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path(HBP:Neurodegeneration)

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Entity

Name
Neurodegeneration
Namespace
HBP
Namespace Version
20181221
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/bd0996a28201cad363557315043c6392e31abf58/export/hbp-names.belns

Appears in Networks 14

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

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

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

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0

This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al

Anti-aggregant tau mutant promotes neurogenesis v1.0.0

Protein phosphatase 2A dysfunction in Alzheimer’s disease 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

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

Caenorhabditis elegans models of tauopathy v1.0.0

Tau in physiology and pathology v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

Activity-dependent neuroprotective protein deficiency models synaptic and developmental phenotypes of autism-like syndrome v1.0.0

In-Edges 48

a(CHEBI:galanthamine) decreases path(HBP:Neurodegeneration) View Subject | View Object

The nicotinic APL action of galantamine appears to be an important determinant of its clinical effectiveness (reviewed in Refs. 98, 291, 371). Acting primarily as a nicotinic APL, galantamine improves synaptic transmission and decreases neurodegeneration, two effects essential for its cognitive-enhancing properties (40, 108, 241, 409, 521). PubMed:19126755

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p(MGI:Chrnb2) negativeCorrelation path(HBP:Neurodegeneration) View Subject | View Object

The importance of retaining the high-affinity nicotine binding sites to brain integrity has been demonstrated in studies of mice with a null mutation in the gene that encodes the beta2 nAChR subunit, a structural subunit of the high-affinity nicotine binding site (150, 184, 215, 311); these mice experience early onset neurodegeneration (528). PubMed:19126755

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Review

a(CHEBI:"amyloid-beta") causesNoChange path(HBP:Neurodegeneration) View Subject | View Object

APP and APP/presenilin-1 (PS-1) mice do not show neurodegeneration (Irizarry et al., 1997) and yet show several features of AD, including accumulation of plaques and defects in learning (Hsiao et al., 1996), suggesting that many features of AD are not the result of neuronal loss. These animals nonetheless have swollen cholinergic nerve terminals at 12 months, suggesting defective nerve sprouting (Hernandez et al., 2001). PubMed:19293145

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p(HGNC:PSEN1) causesNoChange path(HBP:Neurodegeneration) View Subject | View Object

APP and APP/presenilin-1 (PS-1) mice do not show neurodegeneration (Irizarry et al., 1997) and yet show several features of AD, including accumulation of plaques and defects in learning (Hsiao et al., 1996), suggesting that many features of AD are not the result of neuronal loss. These animals nonetheless have swollen cholinergic nerve terminals at 12 months, suggesting defective nerve sprouting (Hernandez et al., 2001). PubMed:19293145

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path(MESH:"Parkinsonian Disorders") increases path(HBP:Neurodegeneration) View Subject | View Object

Therefore, patients with AR-JP—who cannot degrade it because of the mutation in the Parkin E3 (see above)—develop neurodegeneration PubMed:14556719

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MeSH
Parkinsonian Disorders

act(p(HGNCGENEFAMILY:Calpains)) increases path(HBP:Neurodegeneration) View Subject | View Object

On the one hand, expressing a 17-kDa fragment of tau based on calpain cleavage site mapping in hippocampal neurons led to neurite retraction and the appearance of varicosities after 48 h (52). Additionally, suppressing calpain activity in a fly model of tauopathy prevented neurodegeneration, as did expressing a calpain-resistant form of tau (54). PubMed:24027553

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MeSH
Tauopathies
Text Location
Review

p(MGI:Atg7) decreases path(HBP:Neurodegeneration) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

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MeSH
Neurons
Text Location
Review

p(MGI:Mapt, pmod(Ph)) increases path(HBP:Neurodegeneration) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

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MeSH
Neurons
Text Location
Review

p(MGI:Mapt, var("p.P301L")) association path(HBP:Neurodegeneration) View Subject | View Object

PSA was identified as a potential player in tau pathology through a microarray analysis of gene expression in disease-vulnerable vs. disease-resistant brain regions in JNPL3 mice that overexpress a mutant form of tau (P301L) found in the disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). These mice develop neurodegeneration in the cortex while the cerebellum is relatively spared [although in the original description of these animals pathology was found in the deep cerebellar nuclei (27)]. PubMed:24027553

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MeSH
Cerebral Cortex
Text Location
Review

p(HGNC:MAPT, pmod(Ph)) positiveCorrelation path(HBP:Neurodegeneration) View Subject | View Object

We note that these observed increases in tau phosphorylation occurred well before neuronal death (Fig. 1B), consistent with this pathology representing an early stage in neurodegeneration. PubMed:17403556

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Results

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) increases path(HBP:Neurodegeneration) View Subject | View Object

Thus, pro-aggregant TauRDΔK causes neurodegeneration, whereas anti-aggregant TauRDΔKPP leads to neurogenesis, even in regions outside the DG PubMed:29202785

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a(CHEBI:"okadaic acid") increases path(HBP:Neurodegeneration) View Subject | View Object

In vivo use of phosphatase inhibitors such as okadaic acid has been shown in many studies to induce cognitive impairment and widespread neurotoxic effects that are reminiscent of the hallmark pathological processes occurring in AD pathology, i.e., the accumulation of P-tau, amyloidogenesis, synapse loss and neurodegeneration (Malchiodi-Albedi et al., 1997; Arendt et al., 1998; Sun et al.,2003; Kamat et al.,2013) PubMed:24653673

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sec(a(CHEBI:"amyloid-beta")) decreases path(HBP:Neurodegeneration) View Subject | View Object

This inhibition of Aβ secretion during macroautophagy deficiency results in aberrant cytosolic accumulation of Aβ, which ultimately evokes neurodegeneration accompanied with memory loss. PubMed:29758300

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

Impairment in the UPS is cardinal to the development of neurodegeneration, in part because of its reciprocal interplay with protein aggregation PubMed:29758300

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act(a(GO:endosome)) decreases path(HBP:Neurodegeneration) View Subject | View Object

Beyond influencing Ab generation and toxicity, defective endosome functioning plays a crucial Ab-independent role in the failure of retrograde NGF signaling that leads to basal forebrain cholinergic neuron degeneration in the Ts65Dn mouse model of DS (Cooper et al. 2001; Delcroix et al. 2004). PubMed:22908190

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bp(GO:"lysosomal protein catabolic process") decreases path(HBP:Neurodegeneration) View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

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MeSH
Endosomes

bp(GO:"lysosomal protein catabolic process") decreases path(HBP:Neurodegeneration) View Subject | View Object

A close connection between lysosomal network dysfunction and mechanisms of neurodegeneration is well documented (McCray et al. 2008; Nixon et al. 2008; Bellettato et al. 2010; Cherra et al. 2010). PubMed:22908190

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g(HBP:"APOE e4") increases path(HBP:Neurodegeneration) View Subject | View Object

Expression of the ApoE epsilon 4 allele, but not ApoE epsilon 3, in mice administered a neprilysin inhibitor increases Ab immunoreactivity in lysosomes and causes neurodegeneration of hippocampal CA1, entorhinal,and septal neurons (Belinson et al. 2008). PubMed:22908190

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MeSH
CA1 Region, Hippocampal
MeSH
Neurons

a(CHEBI:"alpha,alpha-trehalose") decreases path(HBP:Neurodegeneration) View Subject | View Object

In addition, inducing autophagy in an TOR-independent manner using lithium [53] or trehalose [54–56] has been shown to accelerate clearance of disease proteins in vitro [56] and protect against neurodegeneration in mouse and Drosophila models of Huntington’s disease [53,54]. PubMed:18930136

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MeSH
Huntington Disease

a(CHEBI:"lithium(1+)") decreases path(HBP:Neurodegeneration) View Subject | View Object

In addition, inducing autophagy in an TOR-independent manner using lithium [53] or trehalose [54–56] has been shown to accelerate clearance of disease proteins in vitro [56] and protect against neurodegeneration in mouse and Drosophila models of Huntington’s disease [53,54]. PubMed:18930136

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MeSH
Huntington Disease

a(GO:autolysosome) decreases path(HBP:Neurodegeneration) View Subject | View Object

CLN3-related neurodegeneration appears to be a consequence of reduced autophagosome-lysosome fusion [42]. PubMed:18930136

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act(a(GO:lysosome)) decreases path(HBP:Neurodegeneration) View Subject | View Object

Indeed, primary lysosomal dysfunction in inherited congenital “lysosomal storage disorders” has long been recognized to cause severe neurodegenerative phenotypes characterized pathologically by accumulations of lysosomes and autophagic vacuoles [38] PubMed:18930136

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bp(GO:"cellular protein catabolic process") negativeCorrelation path(HBP:Neurodegeneration) View Subject | View Object

Considering the importance of protein catabolism in maintaining cell homeostasis, it is not surprising that dysregulation of protein turnover is associated with myriad disease states such as cancer and neurodegeneration [5]. PubMed:18930136

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

Indeed, experimental evidence indicates that neurodegeneration is frequently associated with impaired UPS function, although whether this is a cause or consequence of neurodegeneration is a contested issue, as is reviewed elsewhere in this special issue PubMed:18930136

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bp(GO:autophagy) decreases path(HBP:Neurodegeneration) View Subject | View Object

It is becoming increasingly evident that the autophagy-lysosomal system is essential to neuronal homeostasis, and may in some settings be neuroprotective PubMed:18930136

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bp(GO:autophagy) decreases path(HBP:Neurodegeneration) View Subject | View Object

Similarly, in transgenic mice expressing amyloid precursor protein, a mouse model of Alzheimer’s disease, genetic inhibition of autophagy by heterozygous depletion of beclin-1 results in enhancement of neurodegeneration [51]. PubMed:18930136

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MeSH
Alzheimer Disease

act(complex(GO:"proteasome complex")) decreases path(HBP:Neurodegeneration) View Subject | View Object

There have been fewer efforts to manipulate UPS function for therapeutic benefit in neurodegenerative disease, but it was recently shown that use of a proteasome activator enhanced survival in an in vitro model of Huntington’s disease [58], suggesting that augmenting other routes of protein degradation may also provide neuroprotection. PubMed:18930136

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MeSH
Huntington Disease

p(HGNC:ATG5) decreases path(HBP:Neurodegeneration) View Subject | View Object

As mentioned above, dramatic illustration of the interrelatedness of the UPS and autophagy was provided by characterizations of mice with conditional knockout of the essential autophagy genes Atg5 or Atg7 in the central nervous system, which resulted in neurodegeneration with accumulation of ubiquitin-positive pathology [36,37]. PubMed:18930136

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p(HGNC:ATG7) decreases path(HBP:Neurodegeneration) View Subject | View Object

As mentioned above, dramatic illustration of the interrelatedness of the UPS and autophagy was provided by characterizations of mice with conditional knockout of the essential autophagy genes Atg5 or Atg7 in the central nervous system, which resulted in neurodegeneration with accumulation of ubiquitin-positive pathology [36,37]. PubMed:18930136

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p(HGNC:ATP13A2, var("?")) increases path(HBP:Neurodegeneration) View Subject | View Object

Diseasecausing mutations in ATP13A2 result in protein retention in the endoplasmic reticulum and enhanced proteasomal degradation, suggesting that neurodegeneration could be caused by overwhelming the UPS and/or loss of function in lysosomal protein degradation [39]. PubMed:18930136

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p(HGNC:CTSD) decreases path(HBP:Neurodegeneration) View Subject | View Object

The consequences of impaired lysosome function, for example, may be observed in cathepsin D knockout mice and Drosophila melanogaster cathepsin D mutants which show neurodegeneration and associated accumulation of autophagosomes and lysosomes [33–35]. PubMed:18930136

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a(CHEBI:azaperone) decreases path(HBP:Neurodegeneration) View Subject | View Object

The antipsychotic drug azaperone shows neuroprotective effects, improves locomotion, reduces the insoluble tau, and partially abates the neurodegeneration in this tauopathy model (104). PubMed:29191965

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a(PUBCHEM:66766582) decreases path(HBP:Neurodegeneration) View Subject | View Object

Another compound of the ATPZ class also is protective and partially ameliorates the neurodegeneration in this tauopathy model. PubMed:29191965

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p(HGNC:MAPT, frag("?")) increases path(HBP:Neurodegeneration) View Subject | View Object

In addition, the truncation of tau may result in tau fragments that induce neurodegeneration independently of tau aggregation. PubMed:26631930

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p(HBP:"Tau isoform E (412 aa)", var("p.Val337Met")) increases path(HBP:Neurodegeneration) View Subject | View Object

This worm also shows reduced survival, accumulates detergent-insoluble tau, and undergoes late-onset neurodegeneration (66) PubMed:29191965

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composite(p(HBP:"Tau isoform E (412 aa)", var("p.Val337Met")), p(HGNC:DDC)) increases path(HBP:Neurodegeneration) View Subject | View Object

Loss of bas-1 function improved the motor function, reduced insoluble tau and its phosphorylation and ameliorated the tau-induced neurodegeneration without increasing the longevity in TauV337M worms PubMed:29191965

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composite(p(HBP:"Tau isoform E (412 aa)", var("p.Val337Met")), p(HGNC:ZC3H14)) increases path(HBP:Neurodegeneration) View Subject | View Object

Eliminating sut-2 resulted in partial recovery of Unc phenotype, less neurodegeneration and reduction of insoluble tau in the TauV337M worm; whereas sut-2 overexpression exacerbated the pathology PubMed:29191965

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p(HBP:"Tau isoform E (412 aa)", var("p.Pro301Leu")) increases path(HBP:Neurodegeneration) View Subject | View Object

This worm also shows reduced survival, accumulates detergent-insoluble tau, and undergoes late-onset neurodegeneration (66) PubMed:29191965

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a(HBP:"Tau aggregates") increases path(HBP:Neurodegeneration) View Subject | View Object

In addition, the aggregates may occupy space in the cell and thus directly interfere with axonal transport, leading to neurodegeneration PubMed:26631930

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bp(GO:"axonal transport") decreases path(HBP:Neurodegeneration) View Subject | View Object

In addition, the aggregates may occupy space in the cell and thus directly interfere with axonal transport, leading to neurodegeneration PubMed:26631930

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a(HBP:"Tau oligomers") increases path(HBP:Neurodegeneration) View Subject | View Object

In an analogy to the evolution of concepts in the ‘amyloid cascade hypothesis’, which proposes that soluble oligomers — rather than insoluble aggregates of amyloid peptides — are the causative agents of neurodegeneration in AD, recent studies have suggested tau oligomers to be the toxic species, and indeed levels of SDS-stable tau oligomers are increased in AD and PSP brains. PubMed:26631930

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Annotations
MeSH
Brain

tloc(p(HGNC:MAPT), fromLoc(GO:axon), toLoc(MESH:"Dendritic Spines")) association path(HBP:Neurodegeneration) View Subject | View Object

In human AD brains, the missorting of tau into dendrites represents one of the early signs of neurodegeneration PubMed:26631930

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Annotations
MeSH
Alzheimer Disease

act(p(HGNC:MAPT)) decreases path(HBP:Neurodegeneration) View Subject | View Object

In addition, as tau is involved in multiple novel functions, including iron transport, neurogenesis, LTD and neuronal DNA protection (as discussed above), the loss of function of tau may also lead to neurodegeneration via impairment of these processes. PubMed:26631930

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complex(a(MESH:RNA), p(HGNC:MAPT)) increases path(HBP:Neurodegeneration) View Subject | View Object

Nevertheless, the interaction of tau with RNA may induce tau aggregation and thus contribute to neurodegeneration PubMed:26631930

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p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) increases path(HBP:Neurodegeneration) View Subject | View Object

In a Drosophila melanogaster model of tauopathy, the hyperphosphorylation of tau led to the abnormal alignment and accumulation of F‑actin filaments, and thereby induced neurodegeneration PubMed:26631930

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p(HGNC:MAPT, frag("1_368")) increases path(HBP:Neurodegeneration) View Subject | View Object

The truncation of tau at Asn368 has been observed in human AD brains and in a P301S mouse model of tauopathy, in which it leads to the generation of a tau1–368 fragment that is prone to aggregation and shows compromised microtubule-assembly activity, possibly contributing to tau aggregation and neurodegeneration. PubMed:26631930

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Annotations
MeSH
Brain
MeSH
Alzheimer Disease

act(a(GO:synapse)) association path(HBP:Neurodegeneration) View Subject | View Object

In schizophrenia, a progressive synaptic disorder is likely to promote neurodegeneration PubMed:30061532

Appears in Networks:
Annotations
MeSH
Schizophrenia

p(HGNC:WFS1) association path(HBP:Neurodegeneration) View Subject | View Object

In the 3-month-old hippocampi (Figure 4B), we found significant sex-dependent changes for Adnp+/– gene regulation and NAP rescue in the following genes in male mice: (a) apolipoprotein E (Apoe), the lead gene for Alzheimer’s disease risk, which was shown before to be a major gene regulated by ADNP (10, 13); (b) Gm21949, which is suggested to play a role in calcium-mediated responses, action potential conduction in myelinated cells, and axonal outgrowth and guidance (6); (c) lipase A (Lipa), which is related to lipid metabolism and was previously shown to be regulated by the Adnp genotype in mice (3); (d) autism-associated neuroligin 2 (Nlgn2), a postsynaptic membrane cell adhesion protein that mediates the formation and maintenance of synapses between neurons (12); (e) paired box protein 6 (Pax6), a key regulator in glutamatergic neuronal differentiation (38) and cortical development (39), which was shown before by us to be regulated by ADNP (complete knockout of Adnp rendered Pax6 expression undetectable in the brain primordium, contrasting with increased expression in Adnp+/– embryos [ref. 1] and in subcortical brain domains of 2-month-old male Adnp+/– mice [ref. 3]); and (f) Wolframin endoplasmic reticulum transmembrane glycoprotein (Wfs1), which is associated with neurodegeneration and cellular calcium homeostasis regulation and was previously shown to be regulated by NAP (34). PubMed:30106381

Appears in Networks:
Annotations
MeSH
Hippocampus
Gender
Male

Out-Edges 9

path(HBP:Neurodegeneration) negativeCorrelation p(MGI:Chrnb2) View Subject | View Object

The importance of retaining the high-affinity nicotine binding sites to brain integrity has been demonstrated in studies of mice with a null mutation in the gene that encodes the beta2 nAChR subunit, a structural subunit of the high-affinity nicotine binding site (150, 184, 215, 311); these mice experience early onset neurodegeneration (528). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

path(HBP:Neurodegeneration) association p(MGI:Mapt, var("p.P301L")) View Subject | View Object

PSA was identified as a potential player in tau pathology through a microarray analysis of gene expression in disease-vulnerable vs. disease-resistant brain regions in JNPL3 mice that overexpress a mutant form of tau (P301L) found in the disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). These mice develop neurodegeneration in the cortex while the cerebellum is relatively spared [although in the original description of these animals pathology was found in the deep cerebellar nuclei (27)]. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
Text Location
Review

path(HBP:Neurodegeneration) positiveCorrelation p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

We note that these observed increases in tau phosphorylation occurred well before neuronal death (Fig. 1B), consistent with this pathology representing an early stage in neurodegeneration. PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

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

Impairment in the UPS is cardinal to the development of neurodegeneration, in part because of its reciprocal interplay with protein aggregation PubMed:29758300

Appears in Networks:

path(HBP:Neurodegeneration) negativeCorrelation bp(GO:"cellular protein catabolic process") View Subject | View Object

Considering the importance of protein catabolism in maintaining cell homeostasis, it is not surprising that dysregulation of protein turnover is associated with myriad disease states such as cancer and neurodegeneration [5]. PubMed:18930136

Appears in Networks:

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

Indeed, experimental evidence indicates that neurodegeneration is frequently associated with impaired UPS function, although whether this is a cause or consequence of neurodegeneration is a contested issue, as is reviewed elsewhere in this special issue PubMed:18930136

Appears in Networks:

path(HBP:Neurodegeneration) association tloc(p(HGNC:MAPT), fromLoc(GO:axon), toLoc(MESH:"Dendritic Spines")) View Subject | View Object

In human AD brains, the missorting of tau into dendrites represents one of the early signs of neurodegeneration PubMed:26631930

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(HBP:Neurodegeneration) association act(a(GO:synapse)) View Subject | View Object

In schizophrenia, a progressive synaptic disorder is likely to promote neurodegeneration PubMed:30061532

Appears in Networks:
Annotations
MeSH
Schizophrenia

path(HBP:Neurodegeneration) association p(HGNC:WFS1) View Subject | View Object

In the 3-month-old hippocampi (Figure 4B), we found significant sex-dependent changes for Adnp+/– gene regulation and NAP rescue in the following genes in male mice: (a) apolipoprotein E (Apoe), the lead gene for Alzheimer’s disease risk, which was shown before to be a major gene regulated by ADNP (10, 13); (b) Gm21949, which is suggested to play a role in calcium-mediated responses, action potential conduction in myelinated cells, and axonal outgrowth and guidance (6); (c) lipase A (Lipa), which is related to lipid metabolism and was previously shown to be regulated by the Adnp genotype in mice (3); (d) autism-associated neuroligin 2 (Nlgn2), a postsynaptic membrane cell adhesion protein that mediates the formation and maintenance of synapses between neurons (12); (e) paired box protein 6 (Pax6), a key regulator in glutamatergic neuronal differentiation (38) and cortical development (39), which was shown before by us to be regulated by ADNP (complete knockout of Adnp rendered Pax6 expression undetectable in the brain primordium, contrasting with increased expression in Adnp+/– embryos [ref. 1] and in subcortical brain domains of 2-month-old male Adnp+/– mice [ref. 3]); and (f) Wolframin endoplasmic reticulum transmembrane glycoprotein (Wfs1), which is associated with neurodegeneration and cellular calcium homeostasis regulation and was previously shown to be regulated by NAP (34). PubMed:30106381

Appears in Networks:
Annotations
MeSH
Hippocampus
Gender
Male

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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.