Choline Cancer Research Results

Choline, Choline: Click to Expand ⟱
Source:
Type:
Choline is an essential nutrient involved in multiple cellular functions including membrane biosynthesis (as part of phosphatidylcholine), methyl group metabolism, and cholinergic neurotransmission.
– Elevated levels of choline-containing compounds, often measured via magnetic resonance spectroscopy (MRS) or positron emission tomography (PET) using radiolabeled choline analogues, are frequently reported.
– High choline uptake or increased levels of choline metabolites generally correlate with higher tumor grade, greater aggressiveness, and poorer overall survival.
Choline is an essential nutrient with four core biological roles:
-Membrane structure – precursor of phosphatidylcholine (PC) and sphingomyelin
-One-carbon metabolism – methyl donor via betaine → methionine → SAM
-Neurotransmission – precursor of acetylcholine
-Lipoprotein export – required for VLDL assembly and hepatic lipid handling

These functions place choline at the intersection of cell proliferation, epigenetic regulation, and neuronal signaling, which explains its relevance to both cancer and neurodegeneration.


Scientific Papers found: Click to Expand⟱
2772- Bos,    Mechanistic role of boswellic acids in Alzheimer’s disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD
*Inflam↓,
*AChE↓, inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels
*Choline↑,
*NRF2↑, BAs modulate key molecular targets and signalling pathways like 5-lipoxygenase/cyclooxygenase, Nrf2, NF-kB, cholinergic, amyloid-beta (Aβ), and neurofibrillary tangles formation (NFTs) that are involved in AD
*NF-kB↑,
*BBB↑, AKBA has efficiently abled to cross the blood brain barrier (BBB)
*BioAv↑, bioavailability of AKBA was significantly higher in case of sublingual route when compared to intranasal administration, as demonstrated by area under curves (AUCs) analysis
*Half-Life↓, half-life of the drug was about six hours and peak plasma levels of the drug reach 30 hrs after oral administration of 333 mg of BSE.
*Dose↝, drug needs to be administered at a dosing interval of 6 hrs
*PGE2↓, BAs possessed anti-inflammatory activity by inhibiting microsomal prostaglandin E2 synthase-1 (mPGES1)
*ROS↓, prevented oxidative stress-induced neuronal damage and cognitive impairment because of the antioxidant, anti-inflammatory and anti-glutamatergic effects
*cognitive↑,
*antiOx↑,
5LO↓, AKBA significantly reduced pro-inflammatory mediators such as 5-LOX, TNF-α, IL-6 levels and improve cognition
*TNF-α↓,
*IL6↓,
*HO-1↑, AKBA shows neuroprotective effects against ischaemic injury via nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) cascade activation

6635- Cen,    Pharmacokinetics and metabolomics investigation of an orally modified formula of standardized Centella asiatica extract in healthy volunteers
- Trial, Nor, NA
*BioAv↝, The major parent compounds, madecassoside and asiaticoside, were rarely absorbed, instead undergoing biotransformation into active metabolites, madecassic acid and asiatic acid with possibility to be eliminated via fecal route.
*eff↑, Increasing the dose of ECa 233 resulted in significantly greater plasma levels of those active metabolites, with accumulation of asiatic acid after multiple oral administration for seven days.
*Choline↑, Administration of ECa 233 was found to be significantly associated with an increase of choline, an endogenous metabolite with documented benefits for learning and memory.
*memory↑,
*cognitive↑, ECa 233 may be useful in mitigating cognitive impairment, through its role in modulating human metabolites.
*neuroP↑, possesses well-documented neuroprotective effects
*BioAv↑, A previous study found that ECa 233 had limited dissolution of formulation, leading to a restriction of its oral bioavailability7. Hence, the modified formula to improve oral bioavailability of ECa 233 was developed and was used in this clinical stud

3917- PS,    Phosphatidylserine, inflammation, and central nervous system diseases
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, In this review, we discuss the metabolism of PS, the anti-inflammation function of PS in the brain;
*neuroP↑, Therefore, PS and PS liposome could be a promising supplementation for these neurodegenerative and neurodevelopmental diseases.
*cognitive↑, Increasing studies have demonstrated that supplementation of PS significantly improved the cognitive impairment caused by aging, AD, or PD
*Choline↑, a recent study reported PS also increased the release of choline, which is an important neurotransmitter and decrease in AD brains
*IL1β↓, reducing the expression of pro-inflammatory genes in microglia, such as IL1β, IL6, and C-C Motif Chemokine Ligand 2–5
*IL6↓,
*TNF-α↓, Intranasal PS liposomes prior to surgical brain injury induction significantly increases TGFβ, and decreased IL1β and TNFa in brain tissue to attenuate inflammation
*Ach↑, the increase of acetylcholine release enhances the activity of cholinergic neurons and improve the cognitive function of AD patients.
*eff↑, PS combines with ferulic acid and curcumin significantly to inhibit Aβ production, phosphorylated tau, and IL1β release, and increase brain-derived neurotrophic factor and acetylcholine
*eff↑, PS also serves as drug delivery approach for metformin and nicotinamide to ameliorate the cognitive function and inflammation
*BioEnh↑, PS can also serve as a drug delivery tool to elevate the bioavailability of drug, such as epigallocatechin-3-gallate and GDF5.
other↑, PS also has a therapeutic effect for stroke. Ischemia/reperfusion injury has been demonstrated to elicit strong inflammatory responses mediated by activated microglia/macrophages.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,  
Total Targets: 2

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Choline↑, 3,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 2,   Inflam↓, 2,   NF-kB↑, 1,   PGE2↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   BioAv↝, 1,   BioEnh↑, 1,   Dose↝, 1,   eff↑, 3,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 3,   memory↑, 1,   neuroP↑, 3,  
Total Targets: 24

Scientific Paper Hit Count for: Choline, Choline
1 Boswellia (frankincense)
1 Centella asiatica / Gotu kola → asiaticoside
1 Phosphatidylserine
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#:1330  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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