Object

A significant decrease in [3H]epibatidine binding has been observed with aging in the human cortical brain regions and cerebellum (Marutle et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebellum
MeSH
Cerebral Cortex

bp(GO:aging) negativeCorrelation a(HBP:"alpha-7-containing nAChR") View Subject | View Object

The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Brain

bp(GO:aging) negativeCorrelation act(complex(GO:"proteasome complex")) View Subject | View Object

The proteasome activity in the mammalian brain decreases with increasing age (Keller et al., 2002), suggesting that the aged brain is less able to handle the aberrantly folded Abeta PubMed:14556719

Appears in Networks:
Annotations
MeSH
Brain

bp(GO:aging) negativeCorrelation bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") View Subject | View Object

Lindquist and colleagues proposed that inhibition of UPS, which can be caused by ageing or following a pharmacological treatment, can lead to accumulation of PrPc in the cytoplasm where it is spontaneously converted into a PrPsc-like species because it is not rapidly degraded by the UPS (Hooper, 2003; Ma and Lindquist,2002;Ma et al., 2002). PubMed:14556719

Appears in Networks:

bp(GO:aging) increases p(HGNC:PRNP) View Subject | View Object

Lindquist and colleagues proposed that inhibition of UPS, which can be caused by ageing or following a pharmacological treatment, can lead to accumulation of PrPc in the cytoplasm where it is spontaneously converted into a PrPsc-like species because it is not rapidly degraded by the UPS (Hooper, 2003; Ma and Lindquist,2002;Ma et al., 2002). PubMed:14556719

Appears in Networks:

bp(GO:aging) decreases act(p(HGNC:SIRT1)) View Subject | View Object

Activity of the deacetylase SIRT1 declines with age, partially owing to limited availability of its co fac- tor, nicotinamide 24,56,156 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

bp(GO:aging) decreases a(CHEBI:"NAD(+)") View Subject | View Object

Activity of the deacetylase SIRT1 declines with age, partially owing to limited availability of its co fac- tor, nicotinamide 24,56,156 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

bp(GO:aging) increases path(MESH:"Proteostasis Deficiencies") View Subject | View Object

Loss of neuronal proteostasis, a common feature of the aging brain, is accelerated in neurodegenerative disorders, including different types of tauopathies PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

bp(GO:aging) increases path(MESH:"Proteostasis Deficiencies") View Subject | View Object

It is well accepted that loss of proteostasis occurs gradually with age and underlies the basis of severe neurodegenerative disorders such as Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and other types of frontotemporal dementia (Prahlad & Morimoto, 2009; Voisine et al., 2010; Morimoto & Cuervo, 2014) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

bp(GO:aging) negativeCorrelation deg(p(HGNC:MAPT)) View Subject | View Object

Interestingly, tau clearance is known to be impaired in the aging brain [45], supporting the idea that diminished quality control might be conducive to certain tauopathies, such as AD, which are linked to aging PubMed:21882945

Appears in Networks:

bp(GO:aging) positiveCorrelation p(HGNC:FKBP5) View Subject | View Object

In relation to tau biology, FKBP51 enhances the association of Hsp90 with tau, co-localizes with tau in murine neurons, coimmunoprecipitates with tau in AD tissue samples and increases with age in an AD mouse model [136]. PubMed:21882945

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:aging) negativeCorrelation p(HGNC:IDE) View Subject | View Object

Meanwhile, an animal experiment showed that IDE expression will descend with age and diabetes, then resulting in Aβ deposition (Kochkina et al. 2015) PubMed:29626319

Appears in Networks:

bp(GO:aging) positiveCorrelation a(CHEBI:"amyloid-beta") View Subject | View Object

Meanwhile, an animal experiment showed that IDE expression will descend with age and diabetes, then resulting in Aβ deposition (Kochkina et al. 2015) PubMed:29626319

Appears in Networks:

bp(GO:aging) negativeCorrelation p(HGNC:AGER) View Subject | View Object

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

Appears in Networks:
Annotations
Uberon
blood plasma

bp(GO:aging) increases p(RGD:Ptpn1) View Subject | View Object

Interestingly, the middle-aged rats have higher levels of PTP-1B, lower phosphorylation of IRS-1, Akt, GSK3β, mTOR, and TrkB. Also, the aging process increased Tau phosphorylation and β-amyloid content in the hippocampus region. In summary, this study provides new evidence that aging-related PTP1B increasing, contributing to insulin resistance and the onset of the AD. PubMed:29421605

Appears in Networks:

bp(GO:aging) increases p(HGNC:PPP2R2C) View Subject | View Object

It is observed that the expression of B55 γ increases and B55 β decreases gradually after birth and are developmentally regulated [28]. PubMed:23454242

Appears in Networks:

bp(GO:aging) decreases p(HGNC:PPP2R2B) View Subject | View Object

It is observed that the expression of B55 γ increases and B55 β decreases gradually after birth and are developmentally regulated [28]. PubMed:23454242

Appears in Networks:

bp(GO:aging) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Aging, another risk factor of AD, has been found to activate the NLRP1 inflammasome and upregulate IL-18 and IL-1β levels in the hippocampus of aged mice (Mawhinney et al., 2011) PubMed:24561250

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Hippocampus
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:aging) increases act(complex(GO:"NLRP1 inflammasome complex")) View Subject | View Object

Aging, another risk factor of AD, has been found to activate the NLRP1 inflammasome and upregulate IL-18 and IL-1β levels in the hippocampus of aged mice (Mawhinney et al., 2011) PubMed:24561250

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Hippocampus
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:aging) increases p(HGNC:IL1B) View Subject | View Object

Aging, another risk factor of AD, has been found to activate the NLRP1 inflammasome and upregulate IL-18 and IL-1β levels in the hippocampus of aged mice (Mawhinney et al., 2011) PubMed:24561250

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Hippocampus
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:aging) increases p(HGNC:IL18) View Subject | View Object

Aging, another risk factor of AD, has been found to activate the NLRP1 inflammasome and upregulate IL-18 and IL-1β levels in the hippocampus of aged mice (Mawhinney et al., 2011) PubMed:24561250

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Hippocampus
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:aging) increases p(MGI:Otub1) View Subject | View Object

Furthermore, analysis of hippocampal gene expression in aging mice, using publicly available data (NCBI database GDS2082) [73], indicates a significant increase in Otub1 expression with aging (Fig. S4b). PubMed:28083634

Appears in Networks:
Annotations
MeSH
Hippocampus

bp(GO:aging) decreases p(HGNCGENEFAMILY:"DNAJ (HSP40) heat shock proteins") View Subject | View Object

The HSP70 and HSP40 family members exhibit significantly altered expression dynamics during aging in the human brain, both being consistently repressed with age (Brehme et al., 2014). PubMed:27491084

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bp(GO:aging) decreases p(FPLX:HSPA) View Subject | View Object

The HSP70 and HSP40 family members exhibit significantly altered expression dynamics during aging in the human brain, both being consistently repressed with age (Brehme et al., 2014). PubMed:27491084

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bp(GO:aging) increases p(FPLX:HSPB) View Subject | View Object

Furthermore, sHSPs were found to be consistently upregulated in the aging human brain and in the context of neurodegenerative diseases (Brehme et al., 2014). PubMed:27491084

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MeSH
Brain

bp(GO:aging) negativeCorrelation act(complex(GO:"proteasome complex")) View Subject | View Object

AD is the most common of numerous age-associated brain diseases, and the activity of brain proteasomes appears to decline with age (Keller et al. 2002). PubMed:22908190

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MeSH
Alzheimer Disease

bp(GO:aging) negativeCorrelation act(complex(GO:"proteasome complex")) View Subject | View Object

Beyond an age-related reduction (Keller et al. 2002), proteasome activities decrease in AD in a brain region–specific manner, particularly in hippocampus, parahippocampal gyrus, superior and middle temporal gyri, and the inferior parietal lobule (Keller et al. 2000), areas that are especially critical for long-term memory formation. PubMed:22908190

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MeSH
Parahippocampal Gyrus
MeSH
Parietal Lobe
MeSH
Temporal Lobe
MeSH
Alzheimer Disease

bp(GO:aging) decreases bp(HBP:Proteostasis) View Subject | View Object

Indeed, studies using model organisms demonstrate that a gradual decline in cellular proteostasis capacity occurs with aging (10). PubMed:23746257

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bp(GO:aging) decreases bp(HBP:Proteostasis) View Subject | View Object

As shown in Caenorhabditis elegans, Drosophila, and the mouse, the ability of cells and tissues to maintain proteostasis declines during aging, concurrent with the capacity to respond to conformational stresses (214–220). PubMed:23746257

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bp(GO:aging) positiveCorrelation bp(HBP:"non-enzymatic protein modification") View Subject | View Object

Proteome is modified post-translationally by either numerous highly regulated enzymatic protein modifications (EPMs) (e.g. phosphorylation, acetylation, ubiquitination, methylation, etc.) or by non-enzymatic protein modifications (NEPMs), which are mostly stochastic and increase with ageing or in age-related diseases (Fig. 1). PubMed:24563850

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bp(GO:aging) association bp(GO:"protein oxidation") View Subject | View Object

Proteome oxidation and instability has been associated with ageing and the progression of several age-related diseases, including cardiovascular disorders, neu- rodegeneration, and cancer [7,95,96]. PubMed:24563850

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bp(GO:aging) increases p(HGNC:MAPT) View Subject | View Object

At more mature ages (DIV14 - DIV21), MAPT localization is mainly found in the axons with only basal levels in the somatodendritic compartment, consistent with earlier findings [20]. PubMed:30145931

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MeSH
Neurons

bp(GO:aging) decreases p(HGNC:MAPT) View Subject | View Object

At more mature ages (DIV14 - DIV21), MAPT localization is mainly found in the axons with only basal levels in the somatodendritic compartment, consistent with earlier findings [20]. PubMed:30145931

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MeSH
Neurons

bp(GO:aging) decreases bp(GO:locomotion) View Subject | View Object

Three transgenic lines were generated based on 1N4R wild-type MAPT or its FTD-17 mutant variants P301L and V337M. The mutant lines showed a stronger Unc phenotype than the wild-type tau lines and the severity of the Unc phenotype progressed with age PubMed:29191965

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bp(GO:aging) increases a(HBP:"Tau aggregates") View Subject | View Object

Cortical neurons of Tg Tau P301S mice also show an in- crease in tau hyperphosphorylation and pSyk with age (Fig. 7). PubMed:28877763

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Cell Ontology (CL)
cerebral cortex neuron

bp(GO:aging) increases p(HGNC:SYK) View Subject | View Object

In contrast, microscopic fields of older Tg APPsw mice containing A β deposits exhibit a strong increase in pSyk burden (799.95 ± 130.19%) com- pared to age-matched WT mice. PubMed:28877763

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MeSH
Alzheimer Disease

bp(GO:aging) increases p(HGNC:SYK) View Subject | View Object

Cortical neurons of Tg Tau P301S mice also show an in- crease in tau hyperphosphorylation and pSyk with age (Fig. 7). PubMed:28877763

Appears in Networks:
Annotations
Cell Ontology (CL)
cerebral cortex neuron

bp(GO:aging) positiveCorrelation a(HBP:"Tau aggregates") View Subject | View Object

However, tau aggregates are also observed in the brains of some aged individuals with a condition known as primary age-related tauopathy (PART) PubMed:26631930

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MeSH
Brain

bp(GO:aging) positiveCorrelation path(MESH:"Osteoarthritis, Knee") View Subject | View Object

Obesity, genetic factors, and aging are some of the most prominent risk factors (Sharma et al., 2006), and in the younger population, previous knee injury is an important contributor to increased prevalence of knee OA – as much as half of those sustaining a knee injury in their 20s had developed posttraumatic knee OA in the following 12 to 14 years (Lohmander et al., 2004, 2007; von Porat et al., 2004). PubMed:30505280

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Text Location
Introduction

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.