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a(MESH:Neurons)

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Entity

Name
Neurons
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 18

albuquerque2009 v1.0.0

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

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

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

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

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

Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 v1.0.0

Anti-aggregant tau mutant promotes neurogenesis v1.0.0

Extracellular Tau and Its Potential Role in the Propagation of Tau Pathology v1.0.0

Tau Biochemistry v1.2.5

Tau Biochemistry Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

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

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

Caenorhabditis elegans models of tauopathy v1.0.0

Tau in physiology and pathology v1.0.0

In-Edges 50

p(HGNC:CHRNA7) association a(MESH:Neurons) View Subject | View Object

For example, while the alpha7 nAChR is primarily a homomeric receptor in neurons (127), combinations of alpha7 nAChR subunits with alpha5, beta2, or beta3 nAChR subunits have been reported to form functional heteromeric receptors in some systems (240, 360, 515). PubMed:19126755

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Text Location
Review

a(CHEBI:acetylcholine) regulates act(a(MESH:Neurons)) View Subject | View Object

Acetylcholine (ACh) is a neurotransmitter that modulates neuronal function in several areas of the CNS associated with AD and/or SZ pathology, including the striatum, cortex, hippocampus, and prefrontal cortex.5 ACh mediates its actions via two families of receptors, termed the muscarinic ACh receptors (mAChRs) and the nicotinic ACh receptors (nAChRs). PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Corpus Striatum
MeSH
Hippocampus
MeSH
Prefrontal Cortex

bp(GO:"synaptic transmission, cholinergic") regulates act(a(MESH:Neurons)) View Subject | View Object

Given its widespread distribution in the brain, it is not surprising that cholinergic neurotransmission is responsible for modulating important neural functions PubMed:26813123

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act(p(FPLX:CHRN)) negativeCorrelation a(MESH:Neurons) View Subject | View Object

Because excess activation of nAChRs damages neuronal health and brain function, organisms have a clear need to restrict the degree of nAChR activation PubMed:21482353

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p(MGI:Lynx1) increases a(MESH:Neurons) View Subject | View Object

These findings indicate that suppression of the cholinergic system by lynx proteins stabilizes neural circuitry PubMed:21482353

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path(MESH:"Alzheimer Disease") decreases a(MESH:Neurons) View Subject | View Object

Alzheimer’s disease is characterized by progressive cognitive decline, accompanied by a loss of neurons and synapses — especially cholinergic synapses — in the basal forebrain, cerebral cortex and hippocampus126 and by a substantial reduction in both muscarinic and nicotinic AChR expression127. PubMed:19721446

Appears in Networks:
Annotations
MeSH
Basal Forebrain
MeSH
Cerebral Cortex
MeSH
Hippocampus
Text Location
Review

a(MESH:Nicotine) decreases a(MESH:Neurons) View Subject | View Object

nAChRs are particularly important in two critical periods of brain life: early pre- and post-natal circuit formation, and age-related cell degeneration. They are involved in neuronal survival, as it has been shown that nicotinic agonists are neu- roprotective in in vivo and in vitro models PubMed:28901280

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p(MESH:"Receptors, Nicotinic") association a(MESH:Neurons) View Subject | View Object

nAChRs are particularly important in two critical periods of brain life: early pre- and post-natal circuit formation, and age-related cell degeneration. They are involved in neuronal survival, as it has been shown that nicotinic agonists are neu- roprotective in in vivo and in vitro models PubMed:28901280

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complex(a(HBP:"protein aggregates"), a(MESH:Neurons)) hasComponent a(MESH:Neurons) View Subject | View Object

Appears in Networks:

complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons)) hasComponent a(MESH:Neurons) View Subject | View Object

Appears in Networks:

a(CHEBI:adenosine) decreases act(a(MESH:Neurons)) View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

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a(PUBCHEM:64627) increases act(a(MESH:Neurons)) View Subject | View Object

64627 increases neuronal activity (Fos mRNA) both in proaggregant Tau transgenic slices and controls, although in case of the proaggregant slices neuronal activity is almost doubled, yielding levels similar to those of treated littermate control slices (Fig. 4D) PubMed:27671637

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composite(a(PUBCHEM:64627), p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del"))) increases act(a(MESH:Neurons)) View Subject | View Object

Having observed that 64627 restores presynaptic functioning (i.e., PPF, Fig. 4F), neuronal activity (induction of Fos, Fig. 4D), and dendritic spine levels in proaggregant Tau transgenic organotypic slices (Fig. 5 A and B), we tested whether we could restore long-term spatial memory in proaggregant Tau transgenic mice as well PubMed:27671637

Appears in Networks:
Annotations
MeSH
Mitochondria

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) negativeCorrelation act(a(MESH:Neurons)) View Subject | View Object

Surprisingly, expression of neuronal activity marker cFos, astrocytic activity marker Gfap, and oxidative stress marker Hmox1 were reduced in the proaggregant Tau transgenic slices, whereas antiaggregant Tau transgenic slices were not different from littermate controls (Fig. 4A) PubMed:27671637

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act(p(MGI:Adora1)) decreases act(a(MESH:Neurons)) View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

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p(MGI:Fos) biomarkerFor act(a(MESH:Neurons)) View Subject | View Object

Surprisingly, expression of neuronal activity marker cFos, astrocytic activity marker Gfap, and oxidative stress marker Hmox1 were reduced in the proaggregant Tau transgenic slices, whereas antiaggregant Tau transgenic slices were not different from littermate controls (Fig. 4A) PubMed:27671637

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p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

This revealed an impressive increase in mature neurons in all regions of the hippocampus (47% in CA1; 69% in CA3 and 81% in DG) in the anti-aggregant TauRDΔKPP slices compared to age-matched controls (Fig. 2c, bars 2, 5 and 8) PubMed:29202785

Appears in Networks:
Annotations
MeSH
Hippocampus

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

Notably, after switch-off of antiaggregant TauRDΔKPP there was a change in the number of BrdU stained cells in all regions of the hippocampus (CA1 region 32%, CA3 region 22% and DG 33% reduction) compared to switch-ON conditions (Fig. 7a, bars 4, 8 and 12) PubMed:29202785

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Dentate Gyrus

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

Similarly in the number of NeuN positive cells, there was a 22% reduction in CA1, 33% in CA3 and 37% reduction in DG compared to switch-On conditions (Fig. 7b, bars 4, 8 and 12) PubMed:29202785

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p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

BrdU positive cells were present in CA1, CA3 and DG in both the controls and antiaggregant TauRDΔKPP groups (Fig. 8a, b), but their numbers were increased strongly by 80% only in the CA3 region of the anti-aggregant TauRDΔKPP mice (Fig. 8b, bar 4), with 20% change in the CA1 and no change in the DG (Fig. 8b, bar 2 and 6) PubMed:29202785

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Dentate Gyrus

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

Additionally, there was an increase by 25% of the hippocampal volume in anti-aggregant TauRDΔKPP mice, compared to controls at P8 (Fig. 8c, bar 2), presumably due to the increased number of neurons PubMed:29202785

Appears in Networks:
Annotations
MeSH
Hippocampus

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

Surprisingly, the anti-aggregant TauRDΔKPP mice had an increased neuronal number significantly in the CA3 region (20%, Fig. 9b, bar 5), in contrast to the pro-aggregant TauRDΔK mice where neuronal loss (e.g. CA1 ~50%, CA3 ~10%, DG ~25%) was observed in all regions of the hippocampus (Fig. 9b, bar 3, 6, 9) PubMed:29202785

Appears in Networks:
Annotations
MeSH
CA3 Region, Hippocampal

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases a(MESH:Neurons) View Subject | View Object

This suggests that the expression of anti-aggregant TauRDΔKPP is needed for the increased proliferation of newborn neurons, and since these new born neurons need endogenous mouse Tau for their migration, differentiation, and maturation, there is enhanced expression of endogenous mouse Tau PubMed:29202785

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p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) decreases a(MESH:Neurons) View Subject | View Object

This may be due to the strong Tau pathology of the toxic pro-aggregant TauRDΔK leading to Tau aggregation, loss of synapses and loss of neurons PubMed:29202785

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p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) decreases a(MESH:Neurons) View Subject | View Object

By contrast, the pro-aggregant TauRDΔK slices showed a pronounced reduction in neuronal numbers, particularly in the CA1 (-44%), CA3 (-33%) and DG (-22%) regions compared to controls (Fig. 2c, bars 3, 6 and 9) PubMed:29202785

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Dentate Gyrus

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) decreases a(MESH:Neurons) View Subject | View Object

Surprisingly, the anti-aggregant TauRDΔKPP mice had an increased neuronal number significantly in the CA3 region (20%, Fig. 9b, bar 5), in contrast to the pro-aggregant TauRDΔK mice where neuronal loss (e.g. CA1 ~50%, CA3 ~10%, DG ~25%) was observed in all regions of the hippocampus (Fig. 9b, bar 3, 6, 9) PubMed:29202785

Appears in Networks:
Annotations
MeSH
Hippocampus

p(HGNC:MAPT, loc(GO:"extracellular region")) increases act(a(MESH:Neurons)) View Subject | View Object

the application of extracellular tau increases the electrical activity of iPSC-derived or primary cortical neurons PubMed:29238289

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p(HGNC:MAPT, loc(GO:"extracellular region")) decreases a(MESH:Neurons) View Subject | View Object

Moreover, extracellular tau may elicit cellular toxicity under certain conditions. PubMed:29238289

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p(HGNC:MAPT) increases act(a(MESH:Neurons)) View Subject | View Object

this observation suggests that the activity-dependent release of tau participates in a positive feedback loop on neuronal activity. PubMed:29238289

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complex(p(HGNC:MAPT), p(MESH:"Receptors, Muscarinic")) decreases a(MESH:Neurons) View Subject | View Object

The addition of tau into the cell culture media binds to muscarinic acetylcholine receptors and increases intracellular calcium, eventually leading to cell death PubMed:29238289

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complex(GO:"neurofibrillary tangle") causesNoChange act(a(MESH:Neurons)) View Subject | View Object

We found that in the visual cortex, neurons containing conspicuous quantities of mislocalized and aggregated tau nonetheless appear to have a normal capacity to integrate dendritic inputs and respond robustly to visual stimuli and also maintain normal somatic baseline calcium levels. In particular, we show that individual NFT-bearing neurons can respond robustly after integrating sensory inputs and are functionally indistinguishable from neighboring non–NFT-bearing neurons. These results demonstrate that NFT-bearing neurons remain functionally integrated in cortical circuits. PubMed:24368848

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Annotations
Uberon
visual cortex
MeSH
Frontotemporal Dementia

act(a(CHEBI:acrolein)) decreases a(MESH:Neurons) View Subject | View Object

We were prompted to carry out this study because Acr is mainly localized in the neurons [54], is found in association with NFTs and dystrophic neurites surrounding senile plaques [55], is highly toxic to neurons, is found elevated 2–5 fold in affected regions of AD brain. EC can sequester highly reactive and toxic byproducts of oxidation such as acrolein. PubMed:23531502

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p(HGNC:MAPT, pmod(Ac, Lys, 280)) decreases a(MESH:Neurons) View Subject | View Object

We also tested for ac-tau 280 in early stage Alzheimer's disease (Braak stage 1). Histopathological examination using the ac tau 280 antibody was performed in three Alzheimer's cases and three CTE patients. Presence of ac-tau 280 was confirmed in all cases at early sites of disease manifestation. These findings suggest that tau acetylation may precede tau phosphorylation and could be the first PubMed:29276758

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Annotations
MeSH
Alzheimer Disease

act(p(HBP:RAC1b)) positiveCorrelation act(a(MESH:Neurons)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

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p(MGI:Cdk5) negativeCorrelation act(a(MESH:Neurons)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

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p(MGI:Cdk5r1) positiveCorrelation act(a(MESH:Neurons)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

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p(MESH:Proteins, pmod(HBP:misfolding)) decreases a(MESH:Neurons) View Subject | View Object

Accumulation of misfolded proteins and damaged organelles is highly detrimental for neuronal homeostasis and survival. PubMed:29758300

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bp(GO:endocytosis) increases act(a(MESH:Neurons)) View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

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p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) decreases a(MESH:Neurons) View Subject | View Object

As shown earlier, TauRDΔK-expressing mice display loss of neurons in the CA3 and other regions of the hippocampus [11,24]. PubMed:28528849

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Annotations
MeSH
CA3 Region, Hippocampal

a(HBP:"Tau oligomers") decreases a(MESH:Neurons) View Subject | View Object

Indeed, evidence from both human and mouse studies indicates that soluble oligomers rather than insoluble aggregates are toxic to normal neurons (70). PubMed:29191965

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composite(p(HBP:"Tau isoform D (383 aa)", var("p.Pro301Leu")), p(HGNC:CDK5)) decreases a(MESH:Neurons) View Subject | View Object

Similarly, elimination of CDK-5 improved the touch response in the mutant TauR406W-line, but failed to improve it inother line PubMed:29191965

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p(HBP:"Tau isoform D (383 aa)", var("p.Pro301Leu")) decreases act(a(MESH:Neurons)) View Subject | View Object

Frontotemporal dementia with parkinsonism–mutant tau expression (0N4R-tau P301L and 0N4R-tau R406W), on the other hand, resulted in a reduced touch response that worsened with age PubMed:29191965

Appears in Networks:
Annotations
MeSH
Frontotemporal Dementia

p(HBP:"Tau isoform D (383 aa)", var("p.Pro301Leu")) decreases act(a(MESH:Neurons)) View Subject | View Object

At the later stages, the mutant-tau lines showed microtubule loss and non-apoptotic neuronal death, paralleled by a complete loss of touch response (62). PubMed:29191965

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p(HBP:"Tau isoform D (383 aa)", var("p.Arg406Trp")) decreases act(a(MESH:Neurons)) View Subject | View Object

Frontotemporal dementia with parkinsonism–mutant tau expression (0N4R-tau P301L and 0N4R-tau R406W), on the other hand, resulted in a reduced touch response that worsened with age PubMed:29191965

Appears in Networks:
Annotations
MeSH
Frontotemporal Dementia

p(HBP:"Tau isoform D (383 aa)", var("p.Arg406Trp")) decreases act(a(MESH:Neurons)) View Subject | View Object

At the later stages, the mutant-tau lines showed microtubule loss and non-apoptotic neuronal death, paralleled by a complete loss of touch response (62). PubMed:29191965

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p(HBP:"Tau isoform F (441 aa)", var("p.Ala152Thr")) decreases act(a(MESH:Neurons)) View Subject | View Object

Although the wild-type tau lines showed a mild late-onset dose-dependent Unc phenotype, TauA152T worms showed early-onset paralysis and acute neuronal dysfunction. PubMed:29191965

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a(HBP:"Tau aggregates") decreases act(a(MESH:Neurons)) View Subject | View Object

In the longer term, however, these tau aggregates may sequester other cell components, finally compromising neuronal functions PubMed:26631930

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p(HGNC:MAPT) regulates act(a(MESH:Neurons)) View Subject | View Object

These studies indicate that the endogenous tau plays a part in regulating neuronal activity PubMed:26631930

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p(HGNC:MAPT) increases a(MESH:Neurons) View Subject | View Object

Intraneuronal iron accumulation, neuronal loss in the substantia nigra and a severe decline in locomotor functions were observed in 12‑month-old tau-knockoutmice PubMed:26631930

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Annotations
MeSH
Substantia Nigra

p(HGNC:MAPT) increases act(a(MESH:Neurons)) View Subject | View Object

Although tau function can be partly compensated by other, redundant microtubule-associated proteins (for example, MAP1A), the behavioural impairments observed in aged (~12‑month-old) tau-knockout mice indicate that tau is necessary for normal neuronal and brain function. PubMed:26631930

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Out-Edges 16

a(MESH:Neurons) increases deg(a(CHEBI:nicotine)) View Subject | View Object

Metabolic degradation of nicotine and rapid clearance is a mechanism that protects neurons from greater nicotine concentrations, since nicotine readily crosses the mammalian blood-brain barrier and accumulates in the lipophilic brain environment to concentrations that may exceed plasma concentrations by one order of magnitude. Nevertheless, neurotoxicity to nicotine is not uncommon, as attested to by the recent increase in hospital emergency room visits by smokers who concurrently use the transdermal nicotine patch (503). PubMed:19126755

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Text Location
Review

a(MESH:Neurons) decreases r(HGNC:CHRNA3) View Subject | View Object

For instance, the alpha3 nAChR transcript generally dominates in the prenatal brain or in injured neurons, whereas its expression tends to be downregulated in the adult or healthy neuron, and alpha4 transcription is increased. PubMed:19126755

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Text Location
Review

a(MESH:Neurons) increases r(HGNC:CHRNA4) View Subject | View Object

For instance, the alpha3 nAChR transcript generally dominates in the prenatal brain or in injured neurons, whereas its expression tends to be downregulated in the adult or healthy neuron, and alpha4 transcription is increased. PubMed:19126755

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Annotations
Text Location
Review

a(MESH:Neurons) association p(HGNC:CHRNA7) View Subject | View Object

For example, while the alpha7 nAChR is primarily a homomeric receptor in neurons (127), combinations of alpha7 nAChR subunits with alpha5, beta2, or beta3 nAChR subunits have been reported to form functional heteromeric receptors in some systems (240, 360, 515). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

a(MESH:Neurons) regulates a(CHEBI:"kynurenic acid") View Subject | View Object

Interestingly, astrocytic KYNA production is regulated by neuronal activity (187) and cellular energy metabolism (213). This dependence of extracellular KYNA concentrations on the functional interplay between neurons and astrocytes is in line with the postulated neuromodulatory role of KYNA (418) and adds to the complexity of the neurochemical networks in the brain. PubMed:19126755

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Annotations
Text Location
Review

a(MESH:Neurons) negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Because excess activation of nAChRs damages neuronal health and brain function, organisms have a clear need to restrict the degree of nAChR activation PubMed:21482353

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a(MESH:Neurons) increases tloc(a(CHEBI:"gamma-aminobutyric acid"), fromLoc(GO:intracellular), toLoc(GO:"extracellular region")) View Subject | View Object

The neurons release additional GABA, activating presynaptic GABAB receptors on the excitatory inputs to pyramidal neurons, which diminish the release of glutamate onto the pyramidal neurons (Figure 2) PubMed:21482353

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a(MESH:Neurons) association p(MESH:"Receptors, Nicotinic") View Subject | View Object

nAChRs are particularly important in two critical periods of brain life: early pre- and post-natal circuit formation, and age-related cell degeneration. They are involved in neuronal survival, as it has been shown that nicotinic agonists are neu- roprotective in in vivo and in vitro models PubMed:28901280

Appears in Networks:

act(a(MESH:Neurons)) negativeCorrelation p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) View Subject | View Object

Surprisingly, expression of neuronal activity marker cFos, astrocytic activity marker Gfap, and oxidative stress marker Hmox1 were reduced in the proaggregant Tau transgenic slices, whereas antiaggregant Tau transgenic slices were not different from littermate controls (Fig. 4A) PubMed:27671637

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act(a(MESH:Neurons)) increases p(HGNC:MAPT) View Subject | View Object

In addition, stimulating neuronal activity in either cultured neurons or in vivo also enhances tau release PubMed:29238289

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act(a(MESH:Neurons)) increases p(HGNC:MAPT) View Subject | View Object

this observation suggests that the activity-dependent release of tau participates in a positive feedback loop on neuronal activity. PubMed:29238289

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a(MESH:Neurons) causesNoChange p(HGNC:MAPT) View Subject | View Object

CSF tau in APP transgenic mice is increased in an age- dependent manner without a global neuronal loss PubMed:29238289

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Annotations
MeSH
Cerebrospinal Fluid

act(a(MESH:Neurons)) increases p(HGNC:CAMKV) View Subject | View Object

These observations suggest that CaMKv blocks RhoA activity by preventing its interaction with Lfc. These results demonstrate that CaMKv regulates spine maintenance through RhoA inhibition. The suppression of the Lfc/RhoA pathway by AMPA receptors is implicated in dendritic spine maintenance10. Given that CaMKv expression is upregulated by synaptic activity, CaMKv may be a key signalling protein that transduces the signals from AMPA receptors to suppress RhoA during activity-dependent spine maintenance. Corroborating this, the AMPA receptor blocker NBQX attenuated CaMKv expression in neurons (Fig. 3i,j). Importantly, CaMKv overexpression completely rescued NBQX-induced spine loss (Fig. 3k,l). These findings collectively reveal that activity-dependent CaMKv expression and the subsequent inhibition of Lfc/RhoA are required to mediate AMPA receptor function in spine maintenance. PubMed:27796283

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act(a(MESH:Neurons)) positiveCorrelation p(MGI:Cdk5r1) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

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act(a(MESH:Neurons)) positiveCorrelation act(p(HBP:RAC1b)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

Appears in Networks:

act(a(MESH:Neurons)) negativeCorrelation p(MGI:Cdk5) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

Appears in Networks:

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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.