IDE Cancer Research Results
IDE, Insulin-Degrading Enzyme: Click to Expand ⟱
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| Type: |
IDE, Insulin-Degrading Enzyme
-Reduced IDE activity in AD contributes to Aβ accumulation.
-Enhancing IDE activity or expression may reduce Aβ burden.
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Scientific Papers found: Click to Expand⟱
*neuroP↑, highlighting neuroprotective mechanisms, such as the inhibition of Aβ production, enhanced Aβ clearance, and suppression of tau hyperphosphorylation.
*Aβ↓,
*p‑tau↓,
*cognitive↑, Research on P. ginseng and its bioactive ginsenosides has shown potential for improving cognitive function in AD models
*eff↑, particularly pronounced effects in individuals lacking apolipoprotein ε4 allele.
*PKA↑, Upregulates the PKA/CREB signaling pathway
*CREB↑,
*BACE↓, Inhibits BACE1 activity
*ADAM10↑, Enhances the expression of ADAM10 and reduces BACE1 expression through the activation of MAPK/ERK and PI3K/AKT
*MAPK↑,
*ERK↑,
*PI3K↑,
*Akt↑,
*NRF2↑, Activates the Nrf2/Keap1 signaling pathway
*PPARγ↓, Inhibits PPARγ phosphorylation and upregulates the expression of IDE
*IDE↑,
*APP↓, downregulates the expression of BACE1 and APP
*PP2A↑, Ginsenoside Rb1 enhances PP2A levels, thereby facilitating tau dephosphorylation and reducing p-tau levels observed in animal studies
*memory↑, The 400 mg dose of ginseng extract significantly improved “Quality of Memory” and “Secondary Memory” at all post-dose time points,
*antiOx↑, multiple effects such as Moringa oleifera (MO) that have strong anti-oxidative, anti-inflammatory, anticholinesterase, and neuroprotective virtues.
*Inflam↓,
*AChE↓,
*neuroP↑,
*Mood↑, MO improved behavioral deficits such as anxiety-like behavior and hyperactivity and cognitive, learning, and memory impairments.
*cognitive↑,
*memory↑,
*Aβ↓, MO treatment abrogated the Aβ burden to wild-type control mice levels via decreasing BACE1 and AEP and upregulating IDE, NEP, and LRP1 protein levels.
*BACE↓,
*AEP↓,
*IDE↑,
*NEP↑,
*LRP1↑,
*PSD95↑, MO improved synaptic plasticity by improving the decreased GluN2B phosphorylation, the synapse-related proteins PSD95 and synapsin1 levels, the quantity and quality of dendritic spines, and neurodegeneration in the treated mice
*STEP↓, These results suggest that MO modulates the PP2B/DARPP-32/PP1 axis to downregulate STEP activity thereby improving GluN2B Tyr1472 phosphorylation in APP/PS1 mice.
*APP↓, data suggest that MO downregulates the amyloidogenic processing of APP as well as improves Aβ clearance to decrease the Aβ burden in these mice.
Showing Research Papers: 1 to 2 of 2
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2
Pathway results for Effect on Cancer / Diseased Cells:
Total Targets: 0
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, NRF2↑, 1,
Core Metabolism/Glycolysis ⓘ
CREB↑, 1, PPARγ↓, 1,
Cell Death ⓘ
Akt↑, 1, MAPK↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, PI3K↑, 1,
Migration ⓘ
APP↓, 2, LRP1↑, 1, PKA↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, ADAM10↑, 1, PSD95↑, 1, p‑tau↓, 1,
Protein Aggregation ⓘ
AEP↓, 1, Aβ↓, 2, BACE↓, 2, IDE↑, 2, NEP↑, 1, PP2A↑, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Functional Outcomes ⓘ
cognitive↑, 2, memory↑, 2, Mood↑, 1, neuroP↑, 2, STEP↓, 1,
Total Targets: 28
Scientific Paper Hit Count for: IDE, Insulin-Degrading Enzyme
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1364 State#:% Dir#:2
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