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path(MESH:"Cognitive Dysfunction")

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Entity

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

Appears in Networks 12

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

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

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

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

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0

Neural Systems Governed by Nicotinic Acetylcholine Receptors: Emerging Hypotheses v1.0.0

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

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

TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading v1.0.0

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 27

a(HBP:HBP00074) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

The levels of HMW AβOs in AD or MCI patients were significantly higher than in normal controls and correlated inversely with MMSE score. PubMed:29196815

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

a(HBP:HBP00074) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

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

p(HGNC:NGFR) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

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

a(HBP:"amyloid-beta oligomers") positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

Early work on AD considered the fibrillar form to be the toxic species. However, a lack of correlation between plaque burden and cognitive score contrasted with a strong positive correlation between total soluble amyloid and cognitive decline pointing to soluble, oligomeric forms as the primary toxic factor (Walsh and Selkoe, 2007). PubMed:19293145

Appears in Networks:

path(MESH:"Alzheimer Disease") association path(MESH:"Cognitive Dysfunction") 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:

a(MESH:"Muscarinic Antagonists") increases path(MESH:"Cognitive Dysfunction") View Subject | View Object

Furthermore, administration of nonselective muscarinic antagonists can induce cognitive deficits and psychosis in humans,16,37 indicating that mAChR activation may provide pro-cognitive and antipsychotic efficacy. PubMed:24511233

Appears in Networks:

path(MESH:"Alzheimer Disease") association path(MESH:"Cognitive Dysfunction") View Subject | View Object

Schizophrenia (SZ) and Alzheimer’s disease (AD) are two devastating disorders of the central nervous system (CNS) that present clinically with cognitive impairments and psychotic symptoms PubMed:24511233

Appears in Networks:
Annotations
MeSH
Central Nervous System

path(MESH:"Alzheimer Disease") association path(MESH:"Cognitive Dysfunction") View Subject | View Object

AD is the most commonly diagnosed form of dementia and currently affects approximately 35 million individuals worldwide.7 AD is a progressive neurodegenerative disease that is characterized by a host of cognitive deficits, including impairments in learning and memory. In addition to the well-documented cognitive impairments, AD patients also display behavioral disturbances, including anxiety, depression, and psychosis PubMed:24511233

Appears in Networks:

path(MESH:Schizophrenia) association path(MESH:"Cognitive Dysfunction") View Subject | View Object

Schizophrenia (SZ) and Alzheimer’s disease (AD) are two devastating disorders of the central nervous system (CNS) that present clinically with cognitive impairments and psychotic symptoms PubMed:24511233

Appears in Networks:
Annotations
MeSH
Central Nervous System

a(GO:synapse) negativeCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

It has been demonstrated that cholinergic synapses are particularly affected by Aβ oligomers early neurotoxicity [218, 219] and that synaptic loss is the major correlate of cognitive impairment PubMed:26813123

Appears in Networks:

act(p(HGNC:CHRM1)) association path(MESH:"Cognitive Dysfunction") View Subject | View Object

Interestingly, M1 receptor signaling affects several of AD major hallmarks, including cholinergic deficit, cognitive dysfunction, and tau and Aβ pathologies PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

In addition to cognitive alterations, psychiatric symptoms are frequently observed in AD patients, including apathy and depression PubMed:26813123

Appears in Networks:
Annotations
MeSH
CA3 Region, Hippocampal

a(MESH:VU0357017) decreases path(MESH:"Cognitive Dysfunction") View Subject | View Object

Moreover, VU0184670 potentiates neuronal NMDAR-mediated currents in hippocampal brain slices and VU0357017 reverses the cognitive deficits induced by an mAChR antagonist in a contextual fear conditioning paradigm, exhibiting improvement of hippocampus-dependent learning[110, 123]. PubMed:24590577

Appears in Networks:
Annotations
MeSH
Hippocampus

composite(p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")), p(MGI:Chrna7)) decreases path(MESH:"Cognitive Dysfunction") View Subject | View Object

In the NOR task (15 months p.i.) as well, both GFP-alpha7 and APP-alpha7 displayed a cognitive impairment (Fig. 5DeE) PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

p(MGI:Chrna7) decreases path(MESH:"Cognitive Dysfunction") View Subject | View Object

In the NOR task (15 months p.i.) as well, both GFP-alpha7 and APP-alpha7 displayed a cognitive impairment (Fig. 5DeE) PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

path(MESH:"Alzheimer Disease") increases path(MESH:"Cognitive Dysfunction") View Subject | View Object

Several studies showed that in AD animal models, the appearance of the cognitive deficits precedes plaque deposition (Casas et al., 2004; Gouras et al., 2000; Kumar et al., 2013; Wirths et al., 2004) PubMed:27522251

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:LYNX1) association path(MESH:"Cognitive Dysfunction") View Subject | View Object

While genetic linkages of lynx family members to neurological disorders have not been found, evidence for cholinergic dysregulation has been linked to a lynx family member expressed in nonneuronal tissues and involved in human disease (Chimienti et al., 2003), and as such, alterations in lynx dosage may be useful in ameliorating cognitive decline associated with neuropsychiatric disorders. PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

The cortical nAChR deficits significantly correlate with cognitive impairment in AD patients (Nordberg, in press; Nordberg et al 1995, 1997) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

path(MESH:Tauopathies) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

Given that in animal models of AD reducing tau levels attenuates neuronal dysfunction (7, 8), and in humans the extent of tau pathology correlates with cognitive decline (9), there is a growing interest in defining the degradative pathways that remove tau from the cell. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Alzheimer Disease
Text Location
Review

r(HGNC:TFEB) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

Transcriptional levels of TFEB and several of its well-known lysosomal targets were stratified by no demen- tia, mild cognitive impairment, and dementia,these transcript levels positively correlate with cognitive decline PubMed:30108137

Appears in Networks:

bp(MESH:"Cerebrovascular Circulation") association path(MESH:"Cognitive Dysfunction") View Subject | View Object

Aberrant cerebral blood flow is a functional defect that occurs in AD and tauNFT mice, and is closely associated with cognitive impairment (Wells et al., 2015) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons

p(HGNC:CDKN2A) association path(MESH:"Cognitive Dysfunction") View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

path(MESH:"Cerebral Small Vessel Diseases") increases path(MESH:"Cognitive Dysfunction") View Subject | View Object

WMH is driven by cerebral small vessel disease, which causes chronic ischemia and increased risk of cognitive decline and dementia (reviewed, (Prins & Scheltens, 2015)) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons

path(MESH:"Supranuclear Palsy, Progressive") increases path(MESH:"Cognitive Dysfunction") View Subject | View Object

PSP is an age-associated tauopathy that clinically manifests as parkinsonism with additional motor abnormalities and cognitive dysfunction (Orr et al., 2017), and is neuropathologically defined by accumulation of four-repeat (4R) tau, NFTs, gliosis and neurodegeneration (Flament et al., 1991) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Supranuclear Palsy, Progressive

g(DBSNP:rs8052688) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

The genotype distribution of a polymorphism in intron 7 (rs761059) differed between AD cases and controls, with an adjusted odds ratio (OR) of 1.45 (p=0.046, 95% CI: 1.01-2.08). One haplotype (ht2 CAGAG) was found in 14.0% of the AD patients and in 11.1% of the controls (p=0.04, OR=1.43. 95% CI; 1.01-2.01). Stratification by the ApoE gave no significant difference between the groups but when stratified by gender, two SNPs (rs8052688, rs8063) were significantly associated with the risk of MCI among women. PubMed:19765634

Appears in Networks:
Annotations
Gender
Female

g(DBSNP:rs8063) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

The genotype distribution of a polymorphism in intron 7 (rs761059) differed between AD cases and controls, with an adjusted odds ratio (OR) of 1.45 (p=0.046, 95% CI: 1.01-2.08). One haplotype (ht2 CAGAG) was found in 14.0% of the AD patients and in 11.1% of the controls (p=0.04, OR=1.43. 95% CI; 1.01-2.01). Stratification by the ApoE gave no significant difference between the groups but when stratified by gender, two SNPs (rs8052688, rs8063) were significantly associated with the risk of MCI among women. PubMed:19765634

Appears in Networks:
Annotations
Gender
Female

p(HGNC:MAPT, pmod(Ph, Ser, 422)) increases path(MESH:"Cognitive Dysfunction") View Subject | View Object

We performed immunohistochemistry and immunofluorescence on fixed brain sections and biochemical analysis of fresh brain extracts to characterize the presence of PAD-exposed tau (TNT1 antibody), tau oligomers (TOC1 antibody), tau phosphorylated at S422 (pS422 antibody), and tau truncated at D421 (TauC3 antibody) in the brains of 9-11 cases with CTE and cases of nondemented aged controls and AD (Braak VI) (n = 6, each). These 4 markers are particularly useful in understanding potential posttraumatic events in CTE because PAD exposure impairs axonal transport (24), oligomers confer toxicity (28, 38–40), pS422 correlates with cognitive decline (15), and D421 truncated tau may be related to cell toxicity (41, 42). All 3 early tau markers (ie, TNT1, TOC1, and pS422) were present in CTE and displayed extensive colocalization in perivascular tau lesions that are considered diagnostic for CTE. PubMed:26671985

Appears in Networks:
Annotations
MeSH
Chronic Traumatic Encephalopathy

Out-Edges 20

path(MESH:"Cognitive Dysfunction") positiveCorrelation a(HBP:HBP00074) View Subject | View Object

The levels of HMW AβOs in AD or MCI patients were significantly higher than in normal controls and correlated inversely with MMSE score. PubMed:29196815

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

path(MESH:"Cognitive Dysfunction") positiveCorrelation a(HBP:HBP00074) View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

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

path(MESH:"Cognitive Dysfunction") positiveCorrelation p(HGNC:NGFR) View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

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

path(MESH:"Cognitive Dysfunction") association path(MESH:"Alzheimer Disease") 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:

path(MESH:"Cognitive Dysfunction") positiveCorrelation a(HBP:"amyloid-beta oligomers") View Subject | View Object

Early work on AD considered the fibrillar form to be the toxic species. However, a lack of correlation between plaque burden and cognitive score contrasted with a strong positive correlation between total soluble amyloid and cognitive decline pointing to soluble, oligomeric forms as the primary toxic factor (Walsh and Selkoe, 2007). PubMed:19293145

Appears in Networks:

path(MESH:"Cognitive Dysfunction") association path(MESH:"Alzheimer Disease") View Subject | View Object

Schizophrenia (SZ) and Alzheimer’s disease (AD) are two devastating disorders of the central nervous system (CNS) that present clinically with cognitive impairments and psychotic symptoms PubMed:24511233

Appears in Networks:
Annotations
MeSH
Central Nervous System

path(MESH:"Cognitive Dysfunction") association path(MESH:"Alzheimer Disease") View Subject | View Object

AD is the most commonly diagnosed form of dementia and currently affects approximately 35 million individuals worldwide.7 AD is a progressive neurodegenerative disease that is characterized by a host of cognitive deficits, including impairments in learning and memory. In addition to the well-documented cognitive impairments, AD patients also display behavioral disturbances, including anxiety, depression, and psychosis PubMed:24511233

Appears in Networks:

path(MESH:"Cognitive Dysfunction") association path(MESH:Schizophrenia) View Subject | View Object

Schizophrenia (SZ) and Alzheimer’s disease (AD) are two devastating disorders of the central nervous system (CNS) that present clinically with cognitive impairments and psychotic symptoms PubMed:24511233

Appears in Networks:
Annotations
MeSH
Central Nervous System

path(MESH:"Cognitive Dysfunction") positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

In addition to cognitive alterations, psychiatric symptoms are frequently observed in AD patients, including apathy and depression PubMed:26813123

Appears in Networks:
Annotations
MeSH
CA3 Region, Hippocampal

path(MESH:"Cognitive Dysfunction") negativeCorrelation a(GO:synapse) View Subject | View Object

It has been demonstrated that cholinergic synapses are particularly affected by Aβ oligomers early neurotoxicity [218, 219] and that synaptic loss is the major correlate of cognitive impairment PubMed:26813123

Appears in Networks:

path(MESH:"Cognitive Dysfunction") association act(p(HGNC:CHRM1)) View Subject | View Object

Interestingly, M1 receptor signaling affects several of AD major hallmarks, including cholinergic deficit, cognitive dysfunction, and tau and Aβ pathologies PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Cognitive Dysfunction") increases path(MESH:"Plaque, Amyloid") View Subject | View Object

Several studies showed that in AD animal models, the appearance of the cognitive deficits precedes plaque deposition (Casas et al., 2004; Gouras et al., 2000; Kumar et al., 2013; Wirths et al., 2004) PubMed:27522251

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Cognitive Dysfunction") association p(HGNC:LYNX1) View Subject | View Object

While genetic linkages of lynx family members to neurological disorders have not been found, evidence for cholinergic dysregulation has been linked to a lynx family member expressed in nonneuronal tissues and involved in human disease (Chimienti et al., 2003), and as such, alterations in lynx dosage may be useful in ameliorating cognitive decline associated with neuropsychiatric disorders. PubMed:21482353

Appears in Networks:

path(MESH:"Cognitive Dysfunction") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

The cortical nAChR deficits significantly correlate with cognitive impairment in AD patients (Nordberg, in press; Nordberg et al 1995, 1997) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

path(MESH:"Cognitive Dysfunction") positiveCorrelation path(MESH:Tauopathies) View Subject | View Object

Given that in animal models of AD reducing tau levels attenuates neuronal dysfunction (7, 8), and in humans the extent of tau pathology correlates with cognitive decline (9), there is a growing interest in defining the degradative pathways that remove tau from the cell. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Alzheimer Disease
Text Location
Review

path(MESH:"Cognitive Dysfunction") positiveCorrelation r(HGNC:TFEB) View Subject | View Object

Transcriptional levels of TFEB and several of its well-known lysosomal targets were stratified by no demen- tia, mild cognitive impairment, and dementia,these transcript levels positively correlate with cognitive decline PubMed:30108137

Appears in Networks:

path(MESH:"Cognitive Dysfunction") association p(HGNC:CDKN2A) View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

path(MESH:"Cognitive Dysfunction") association bp(MESH:"Cerebrovascular Circulation") View Subject | View Object

Aberrant cerebral blood flow is a functional defect that occurs in AD and tauNFT mice, and is closely associated with cognitive impairment (Wells et al., 2015) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons

path(MESH:"Cognitive Dysfunction") positiveCorrelation g(DBSNP:rs8052688) View Subject | View Object

The genotype distribution of a polymorphism in intron 7 (rs761059) differed between AD cases and controls, with an adjusted odds ratio (OR) of 1.45 (p=0.046, 95% CI: 1.01-2.08). One haplotype (ht2 CAGAG) was found in 14.0% of the AD patients and in 11.1% of the controls (p=0.04, OR=1.43. 95% CI; 1.01-2.01). Stratification by the ApoE gave no significant difference between the groups but when stratified by gender, two SNPs (rs8052688, rs8063) were significantly associated with the risk of MCI among women. PubMed:19765634

Appears in Networks:
Annotations
Gender
Female

path(MESH:"Cognitive Dysfunction") positiveCorrelation g(DBSNP:rs8063) View Subject | View Object

The genotype distribution of a polymorphism in intron 7 (rs761059) differed between AD cases and controls, with an adjusted odds ratio (OR) of 1.45 (p=0.046, 95% CI: 1.01-2.08). One haplotype (ht2 CAGAG) was found in 14.0% of the AD patients and in 11.1% of the controls (p=0.04, OR=1.43. 95% CI; 1.01-2.01). Stratification by the ApoE gave no significant difference between the groups but when stratified by gender, two SNPs (rs8052688, rs8063) were significantly associated with the risk of MCI among women. PubMed:19765634

Appears in Networks:
Annotations
Gender
Female

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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.