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a(CHEBI:galanthamine)

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Entity

Name
galanthamine
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 10

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

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

Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System v1.0.0

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

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

Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice 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

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

In-Edges 7

a(CHEBI:"nicotinic antagonist") causesNoChange act(a(CHEBI:galanthamine)) View Subject | View Object

Surprisingly, however, activation of nAChRs by galantamine or physostigmine was insensitive to blockade by competitive nAChR antagonists, was detected even when the receptors were desensitized by high agonist concentrations, and was inhibited by the monoclonal antibody FK1 (350, 370, 372, 413, 428, 429). PubMed:19126755

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a(HBP:"FK1 antibody") decreases act(a(CHEBI:galanthamine)) View Subject | View Object

Surprisingly, however, activation of nAChRs by galantamine or physostigmine was insensitive to blockade by competitive nAChR antagonists, was detected even when the receptors were desensitized by high agonist concentrations, and was inhibited by the monoclonal antibody FK1 (350, 370, 372, 413, 428, 429). PubMed:19126755

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p(HGNC:CHRNA7) increases act(a(CHEBI:galanthamine)) View Subject | View Object

In SHSY5Y cells, RNA interference (RNAi) knockdown of alpha7 enhanced Abeta toxicity (Qi et al., 2007), and alpha7 antagonists, but not alpha4beta2 antagonists, block galantamine protection of cultured rat neurons (Kihara et al., 2004). Donepezil protects cultured rat cortical neurons against Abeta toxicity through both alpha7 and non-alpha7 nAChRs (Takada et al., 2003). It is therefore likely that alpha7 nAChRs are the primary mediators of nicotine neuroprotection, but in some cells, non-alpha7 subtypes are also likely to contribute. PubMed:19293145

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a(MESH:methyllycaconitine) decreases act(a(CHEBI:galanthamine)) View Subject | View Object

Notably, PHA could completely block the Ab-impaired task acquisition and reduce escape-latency to the normal level. Furthermore, the effect of PHA against the Ab-impaired task acquisition could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). It was also noted that blockade of a7 nAChR by MLA in the Gal-treated group resulted in a significant prolongation of the escape-latency on comparing with the Gal group (p<0.001) (Fig. 2). PubMed:25881725

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a(MESH:methyllycaconitine) decreases act(a(CHEBI:galanthamine)) View Subject | View Object

MLA could completely block the PHA-induced spatial memory improvement (p<0.001). Furthermore, the effect of Gal against the Ab-impaired reference memory could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). However, a7 nAChR blockage in the Gal group has a lesser effect on reference memory in comparison of blockage of that receptor in the PHA group (p<0.05) (Fig. 4). PubMed:25881725

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a(MESH:methyllycaconitine) decreases act(a(CHEBI:galanthamine)) View Subject | View Object

Inter-group analysis showed that the protein level decreased by pretreatment with selective a7 nAChR antagonist MLA (p<0.001). PHA and Gal prevent receptor destroying in AD animals, but this effect is completely abolished by MLA (p<0.001) (Fig. 9). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown). PubMed:25881725

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MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

complex(a(CHEBI:galanthamine), p(FPLX:CHRN)) hasComponent a(CHEBI:galanthamine) View Subject | View Object

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Out-Edges 33

a(CHEBI:galanthamine) increases act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) View Subject | View Object

An alternative means to increase nicotinic functions in the brain is to sensitize the nAChRs to activation by the endogenous agonist(s) using the so-called nicotinic allosteric potentiating ligands (APLs), which include drugs such as physostigmine and galantamine, a drug currently approved for the treatment of AD. PubMed:19126755

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a(CHEBI:galanthamine) increases act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) View Subject | View Object

In the early 1990s, galantamine, an alkaloid originally extracted from the bulbs and flowers of the wild Caucasian snowdrop Galanthus nivalis and other related Amaryllidacea species, was found to act like physostigmine on muscle and neuronal nAChRs (370, 372). PubMed:19126755

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a(CHEBI:galanthamine) increases act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) View Subject | View Object

Surprisingly, however, activation of nAChRs by galantamine or physostigmine was insensitive to blockade by competitive nAChR antagonists, was detected even when the receptors were desensitized by high agonist concentrations, and was inhibited by the monoclonal antibody FK1 (350, 370, 372, 413, 428, 429). PubMed:19126755

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Review

a(CHEBI:galanthamine) increases act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) 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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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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a(CHEBI:galanthamine) increases bp(GO:"synaptic transmission, cholinergic") 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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Review

a(CHEBI:galanthamine) decreases p(HGNC:ACHE) View Subject | View Object

Drugs currently approved to treat mild-to-moderate AD, including galantamine, donepezil, and rivastigmine, all inhibit AChE, the enzyme that hydrolyzes ACh (462). PubMed:19126755

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a(CHEBI:galanthamine) isA a(CHEBI:"EC 3.1.1.8 (cholinesterase) inhibitor") View Subject | View Object

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

Current licensed pharmacological treatments for AD consist largely of three acetylcholinesterase (AChE) inhibitors: rivastigmine, galantamine, and donepezil (Aguglia et al., 2004; Ritchie et al., 2004), although memantine, a blocker of L-glutamate receptors of the Nmethyl- D-aspartate (NMDA) subtype, is also deployed in late stages of the disease PubMed:19293145

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act(a(CHEBI:galanthamine)) increases bp(MESH:Neuroprotection) View Subject | View Object

In SHSY5Y cells, RNA interference (RNAi) knockdown of alpha7 enhanced Abeta toxicity (Qi et al., 2007), and alpha7 antagonists, but not alpha4beta2 antagonists, block galantamine protection of cultured rat neurons (Kihara et al., 2004). Donepezil protects cultured rat cortical neurons against Abeta toxicity through both alpha7 and non-alpha7 nAChRs (Takada et al., 2003). It is therefore likely that alpha7 nAChRs are the primary mediators of nicotine neuroprotection, but in some cells, non-alpha7 subtypes are also likely to contribute. PubMed:19293145

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a(CHEBI:galanthamine) increases p(HGNC:BCL2) View Subject | View Object

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005). PubMed:19293145

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MeSH
Neurons

a(CHEBI:galanthamine) increases act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) View Subject | View Object

Nicotine stimulates the secretion of betaAPP, which is trophic and neuroprotective against Abeta, from PC12 cells through an alpha7 and calcium-dependent pathway (Kim et al., 1997) as well as increasing the secretion of soluble APP and lowering the Abeta-containing sAPP-gamma in rats (Lahiri et al., 2002), again through nAChR-dependent mechanisms. Galantamine, a nAChR potentiator and AChE inhibitor, also increases the secretion of sAPP from human SH-SY5Y neuroblastoma cells (Lenzken et al., 2007) through the activation of nAChRs. It therefore seems that activation of nAChRs shifts the balance of APP processing away from beta-amyloidogenic to soluble APP production. PubMed:19293145

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Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:galanthamine) isA a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") View Subject | View Object

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a(CHEBI:galanthamine) isA a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") View Subject | View Object

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a(CHEBI:galanthamine) increases act(p(FPLX:CHRN)) View Subject | View Object

The most commonly prescribed treatments for AD are acetylcholinesterase inhibitors, which decrease the hydrolysis rate of ACh and, thereby, enhance cholinergic signaling. One such drug, galantamine (Reminyl), also potentiates nAChRs (66). PubMed:17009926

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MeSH
Alzheimer Disease

a(CHEBI:galanthamine) decreases path(MESH:Death) View Subject | View Object

In a double-blind study designed to assess patients survival with mild to moderately severe AD, the long-term treatment (2 years) with galantamine significantly reduced mortality and cognition decline, besides improving daily live activities in mild to moderate AD patients PubMed:26813123

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MeSH
Alzheimer Disease

a(CHEBI:galanthamine) increases bp(GO:cognition) View Subject | View Object

In a double-blind study designed to assess patients survival with mild to moderately severe AD, the long-term treatment (2 years) with galantamine significantly reduced mortality and cognition decline, besides improving daily live activities in mild to moderate AD patients PubMed:26813123

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MeSH
Alzheimer Disease

a(CHEBI:galanthamine) increases act(p(HGNC:ACHE)) View Subject | View Object

It is likely that the therapeutic benefit of cholinesterase inhibitors occurs at least in part through activation of the nAChRs, by the direct action of increased levels and/or through a direct activation of the allosteric site on the nAChR (Maelicke et al 1995, 2000) PubMed:11230871

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a(CHEBI:galanthamine) decreases act(p(MGI:App, frag("25_35"))) View Subject | View Object

Moreover in Ab-received mice, treatment with PHA and Gal improved the acquisition performance on comparing with the normal saline group (p<0.001) PubMed:25881725

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a(CHEBI:galanthamine) increases bp(GO:learning) View Subject | View Object

Moreover in Ab-received mice, treatment with PHA and Gal improved the acquisition performance on comparing with the normal saline group (p<0.001) PubMed:25881725

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a(CHEBI:galanthamine) increases path(MESH:"Spatial Memory") View Subject | View Object

The analysis also showed significant enhancing effects of PHA and Gal on the time spent in the target quadrant on comparing with the normal saline in AD mice (p<0.001). Also, in comparison with the control group, PHA-treated AD animals did not have a significant difference (p>0.05) on the time spent in the target quadrant, but in the Gal group it was significantly lower (p<0.001) (Fig. 3). PubMed:25881725

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MeSH
Alzheimer Disease

a(CHEBI:galanthamine) causesNoChange r(MGI:Chrna7) View Subject | View Object

Also, no alterations in the expression of a7 nAChR mRNA were observed in pretreatment with normal saline or MLA in PHA- or Gal-treated groups (p>0.05). In the same way, the pattern of mRNA expression in the cortex (data not shown) was similar to the hippocampus (Fig. 7). PubMed:25881725

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MeSH
Cerebral Cortex
MeSH
Hippocampus

a(CHEBI:galanthamine) increases p(MGI:Chrna7) View Subject | View Object

The analysis also showed significant effects of PHA and Gal on the protein levels on comparing with normal saline in AD mice (p<0.001). Moreover, Gal could not completely protect the a7 nAChR protein level in AD animals. This group has a lesser a7 nAChR protein level in comparison with the control group (p<0.001) (Fig. 8). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown) PubMed:25881725

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MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:galanthamine) increases p(MGI:Chrna7) View Subject | View Object

Inter-group analysis showed that the protein level decreased by pretreatment with selective a7 nAChR antagonist MLA (p<0.001). PHA and Gal prevent receptor destroying in AD animals, but this effect is completely abolished by MLA (p<0.001) (Fig. 9). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown). PubMed:25881725

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Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:galanthamine) regulates p(HGNC:CHRNA7) View Subject | View Object

Two compounds that are currently in clinical use might have direct effects on the alpha7 nAChR. The anticholinesterase inhibitor galantamine has modulatory effects on alpha7 nAChR and was reportedly beneficial for patients with schizophrenia in a case study184 PubMed:19721446

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a(CHEBI:galanthamine) decreases path(MESH:Schizophrenia) View Subject | View Object

Two compounds that are currently in clinical use might have direct effects on the alpha7 nAChR. The anticholinesterase inhibitor galantamine has modulatory effects on alpha7 nAChR and was reportedly beneficial for patients with schizophrenia in a case study184 PubMed:19721446

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a(CHEBI:galanthamine) increases bp(GO:cognition) View Subject | View Object

Only five drugs (Figure 1) have been approved by the U. S. Food and Drug Administration (FDA), four of which are cholinesterase inhibitors (tacrine, 15 donepezil, 16 rivastigmine 17 and galantamine 18 ) and one of which is a N-methyl-D-aspartate (NMDA) receptor antagonist (memantine 19 ). a N-methyl-D-aspartate (NMDA) receptor antagonist (memantine 19 ). These pharmacological agents have had limited effect in improving the cognitive function of AD patients and do not slow the progression of the disease. Clinical studies have shown that these agents temporarily stabilize cognitive impairment and help to maintain global function, delaying the need for patient palliative care by only a few month PubMed:30444369

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MeSH
Alzheimer Disease

a(CHEBI:galanthamine) decreases act(p(FPLX:Cholinesterase)) View Subject | View Object

Only five drugs (Figure 1) have been approved by the U. S. Food and Drug Administration (FDA), four of which are cholinesterase inhibitors (tacrine, 15 donepezil, 16 rivastigmine 17 and galantamine 18 ) and one of which is a N-methyl-D-aspartate (NMDA) receptor antagonist (memantine 19 ). a N-methyl-D-aspartate (NMDA) receptor antagonist (memantine 19 ). These pharmacological agents have had limited effect in improving the cognitive function of AD patients and do not slow the progression of the disease. Clinical studies have shown that these agents temporarily stabilize cognitive impairment and help to maintain global function, delaying the need for patient palliative care by only a few month PubMed:30444369

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a(CHEBI:galanthamine) decreases act(p(HGNC:ACHE)) View Subject | View Object

It inhibits AChE competitively and reversibly, causing elevated cerebral concen-trations of ACh, and thus, enhancing cholinergic activity. PubMed:29179999

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a(CHEBI:galanthamine) increases a(CHEBI:acetylcholine) View Subject | View Object

It inhibits AChE competitively and reversibly, causing elevated cerebral concen-trations of ACh, and thus, enhancing cholinergic activity. PubMed:29179999

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MeSH
Cerebral Cortex

a(CHEBI:galanthamine) increases sec(a(CHEBI:acetylcholine)) View Subject | View Object

Besides, galantamine allosterically interacted with nicotinic ACh receptors to increase the agonistic activity of these receptors and amplified the ACh reaction through stimulating ACh release [165–167]. PubMed:29179999

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a(CHEBI:galanthamine) increases act(p(HGNC:HMOX1)) View Subject | View Object

The protective effects of galantamine in brain microvascular endothelial cells were mediated via protective gene, heme oxygenase-1 induction through NF-B activation [168] PubMed:29179999

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a(CHEBI:galanthamine) increases act(p(FPLX:NFkappaB)) View Subject | View Object

The protective effects of galantamine in brain microvascular endothelial cells were mediated via protective gene, heme oxygenase-1 induction through NF-B activation [168] PubMed:29179999

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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.