General Information:

Id: 2,533
Diseases: Alzheimer disease - [OMIM]
Mammalia
review
Reference: Di Paolo G and Kim TW(2011) Linking lipids to Alzheimers disease: cholesterol and beyond. Nat. Rev. Neurosci. 12: 284-296 [PMID: 21448224]

Interaction Information:

Comment Dysregulation of lipid pathways has been implicated in a growing number of neurodegenerative disorders, such as Alzheimer disease (AD).
Formal Description
Interaction-ID: 23580

affects_activity of

phenotype

neurodegeneration

Comment Patients with AD display loss of synapses and neurons, as well as extracellular senile plaques and intracellular neurofibrillary tangles (NFTs).
Formal Description
Interaction-ID: 23590

is localized in

cellular component

intracellular

Comment Patients with AD display loss of synapses and neurons, as well as extracellular senile plaques and intracellular neurofibrillary tangles (NFTs).
Formal Description
Interaction-ID: 23591

is localized in

cellular component

extracellular region

Comment Brains with AD display a higher occurrence of adipose inclusions or lipoid granules, suggesting aberrant lipid metabolism.
Formal Description
Interaction-ID: 23592

increases_activity of

in brain
Comment APOE encodes a protein that serves as acrucial regulator of cholesterol metabolism in the brain and of triglyceride metabolism throughout the body.
Formal Description
Interaction-ID: 23593

gene/protein

APOE

affects_activity of

in brain
Drugbank entries Show/Hide entries for APOE
Comment The epsilon 4 allele of the apolipoprotein E (APOE) gene was identified as the strongest genetic risk factor for AD.
Formal Description
Interaction-ID: 23594

gene/protein mutant

APOE (isoform E4)

increases_activity of

Comment APOE encodes a protein that serves as acrucial regulator of cholesterol metabolism in the brain and of triglyceride metabolism throughout the body.
Formal Description
Interaction-ID: 23600

gene/protein

APOE

affects_activity of

in body
Drugbank entries Show/Hide entries for APOE
Comment APOE mediates the uptake of lipoprotein particles in the brain via the low-density lipoprotein (LDL) receptor related protein (LRP) and the very low-density family lipoprotein receptor.
Formal Description
Interaction-ID: 23601

gene/protein

APOE

affects_activity of

into brain
Drugbank entries Show/Hide entries for APOE
Comment APOE in amyloid pathology is supported by evidence that it binds amyloid-beta and modulates the aggregation and clearance of amyloid-beta.
Formal Description
Interaction-ID: 23602

gene/protein

APOE

interacts (colocalizes) with

gene/protein

Amyloid beta peptide

Drugbank entries Show/Hide entries for APOE
Comment Pharmacological inhibition of ACAT1 (for example, using CP-113,818) leads to the reduction of both amyloid-beta and cholesteryl ester.
Formal Description
Interaction-ID: 23603

drug/chemical compound

CP-113,818

decreases_activity of

gene/protein

SOAT1

Drugbank entries Show/Hide entries for SOAT1
Comment Pharmacological inhibition of ACAT1 (for example, using CP-113,818) leads to the reduction of both amyloid-beta and cholesteryl ester.
Formal Description
Interaction-ID: 23711

gene/protein

SOAT1

increases_quantity of

gene/protein

Amyloid beta peptide

Drugbank entries Show/Hide entries for SOAT1
Comment Genetic ablation of ACAT1 reduces both amyloid-beta pathology and cognitive impairments in a mouse model of AD.
Formal Description
Interaction-ID: 23712

gene/protein

SOAT1

increases_activity of

phenotype

amyloidosis

in a mouse model of AD; genetic ablation of ACAT1 reduces both amyloid-beta pathology and cognitive impairments;
Drugbank entries Show/Hide entries for SOAT1
Comment Genetic ablation of ACAT1 reduces both amyloid-beta pathology and cognitive impairments in a mouse model of AD.
Formal Description
Interaction-ID: 23713

gene/protein

SOAT1

increases_activity of

phenotype

cognitive impairment

in a mouse model of AD; genetic ablation of ACAT1 reduces both amyloid-beta pathology and cognitive impairments;
Drugbank entries Show/Hide entries for SOAT1
Comment ACAT1 ablation also increases levels of oxysterol, 24(S)-hydroxycholesterol, suggesting a potential role of this cholesterol metabolite in decreasing amyloidogenesis.
Formal Description
Interaction-ID: 23714

gene/protein

SOAT1

decreases_quantity of

drug/chemical compound

24-Hydroxycholesterol

ACAT1 ablation increases levels of oxysterol,24(S)-hydroxycholesterol;
Drugbank entries Show/Hide entries for SOAT1
Comment Cholesterol efflux also controls amyloid-beta generation.
Formal Description
Interaction-ID: 23804

affects_quantity of

gene/protein

Amyloid beta peptide

Comment ATP-binding cassette transporter A1 (ABCA1) serves as an important regulator of the levels and lipidation status of APOE by stimulating efflux of excess intracellular cholesterol to extracellular lipid acceptors, including unlipidated APOE and deletion of ABCA1 gene in mouse models of AD dramatically decreases the levels of APOE both in the brain and in the periphery, which correlates with greater amyloid-beta deposits.
Formal Description
Interaction-ID: 23805

gene/protein

ABCA1

affects_quantity of

gene/protein

APOE

Drugbank entries Show/Hide entries for ABCA1 or APOE
Comment ATP-binding cassette transporter A1 (ABCA1) serves as an important regulator of the levels and lipidation status of APOE by stimulating efflux of excess intracellular cholesterol to extracellular lipid acceptors, including unlipidated APOE.
Formal Description
Interaction-ID: 23806

gene/protein

ABCA1

affects_processing of

gene/protein

APOE

Drugbank entries Show/Hide entries for ABCA1 or APOE
Comment ATP-binding cassette transporter A1 (ABCA1) serves as an important regulator of the levels and lipidation status of APOE by stimulating efflux of excess intracellular cholesterol to extracellular lipid acceptors, including unlipidated APOE.
Formal Description
Interaction-ID: 23807

gene/protein

ABCA1

affects transport of

gene/protein

APOE

Drugbank entries Show/Hide entries for ABCA1 or APOE
Comment Increased levels of ABCA1 were found to lower amyloid-beta levels in cultured cells.
Formal Description
Interaction-ID: 23808

gene/protein

ABCA1

affects_quantity of

gene/protein

Amyloid beta peptide

in cultured cells
Drugbank entries Show/Hide entries for ABCA1
Comment Reducing membrane cholesterol levels through cholesterol-extracting compounds, such as beta-methyl cyclodextrin (betaMCD), decreases activity of both BACE1 and gamma-secretase, leading to an additive reduction in amyloid-beta generation.
Formal Description
Interaction-ID: 23822

drug/chemical compound

Methyl-beta-cyclodextrin

decreases_quantity of

drug/chemical compound

Cholesterol

Drugbank entries Show/Hide entries for
Comment Reducing membrane cholesterol levels through cholesterol-extracting compounds, such as beta-methyl cyclodextrin (betaMCD), decreases activity of both BACE1 and gamma-secretase, leading to an additive reduction in amyloid-beta generation.
Formal Description
Interaction-ID: 23825

drug/chemical compound

Cholesterol

increases_activity of

gene/protein

BACE1

Drugbank entries Show/Hide entries for Cholesterol or BACE1
Comment Reducing membrane cholesterol levels through cholesterol-extracting compounds, such as beta-methyl cyclodextrin (betaMCD), decreases activity of both BACE1 and gamma-secretase, leading to an additive reduction in amyloid-beta generation.
Formal Description
Interaction-ID: 23826

drug/chemical compound

Cholesterol

increases_activity of

Drugbank entries Show/Hide entries for Cholesterol
Comment Reducing membrane cholesterol levels through cholesterol-extracting compounds, such as beta-methyl cyclodextrin (betaMCD), decreases activity of both BACE1 and gamma-secretase, leading to an additive reduction in amyloid-beta generation.
Formal Description
Interaction-ID: 23827

drug/chemical compound

Cholesterol

affects_quantity of

gene/protein

Amyloid beta peptide

Drugbank entries Show/Hide entries for Cholesterol
Comment Inclusion of cholesterol or sphingolipids in phosphatidylcholine-containing vesicles leads to increased gamma-secretase activity.
Formal Description
Interaction-ID: 24058

drug/chemical compound

Sphingolipid

increases_activity of

in phosphatidylcholine-containing vesicles
Comment Cholesterol- and sphingolipid enriched membrane microdomains called 'lipid rafts' play a role in the amyloidogenic processing of APP.
Formal Description
Interaction-ID: 24059

cellular component

membrane raft

affects_activity of

phenotype

amyloidosis

Comment A substantial pool of BACE1 is localized to lipid rafts mainly through palmitoylation of its transmembrane and cytoplasmic domains.
Formal Description
Interaction-ID: 24060

gene/protein

BACE1

interacts (colocalizes) with

cellular component

membrane raft

Cholesterol depletion decreases the association of BACE1 with lipid rafts.
Drugbank entries Show/Hide entries for BACE1
Comment Cholesterol depletion decreases the association of BACE1 with lipid rafts, which correlates with decreased amyloidogenic processing of APP.
Formal Description
Interaction-ID: 24061

drug/chemical compound

Cholesterol

affects_processing of

gene/protein

APP

The amyloidogenic processing of APP is affected.
Drugbank entries Show/Hide entries for Cholesterol or APP
Comment Cholesterol depletion decreases the association of BACE1 with lipid rafts, which correlates with decreased amyloidogenic processing of APP.
Formal Description
Interaction-ID: 24063

drug/chemical compound

Cholesterol

affects_activity of

phenotype

amyloidosis

Drugbank entries Show/Hide entries for Cholesterol
Comment Cholesterol depletion decreases the association of BACE1 with lipid rafts, which correlates with decreased amyloidogenic processing of APP.
Formal Description
Interaction-ID: 24064

phenotype

amyloidosis

affects_processing of

gene/protein

APP

Drugbank entries Show/Hide entries for APP
Comment Acute cell exposure to cholesterol promotes the co-clustering of APP and BACE1 in lipid raft domains, as well as their rapid endocytosis.
Formal Description
Interaction-ID: 24085

drug/chemical compound

Cholesterol

affects_activity of

process

endocytosis

of APP and BACE1
Drugbank entries Show/Hide entries for Cholesterol
Comment Acute cell exposure to cholesterol promotes the co-clustering of APP and BACE1 in lipid raft domains, as well as their rapid endocytosis.
Formal Description
Interaction-ID: 24086

gene/protein

BACE1

interacts (colocalizes) with

gene/protein

APP

in lipid raft domains; promoted by cholesterol
Drugbank entries Show/Hide entries for BACE1 or APP
Comment Core components of the gamma-secretase complex, including presenilins, are also associated with lipid rafts.
Formal Description
Interaction-ID: 24087

gene/protein

PSEN1

is localized in

cellular component

membrane raft

Comment Core components of the gamma-secretase complex, including presenilins, are also associated with lipid rafts.
Formal Description
Interaction-ID: 24088

gene/protein

PSEN2

is localized in

cellular component

membrane raft

Comment Core components of the gamma-secretase complex, including presenilins, are also associated with lipid rafts.
Formal Description
Interaction-ID: 24089

is localized in

cellular component

membrane raft

Comment Inhibition of gamma-secretase activity leads to the accumulation of APP COOH-terminal products in lipid rafts.
Formal Description
Interaction-ID: 24090

decreases_quantity of

gene/protein

APP (CTF)

in lipid rafts
Comment Sphingolipids, including ceramide, sphingomyelin and glycosphingolipids (GSLs) are major components of lipid rafts, playing a number of crucial parts in cell functions associated with normal as well as diseased states.
Formal Description
Interaction-ID: 24094

drug/chemical compound

N-Acylsphingosine

is localized in

cellular component

membrane raft

Comment Sphingolipids, including ceramide, sphingomyelin and glycosphingolipids (GSLs) are major components of lipid rafts, playing a number of crucial parts in cell functions associated with normal as well as diseased states.
Formal Description
Interaction-ID: 24095

drug/chemical compound

Sphingomyelin

is localized in

cellular component

membrane raft

Comment Sphingolipids, including ceramide, sphingomyelin and glycosphingolipids (GSLs) are major components of lipid rafts, playing a number of crucial parts in cell functions associated with normal as well as diseased states.
Formal Description
Interaction-ID: 24096

drug/chemical compound

Glycosphingolipid

is localized in

cellular component

membrane raft

Comment Ceramide levels are elevated at the earliest clinically recognizable stage of AD, perhaps mediating oxidative stress-induced neuronal death.
Formal Description
Interaction-ID: 24097

increases_quantity of

drug/chemical compound

N-Acylsphingosine

at AD early stage
Comment Ceramide also regulates BACE1-mediated processing of APP independently of its role in oxidative cell death.
Formal Description
Interaction-ID: 24098

drug/chemical compound

N-Acylsphingosine

affects_processing of

gene/protein

APP

if BACE1-mediated
Drugbank entries Show/Hide entries for APP
Comment Inhibition of sphingomyelinase, the enzyme that mediates the conversion of sphingomyelin to ceramide, and the resulting sphingomyelin accumulation, reduces amyloid-beta secretion owing to inhibition of gamma-secretase activity.
Formal Description
Interaction-ID: 24099

gene/protein

Sphingomyelinase

decreases_quantity of

drug/chemical compound

Sphingomyelin

Comment Inhibition of sphingomyelinase, the enzyme that mediates the conversion of sphingomyelin to ceramide, and the resulting sphingomyelin accumulation, reduces amyloid-beta secretion owing to inhibition of gamma-secretase activity.
Formal Description
Interaction-ID: 24100

gene/protein

Sphingomyelinase

increases_quantity of

drug/chemical compound

N-Acylsphingosine

Comment Suppression of the entire sphingolipid biosynthetic pathway by inhibition of serine palmitoyl transferase leads to increased production of amyloid-beta 42 (Abeta42; the 42-amino-acid form of amyloid-beta), whereas Abeta40 levels remain unchanged.
Formal Description
Interaction-ID: 24102

complex/PPI

Serine-palmitoyltransferase complex

decreases_quantity of

Comment Suppression of the entire sphingolipid biosynthetic pathway by inhibition of serine palmitoyl transferase leads to increased production of amyloid-beta 42 (Abeta42; the 42-amino-acid form of amyloid-beta), whereas Abeta40 levels remain unchanged.
Formal Description
Interaction-ID: 24103

complex/PPI

Serine-palmitoyltransferase complex

NOT affects_quantity of

Comment Sphingolipids modulate activity of BACE1.
Formal Description
Interaction-ID: 24130

drug/chemical compound

Sphingolipid

affects_activity of

gene/protein

BACE1

Drugbank entries Show/Hide entries for BACE1
Comment GGPP and, to a lesser extent, FPP are significantly elevated in the frontal cortex of patients with AD, consistent with increased levels of their respective synthases.
Formal Description
Interaction-ID: 24131

increases_quantity of

drug/chemical compound

Geranylgeranyl pyrophosphate

in the frontal cortex; of patients with AD, consistent with increased level of the synthase
Comment GGPP and, to a lesser extent, FPP are significantly elevated in the frontal cortex of patients with AD, consistent with increased levels of their respective synthases.
Formal Description
Interaction-ID: 24146

increases_quantity of

drug/chemical compound

Farnesyl pyrophosphate

in the frontal cortex; of patients with AD, consistent with increased level of the synthase
Comment Wortmannin, a classical inhibitor of the phosphatidylinositol 3-kinase (PI3K) pathway was shown to reduce the levels of amyloid- both in vitro and in vivo, thus further highlighting a potential role of phosphoinositides in AD pathogenesis.
Formal Description
Interaction-ID: 24147

drug/chemical compound

Wortmannin

affects_quantity of

gene/protein

Amyloid beta peptide

Comment Gamma-secretase complex activity in liposomes is exquisitely sensitive to the presence of PtdIns(4,5)P2.
Formal Description
Interaction-ID: 24149

drug/chemical compound

Phosphatidylinositol-4,5-bisphosphate

affects_activity of

in liposomes
Comment Cellular PtdIns(4,5)P2 levels inversely correlate with secreted Abeta42 levels in cultured fibroblasts.
Formal Description
Interaction-ID: 24150

drug/chemical compound

Phosphatidylinositol-4,5-bisphosphate

affects_quantity of

in cultured fibroblasts
Comment PLD1 negatively regulates the processing of APP by PS1, probably through modulation of PS1 activity.
Formal Description
Interaction-ID: 24156

gene/protein

PLD1

affects_processing of

gene/protein

APP

Drugbank entries Show/Hide entries for PLD1 or APP
Comment PLD1 also promotes the cell surface delivery of PS1 and physically interacts with this protein.
Formal Description
Interaction-ID: 24157

gene/protein

PLD1

interacts (colocalizes) with

gene/protein

PSEN1

Drugbank entries Show/Hide entries for PLD1
Comment Gangliosides are abundant membrane glycosphingolipids that are primary modulators of amyloid-beta aggregation. They are concentrated in the luminal leaflet of various cellular organelles and the outer leaflet of the plasma membrane, where they are found in raftlike lipid microdomains that also contain cholesterol.
Formal Description
Interaction-ID: 24158

drug/chemical compound

Ganglioside

affects_activity of

Comment Gangliosides, such as GM1, bind amyloid-beta and alter the conformation from random coils to more ordered structures with increased beta-sheet content, which correlates with toxicity. The presence of GM1-bound amyloid-beta (GAbeta) is associated with early pathological changes in A.
Formal Description
Interaction-ID: 24159

drug/chemical compound

Ganglioside GM1

interacts (colocalizes) with

gene/protein

Amyloid beta peptide

Comment Cell surface GM1 acts as a 'seed' for amyloid-beta aggregation in neurons as well as in nerve terminal preparations.
Formal Description
Interaction-ID: 24160

drug/chemical compound

Ganglioside GM1

increases_quantity of

in neuron
Comment The seeding property of GM1 increases with the ageing process and is facilitated by cholesterol-rich environments, indicating that the process might occur in membrane rafts.
Formal Description
Interaction-ID: 24161

process

aging

increases_activity of

drug/chemical compound

Ganglioside GM1

Comment Ablation of beta-1,4 N-acetylgalactosaminyltransferase 1 (also known as GM2/GD2 synthase) in a transgenic mouse model of AD leads to an accumulation of GM3 and a loss of GM1.
Formal Description
Interaction-ID: 24162

gene/protein

B4GALNT1

increases_quantity of

drug/chemical compound

Ganglioside GM3

in a transgenic mouse model of AD
Comment Ablation of beta-1,4 N-acetylgalactosaminyltransferase 1 (also known as GM2/GD2 synthase) in a transgenic mouse model of AD leads to an accumulation of GM3 and a loss of GM1.
Formal Description
Interaction-ID: 24163

gene/protein

B4GALNT1

decreases_quantity of

drug/chemical compound

Ganglioside GM1

in a transgenic mouse model of AD
Comment Genetic ablation of GD3 synthase (GD3S) improves cognitive function and decreases the amyloid-beta plaque burden in a bigenic mouse expressing FAD mutant versions of the APP and PSEN1 genes.
Formal Description
Interaction-ID: 24164

gene/protein

ST8SIA1

affects_activity of

phenotype

cognitive impairment

in a bigenic mouse expressing FAD mutant versions of the APP and PSEN1 genes
Comment Genetic ablation of GD3 synthase (GD3S) improves cognitive function and decreases the amyloid-beta plaque burden in a bigenic mouse expressing FAD mutant versions of the APP and PSEN1 genes.
Formal Description
Interaction-ID: 24165

gene/protein

ST8SIA1

affects_quantity of

in a bigenic mouse expressing FAD mutant versions of the APP and PSEN1 genes
Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 24182

drug/chemical compound

Zn2+

interacts (colocalizes) with

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 24183

increases_activity of

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 24184

gene/protein

Amyloid beta peptide

increases_activity of

Amyloid-beta interacts with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques
Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 24185

drug/chemical compound

Cu2+

interacts (colocalizes) with

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 24186

cooccurs with

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 24187

increases_activity of

via Amyloid-beta interacts with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques
Comment Amyloid-beta can reduce metal ions like Zn2+ and Cu2+, thus producing hydrogen peroxide.
Formal Description
Interaction-ID: 24188

gene/protein

Amyloid beta peptide

affects_quantity of

drug/chemical compound

H2O2

via reducing metal ions like Zn2+ and Cu2+
Comment Response to cation stress is part of responses to stress.
Formal Description
Interaction-ID: 36320

affects_activity of

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 66691

gene/protein

Amyloid beta peptide

increases_activity of

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 66692

gene/protein

Amyloid beta peptide

interacts (colocalizes) with

drug/chemical compound

Cu2+

Comment Amyloid-beta has been shown to cause oxidative stress through its interaction with transition metal ions, such as Cu2+ and Zn2+, which are enriched in senile plaques (aggregated amyloid-beta peptides).
Formal Description
Interaction-ID: 66693

gene/protein

Amyloid beta peptide

interacts (colocalizes) with

drug/chemical compound

Zn2+

Comment Inhibition of sphingomyelinase, the enzyme that mediates the conversion of sphingomyelin to ceramide, and the resulting sphingomyelin accumulation, reduces amyloid-beta secretion owing to inhibition of gamma-secretase activity.
Formal Description
Interaction-ID: 77660

drug/chemical compound

Sphingomyelin

decreases_activity of

Comment Inhibition of sphingomyelinase, the enzyme that mediates the conversion of sphingomyelin to ceramide, and the resulting sphingomyelin accumulation, reduces amyloid-beta secretion owing to inhibition of gamma-secretase activity.
Formal Description
Interaction-ID: 77661

drug/chemical compound

Sphingomyelin

decreases_activity of

process

amyloid-beta secretion

due to inhibition of gamma-secretase activity
Comment Inhibition of sphingomyelinase, the enzyme that mediates the conversion of sphingomyelin to ceramide, and the resulting sphingomyelin accumulation, reduces amyloid-beta secretion owing to inhibition of gamma-secretase activity.
Formal Description
Interaction-ID: 79969

decreases_quantity of

drug/chemical compound

Sphingomyelin

Comment Inhibition of sphingomyelinase, the enzyme that mediates the conversion of sphingomyelin to ceramide, and the resulting sphingomyelin accumulation, reduces amyloid-beta secretion owing to inhibition of gamma-secretase activity.
Formal Description
Interaction-ID: 79970

increases_quantity of

drug/chemical compound

N-Acylsphingosine

Comment The seeding property of GM1 increases with the ageing process and is facilitated by cholesterol-rich environments, indicating that the process might occur in membrane rafts.
Formal Description
Interaction-ID: 80188

drug/chemical compound

Cholesterol

increases_activity of

drug/chemical compound

Ganglioside GM1

Drugbank entries Show/Hide entries for Cholesterol
Comment ACAT1 ablation also increases levels of oxysterol, 24(S)-hydroxycholesterol, suggesting a potential role of this cholesterol metabolite in decreasing amyloidogenesis.
Formal Description
Interaction-ID: 88980

gene/protein

SOAT1

decreases_quantity of

drug/chemical compound

Oxysterol

ACAT1 ablation increases levels of oxysterol,24(S)-hydroxycholesterol;
Drugbank entries Show/Hide entries for SOAT1
Comment Cell surface GM1 acts as a 'seed' for amyloid-beta aggregation in neurons as well as in nerve terminal preparations.
Formal Description
Interaction-ID: 94413

drug/chemical compound

Ganglioside GM1

increases_quantity of

in neuron