Acetyl-CoA Cancer Research Results
Acetyl-CoA, Acetyl-CoA/AcCoA: Click to Expand ⟱
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Acetyl-CoA:
A small molecule, specifically a coenzyme.
-Central to metabolism, especially in:
-The citric acid cycle (Krebs cycle)
-Fatty acid synthesis
-Ketogenesis
It carries acetyl groups (2-carbon units) and delivers them to biochemical reactions.
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Scientific Papers found: Click to Expand⟱
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*antiOx↑, Both of alpha lipoic acid and its reduced form have been shown to possess anti-oxidant, cardiovascular, cognitive, anti-ageing, detoxifying, anti-inflammatory, anti-cancer, and neuroprotective pharmacological properties
*cardioP↑,
*cognitive↑, Alpha lipoic acid has the ability to decrease cognitive impairment and may be a successful therapy for Alzheimer’s disease and any disease related dementias
*AntiAge↑,
*Inflam↓,
*AntiCan↑,
*neuroP↑, ALA has neuroprotective effects in experimental brain injury caused by trauma and subarachnoid hemorrhage
*IronCh↑, Also, the ability of ALA to chelate metals can produce an antioxidant effect
*ROS↑, DHLA can exert a pro-oxidant effect of donating its electrons for the reduction of iron, which can then break down peroxide to the prooxidant hydroxyl radical via the Fenton reaction [10]. So, ALA and its reduced form DHLA, can promote antioxidant pr
*Weight↓, α-lipoic acid supplementation at a dose of 300 mg/day might help to could help to promote weight loss and fat mass reduction in healthy overweight/obese women following an energy-restricted balanced diet
*Ach↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*ROS↓, also scavenges
reactive oxygen species, thereby increasing the concentration levels
of reduced Glutathione (GSH).
*GSH↑,
*lipid-P↓, Alpha lipoic acid can scavenge lipid peroxidation products as hydroxynonenal and
acrolein.
*memory↑, learning and memory in the passive avoidance test partially
through its antioxidant activity.
*NRF2↑, α-LA treatment has been shown to increase Nrf2 nuclear localization
*ChAT↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*GlucoseCon↑,
*Acetyl-CoA↑,
*cognitive↑, Our study suggests that ALA therapy could be effective in slowing cognitive decline in patients with AD and IR.
*antiOx↑, Alpha-lipoic acid (ALA) is a naturally occurring disulfide molecule with antioxidant and anti-inflammatory properties.
*Inflam↓,
*neuroP↑, ALA plays many different roles in pathogenic pathways of dementia, acting as a neuroprotective agent.
*Ach↑, It increases acetylcholine production, inhibits hydroxyl radical production, and increases the process of getting rid of reactive oxygen species.
*ROS↓,
*GlucoseCon↑, (ii) increased glucose uptake, supplying more acetyl-CoA for the production of Ach;
*lipid-P↓, (v) scavenging lipid peroxidation products;
*GSH↑, (vi) inducing enzymes of glutathione synthesis
*Acetyl-CoA↑,
*antiOx↑, (ALA), a known antioxidant compound abundant in vegetables and animal tissues, in reducing oxidative stress in the aging brain and preventing cognitive decline.
*ROS↓,
*cognitive∅, no statistically significant effects either on cognitive function, executive function, or mood were found
*lipid-P↓, ALA has been shown to reduce lipid peroxidation and increase the activity of antioxidant molecules in different areas of the brain of experimental animals
*memory↑, ALA has been suggested to improve memory by increasing the activity of choline acetyltransferase (ChAT)
*ChAT↑,
*Acetyl-CoA↑, a crucial step in the biosynthesis of acetylcholine, in the hippocampi of treated rats
*Aβ↓, ALA administration can inhibit the formation of beta-amyloid fibrils and their expansion, thus exerting a direct effect on a known mechanism involved in neurodegenerative diseases
*BioAv↑, ALA is abundantly present in vegetables and animal tissues [17], is promptly bioavailable, and has no known toxic effects on animals and human subjects
*BBB↑, ALA has been demonstrated to successfully cross the blood–brain barrier in animal models
*toxicity∅, and no collateral effects have been observed at the oral daily doses currently employed as supplements (from 50 to 2400 mg/day)
*Ach↑, It synthesizes key biomolecules, including haemoglobin, acetylcholine, and cholesterol synthesis for cell membrane integrity.
*ROS↓, Its deficiency disrupts the TCA cycle, and promotes oxidative stress, neuroinflammation, tau hyperphosphorylation, and Aβ plaque formation, key attributes of AD.
*Inflam↓,
*p‑tau↓,
*Aβ↓,
*Acetyl-CoA↑, Its deficiency prevents the production of CoA, which reduces the levels of acetyl-CoA, impairing neurotransmitter synthesis, ATP production, and tricarboxylic acid cycle function, thereby disrupting neuronal survival and function
*ATP↑,
*ChAT↑, Vitamin B5 deficiency impairs acetylcholine biosynthesis by inhibiting choline acetyltransferase (ChAT), which catalyzes acetyl-CoA and choline conversion
*memory↑, Acetylcholine decline impairs memory, and vitamin B5 deficiency disrupts pathways dependent on CoA-derived acyl groups, impairing fatty acid synthesis and causing neuronal dysfunction
*Risk↓, We found that widespread, severe cerebral deficiency of vitamin B5 occurs in AD.
*Acetyl-CoA↑, Vitamin B5 is the obligate precursor of CoA/acetyl-CoA (acetyl-coenzyme A), which plays myriad key roles in the metabolism of all organs, including the brain.
*Ach↑, In brain, acetyl-CoA is the obligate precursor of the neurotransmitter acetylcholine, and the complex fatty-acyl groups that mediate the essential insulator role of myelin, both processes being defective in AD
*neuroP↑, We conclude that cerebral vitamin B5 deficiency may well cause neurodegeneration and dementia in AD, which might be preventable or even reversible in its early stages, by treatment with suitable oral doses of vitamin B5.
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
Total Targets: 0
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, GSH↑, 2, lipid-P↓, 3, NRF2↑, 1, ROS↓, 4, ROS↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1,
Core Metabolism/Glycolysis ⓘ
Acetyl-CoA↑, 5, GlucoseCon↑, 2,
Transcription & Epigenetics ⓘ
Ach↑, 4,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 3,
Synaptic & Neurotransmission ⓘ
ChAT↑, 3, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↑, 1, cardioP↑, 1, cognitive↑, 2, cognitive∅, 1, memory↑, 3, neuroP↑, 3, Risk↓, 1, toxicity∅, 1, Weight↓, 1,
Total Targets: 27
Scientific Paper Hit Count for: Acetyl-CoA, Acetyl-CoA/AcCoA
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#:1348 State#:% Dir#:2
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