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a(CHEBI:"lithium(1+)")

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Entity

Name
lithium(1+)
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 4

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

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

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

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 0

Out-Edges 15

a(CHEBI:"lithium(1+)") decreases act(p(HGNC:IMPA1)) View Subject | View Object

Lithium ions inhibit inositol monophosphatase to deplete inositol triphosphate. PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") decreases a(PUBCHEM:55310) View Subject | View Object

Lithium ions inhibit inositol monophosphatase to deplete inositol triphosphate. PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") increases bp(GO:autophagy) View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") decreases p(HGNC:SNCA) View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") decreases p(HGNC:SOD1) View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") decreases p(HGNC:HTT) View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") decreases p(HGNC:MAPT) View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") increases bp(GO:"motor behavior") View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"lithium(1+)") increases bp(GO:autophagy) View Subject | View Object

Recent acknowledged drugs can improve autophagy by acting on the process of autophagy-lysosome formation and then increasing tau clearance, such as methylene blue, lithium, and trehalose (Congdon et al. 2012; Kruger et al. 2012; Shimada et al. 2012) PubMed:29626319

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a(CHEBI:"lithium(1+)") increases bp(GO:autophagy) 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

Appears in Networks:
Annotations
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

Appears in Networks:
Annotations
MeSH
Huntington Disease

a(CHEBI:"lithium(1+)") decreases path(MESH:Schizophrenia) View Subject | View Object

In fact, lithium is able to delay METH-induced sensitization, while being a powerful treatment in schizophrenia PubMed:30061532

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a(CHEBI:"lithium(1+)") decreases act(p(HGNC:MTOR)) View Subject | View Object

In fact, lithium is able to delay METH-induced sensitization, while being a powerful treatment in schizophrenia PubMed:30061532

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a(CHEBI:"lithium(1+)") decreases path(MESH:Schizophrenia) View Subject | View Object

These pieces of evidence corroborate findings showing that several autophagy inducers, such as lithium, rapamycin, and Food and Drug Administration (FDA) approved antipsychotic drugs are effective to treat psychosis including schizophrenia PubMed:30061532

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a(CHEBI:"lithium(1+)") decreases path(MESH:"Psychotic Disorders") View Subject | View Object

These pieces of evidence corroborate findings showing that several autophagy inducers, such as lithium, rapamycin, and Food and Drug Administration (FDA) approved antipsychotic drugs are effective to treat psychosis including schizophrenia PubMed:30061532

Appears in Networks:

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.