Ach Cancer Research Results
Ach, Acetylcholine: Click to Expand ⟱
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| Type: |
Acetylcholine (ACh)
↓ Acetylcholine (ACh) levels in AD patients
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Scientific Papers found: Click to Expand⟱
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*other↝, exact causes of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) are not fully understood, researchers believe that regulating the 5-HT system could help alleviate symptoms
*cognitive↑, 5-HT-related drugs may also improve the most prominent cognitive impairment issues in AD.
*memory↑, 5-HT6 receptor antagonists (such as idalopirdine) have the potential to improve memory and learning abilities in clinical trials.
*Ach↑, 5-HT4 receptor agonists can enhance acetylcholine release, which helps improve cognitive function and memory formation.
*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in
acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits
the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models
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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↑,
*ATP↑, Incubation with ALA showed a significant increase in ATP levels in both SH-SY5Y-APP695 and SH-SY5Y-MOCK cells.
*MMP↑, MMP levels were elevated in SH-SY5Y-MOCK cells, treatment with rotenone showed a reduction in MMP, which could be partly alleviated after incubation with ALA in SH-SY5Y-MOCK cells.
*ROS↓, ROS levels were significantly lower in both cell lines treated with ALA.
*GlucoseCon↑, benefits to diabetic neuropathy and impaired glucose uptake, and the regeneration of glutathione (GSH) and vitamins C and E
*GSH↑,
*neuroP↑, ALA seems to have a positive effect on neurodegenerative diseases such as AD
*cognitive↑, ALA improves cognitive performance and could be considered as a promising bioactive substance for AD by affecting multiple mechanisms such as:
*Ach↑, (1) impaired acetylcholine production;
*Inflam↓, (2) hydroxyl radical formation, ROS production, and neuroinflammation;
*Aβ↓, (3) impaired amyloid plaque formation;
OXPHOS↓, ALA has also been shown to restore the expression of OXPHOS complexes in HepG2 cells, ranging in a concentration between 0.5–2 mM
*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↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*PGE2↓, α-LA has mechanisms of epigenetic regulation in genes related to the expression of various inflammatory mediators, such PGE2, COX-2, iNOS, TNF-α, IL-1β, and IL-6
*COX2↓,
*iNOS↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*BioAv↓, α-LA has rapid uptake and low bioavailability and the metabolism is primarily hepatic
*Ach↑, α-LA increases the production of acetylcholine [30], inhibits the production of free radicals [31], and promotes the downregulation of inflammatory processes
*ROS↓,
*cognitive↑, Studies have shown that patients with mild AD who were treated with α-LA showed a slower progression of cognitive impairment
*neuroP↑, α-LA is classified as an ideal neuroprotective antioxidant because of its ability to cross the blood-brain barrier and its uniform uptake profile throughout the central and peripheral nervous systems
*BBB↑,
*Half-Life↓, α-LA presented a mean time to reach the maximum plasma concentration (tmax) of 15 minutes and a mean plasma half-life (t1/2) of 14 minutes
*BioAv↑, LA consumption is recommended 30 minutes before or 2 hours after food intake
*Casp3↓, α-LA had an effect on caspases-3 and -9, reducing the activity of these apoptosis-promoting molecules to basal levels
*Casp9↓,
*ChAT↑, α-LA increased the expression of M2 muscarinic receptors in the hippocampus and M1 and M2 in the amygdala, in addition to ChaT expression in both regions.
*cognitive↑, α-LA acts on these apoptotic signalling pathways, leading to improved cognitive function and attenuation of neurodegeneration.
*eff↑, Based on their results, the authors suggest that treatment with α-LA would be a successful neuroprotective option in AD, at least as an adjuvant to standard treatment with acetylcholinesterase inhibitors.
*cAMP↑, The increase of cAMP caused by α-LA inhibits the release of proinflammatory cytokines, such as IL-2, IFN-γ, and TNF-α.
*IL2↓,
*INF-γ↓,
*TNF-α↓,
*SIRT1↑, Protein expression encoded by SIRT1 showed higher levels after α-LA treatment, especially in liver cells.
*SOD↑, antioxidant enzymes (SOD and GSH-Px) and malondialdehyde (MDA) were analysed by ELISA after 24 h of MCAO, which showed that the enzymatic activities were recovered and MDA was reduced in the α-LA-treated groups i
*GPx↑,
*MDA↓,
*NRF2↑, The ratio of nucleus/cytoplasmic Nrf2 was higher in the α-LA group 40 mg/kg, indicating that the activation of this factor also occurred in a dose-dependent manner
*neuroP↑, potential therapeutic effects for the prevention or treatment of neurodegenerative disease
*Inflam↓, ALA is able to regulate inflammatory cell infiltration into the central nervous system and to down-regulate VCAM-1 and human monocyte adhesion to epithelial cells
*VCAM-1↓, down-regulate vascular cell adhesion molecule-1 (VCAM-1) and the human monocyte adhesion to epithelial cells
*5HT↑, ALA is able to improve the function of the dopamine, serotonin and norepinephrine neurotransmitters
*memory↑, scientific evidence shows that ALA possesses the ability to improve memory capacity in a number of experimental neurodegenerative disease models and in age-related cognitive decline in rodents
*BioAv↝, Between 27 and 34% of the oral intake is available for tissue absorption; the liver is one of the main clearance organs on account of its high absorption and storage capacity
*Half-Life↓, The plasma half-life of ALA is approximately 30 minutes. Peak urinary excretion occurs 3-6 hours after intake.
*NF-kB↓, As an inhibitor of NF-κβ, ALA has been studied in cytokine-mediated inflammation
*antiOx↑, In addition to the direct antioxidant properties of ALA, some studies have shown that both ALA and DHLA and a great capacity to chelate redox-active metals, such as copper, free iron,
zinc and magnesium, albeit in different ways (
*IronCh↑, ALA is able to chelate transition metal ions and, therefore, modulate the iron- and copper-mediated oxidative stress in Alzheimer’s plaques
*ROS↓, iron and copper chelation with DHLA may explain the low level of free radical damage in the brain and the improvement in the pathobiology of Alzheimer’s Disease
*ATP↑, ALA may increase the mitochondrial synthesis of ATP in the brain of elderly rats, thereby increasing the activity of the mitochondrial enzymes
*ChAT↑, ALA may also play a role in the activation of the choline acetyltransferase enzyme (ChAT), which is essential in the anabolism of acetylcholine
*Ach↑,
*cognitive↑, One experimental study has shown that in rats that had been administered ALA there was an inversion in the cognitive dysfunction with an increase in ChAT activity in the hippocampus
*lipid-P↓, administration of ALA reduces lipid peroxidation in different areas of the brain and increases the activity of antioxidants such as ascorbate (vitamin C), α-tocopherol (vitamin E), glutathione,
*VitC↑,
*VitE↑,
*GSH↑,
*SOD↑, and also the activity of superoxide dismutase, catalase, glutathione-peroxidase, glutathione-reductase, glucose-6-P-dehydrogenase
*Catalase↑,
*GPx↑,
*Aβ↓, Both ALA and DHLA have been seen to inhibit the formation of Aβ fibrils
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PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,
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*neuroP↑, Apigenin, a flavonoid found in various herbs and plants, has garnered significant attention for its neuroprotective properties
*antiOx↑, shown to possess potent antioxidant activity, which is thought to play a crucial role in its neuroprotective effects
*ROS↓, Apigenin has been demonstrated to scavenge ROS, thereby reducing oxidative stress and mitigating the damage to neurons
*Inflam↓, apigenin has been found to possess anti-inflammatory properties.
*TNF-α↓, inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-1β, which are elevated in neurodegenerative diseases
*IL1β↓,
*PI3K↑, apigenin has been shown to activate the PI3K/Akt signaling pathway, which is involved in promoting neuronal survival and preventing apoptosis.
*Akt↑,
*BBB↑, Apigenin has additional neuroprotective properties due to its ability to cross the BBB and enter the brain
*NRF2↑, figure 1
*SOD↑, pigenin has also been shown to activate various antioxidant enzymes, such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)
*GPx↑,
*MAPK↓, Apigenin inhibits the MAPK signalling system, which significantly reduces oxidative stress-induced damage in the brain
*Catalase↑, , including SOD, catalase, GPx and heme oxygenase-1 (HO-1) [37].
*HO-1↑,
*COX2↓, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*PGE2↓,
*PPARγ↑, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*TLR4↓,
*GSK‐3β↓, Apigenin can inhibit the activity of GSK-3β,
*Aβ↓, Inhibiting GSK-3 can reduce Aβ production and prevent neurofibrillary disorders.
*NLRP3↓, Apigenin suppresses nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome activation by upregulating PPAR-γ
*BDNF↑, Apigenin causes upregulation of BDNF and TrkB expression in several animal models
*TrkB↑,
*GABA↑, Apigenin enhances GABAergic signaling by increasing the frequency of chloride channel opening, leading to increased inhibitory neurotransmission
*AChE↓, It blocks acetylcholinesterase and increases acetylcholine availability.
*Ach↑,
*5HT↑, Apigenin has been shown to increase 5-HT levels, decrease 5-HT turnover, and prevent dopamine changes.
*cognitive↑, Apigenin increases the availability of acetylcholine in the synapse after inhibiting AChE, thereby enhancing cholinergic neurotransmission and improving cognitive function and memory
*MAOA↓, apigenin acts as a monoamine oxidase (MAO) inhibitor and MAO inhibitors increase the levels of monoamines in the brain
*Inflam↓, anti-inflammatory, anticarcinogenic, and free radical-scavenging activities.
*ROS↓,
*Aβ↓, Recent studies revealed its protective effects against amyloid-β (Aβ)-induced neurotoxicity, but the mechanism was unclear. I
*memory↑, involving improvement of the learning and memory capabilities,
*AChE↓, improvement of cholinergic system involving the inhibition of AChE activity and elevation of ACh level, and modification of BNDF, TrkB, and phospho-CREB levels.
*Ach↑,
*Dose↑, Apigenin, at doses of 10 mg/kg and 20 mg/kg, promoted learning and memory
*BDNF↑, apigenin also increased BDNF level and up-regulated its receptor TrkB and pCREB in A25-35 -induced amnesic mice.
*TrkB↑,
*p‑CREB↑,
*BBB↑, Additionally, we found that treatment with apigenin was effective in preserving anatomical and functional integrity of the BBB per-
meability.
*Ca+2?, A relevant effect of apigenin by suppressing the Ca 2+ influx through both voltage- and receptor-operated calcium channels
might be attributed to the changes of rCBF
*Aβ↓, neuroprotective potential of WA is mediated by reduction of beta-amyloid plaque aggregation, tau protein accumulation, regulation of heat shock proteins, and inhibition of oxidative and inflammatory constituents.
*tau↓,
*HSPs↝, WA inhibited Hsp90 [127] and induced Hsp 27 and Hsp70 expressions
*antiOx↑,
*ROS↓,
*Inflam↓,
*neuroP↑, confirming WA’s neuroprotective potency against AD.
*cognitive↑, In an AD model, cognitive defects induced by ibotenic acid that was significantly reversed by WA isolated from Ashwagandha root
*NF-kB↓, inhibited nuclear factor NF-κB activation
*HO-1↑, WA also increased the neuro-protective protein heme oxygenase-1, which is beneficial to AD prevention
*memory↑, WA additionally enhances memory [133], prevents Aβ production, reconstructs synapses, and regenerates axons
*AChE↓, WA Inhibits AChE and BuChE Activities
*BChE↓,
*ChAT↑, WA has an important role in AD by reversing the reduction in cholinergic markers such as choline acetyltransferase (ChAT) and acetylcholine
*Ach↑, WA increased the level of ACh, the amount of choline acetyltransferase (ChAT)
*ROS↓, EBm promotes free radical scavenger mechanisms
*5LO↓, reduces lipoxygenase activity reducing lipid peroxidation, increases glutathione peroxidase and chelates iron.
*lipid-P↓,
*GPx↑,
*IronCh↑,
*neuroP↑, EBm was seen to protect the cholinergic neurons and reduce anticholinesterase activity comparable to donepezil, rivastigmine, and galantamine.
*AChE↓,
*memory↑, EBm improved the total memory score and maximum improvement was seen in logical memory and paired associate learning in humans and reversed phenytoin-induced memory impairment in experimental model.
*toxicity↓, Mild nausea and gastrointestinal upset are seen in humans.
*SOD↑, EBm was administered to the rats for 21 days. It showed increase in activity of enzymes SOD, CAT, and GPx in prefrontal cortex, hippocampus, and striatum. I
*Catalase↑,
*cognitive↑, administration in indicated doses may act as a remedy for age-associated memory and cognitive decline in AD.
*ChAT↑, OBX reduced cholinergic activity and hence also ChAT in hippocampus. Subsequent administration of EBm and tacrine to the substrate, however, reversed this effect
*Ach↑,
*BP↓, Brahmi decreased systolic and diastolic blood pressure without significantly affecting heart rate.
*neuroP↑, therapeutic potential against multiple neurodegenerative diseases such as Alzheimer's disease (AD).
*Inflam↓, main chemical constituents of this gum include boswellic acids (BAs) like 3-O-acetyl-11-keto-β boswellic acid (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD
*AChE↓, It is also involved in inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels
*Ach↑,
*NRF2↑, activating Nrf2 through binding of ARE, inhibiting NF-kB and AChE activity.
*NF-kB↓,
*Aβ↓, inhibition of amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) induced neurotoxicity and neuroinflammation in AD
*Ach↑, Choline is also the precursor for acetylcholine, a neurotransmitter which activates the alpha7 nicotinic acetylcholine receptor (α7nAchR), and also acts as an agonist for the Sigma‐1 R (σ1R).
*Aβ↓, Lifelong choline supplementation significantly reduced amyloid‐β plaque load and improved spatial memory in APP/PS1 mice.
*memory↑,
*APP↓, Mechanistically, these changes were linked to a decrease of the amyloidogenic processing of APP, reductions in disease‐associated microglial activation, and a downregulation of the α7nAch and σ1 receptors.
*eff↑, Additional dietary choline is a putative treatment option that may prevent AD progression.
*neuroP↑, This suggests that additional choline in diet may be beneficial in preventing neuropathological changes associated with the aging brain.
*Dose↑, The tolerable upper limit (TUL) of choline unlikely to cause side effects for adult females and males (>19 years of age) is 3,500 mg/day, which is 8.24 times higher than the 425 mg/day recommendation for females and 6.36 times higher than the 550 mg/
*memory↑, The cholinergic system plays an important role in memory and attention and the loss of cholinergic neurons from the nucleus basalis of Meynert that takes place in the AD patient’s brain appears to be a very important factor contributing to AD memory
*Sleep↑, Another important function of the cholinergic system is to regulate the sleep cycle
*Ach↑, The enzyme choline acetyltransferase (ChAT) can synthesize ACh from choline and acetyl-coenzyme A (acetyl-CoA).
*AChE↓, aqueous and methanolic saffron extract presented a moderate activity as AChE inhibitor (up to 30%),
*memory↑, f 50-200 mg/kg of crocin enhanced memory impairment
*cognitive↑, crocin (30 mg/kg) for 3 weeks significantly improved cognitive impairment caused by intracerebroventricular injection of STZ,
*MDA↑, improved cognitive tasks and produced a significant decrease of malondialdehyde (MDA) levels and increase of total thiol content and glutathione peroxidase (GPx) activity in STZ-lesioned rats
*Thiols↑,
*GPx↑,
*antiOx↑, crocetin is only one and strong antioxidant, providing protection in rescuing cell viability, blocking reactive oxygen species (ROS) production and reducing caspase-3 activation
*ROS↓, crocin can prevent oxidative stress damage to hippocampus, memory and learning impairments
*Casp3↓,
*neuroP↑, neuroprotective effects of crocin against AD
*SOD↑, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*Ach↑,
*ChAT↑,
*BBB↑, shown that crocetin, able to pass through BBB, inhibits fibril Aβ formation,
*Aβ↓,
*tau↓, inhibitory effects of crocin on tau protein neurofibrillary tangles in AD.
*cognitive↑, (15 mg twice a day) or a capsule of placebo (two capsules a day) for 16 weeks. The results of this study indicated that saffron produces a significant improvement in cognitive performance
*Inflam↓, anticholinergic, anti-inflammatory and antioxidant features
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*ROS↓, suppressed intracellular reactive oxygen species (ROS) accumulation and Ca2+ overload compared with untreated cells.
*Ca+2↓, crocin strongly inhibited the overload of Ca2+ compared with the l-Glu-damaged HT22 cells,
*BAX↓, crocin significantly decreased the expression levels of Bax, Bad and cleaved caspase-3
*BAD↓,
*Casp3↓,
*cognitive↑, crocin substantially improved the cognition and memory abilities of the mice as measured by their coordination of movement in an open field test,
*memory↑,
*Aβ↓, Crocin improved cognitive abilities of AD mice, and reduced Aβ deposition in their brains
*GPx↑, crocin was able to reduce the Aβ1-42 content in the mouse brains, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*SOD↑,
*ChAT↑,
*Ach↑,
*AChE↓, and reduce the levels of ROS and acetylcholinesterase in the serum, cerebral cortex and hypothalamus compared with untreated mice.
*ROS↓,
*p‑Akt↑, crocin upregulated the phosphorylation levels of Akt and mTOR in 24-h l-Glu-exposed cells.
*p‑mTOR↑,
*neuroP↑, crocin-mediated neuroprotection of l-Glu-damaged HT22 cells.
*memory↑, value of saffron and its’ components, alone, or in combination with the other pharmaceuticals, for improving learning and memory abilities and controlling seizures
*cognitive↑, use of saffron in cognitive disturbance and epilepsy
*BioAv↑, Crocin is converted to crocetin by gastrointestinal cells (Hosseini et al., 2018), and is then absorbed and distributed to body tissues including the central nervous system
*ROS↓, -pretreated rats, cognitive performance was restored through attenuation of oxidative stress
*IL1↓, Crocin suppressed formation of advanced glycation products and brain inflammatory mediators [interleukin (IL)-1, tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κB].
*TNF-α↓,
*NF-kB↓,
*neuroP↑, neuroprotective effects against oxidative stress was suggested to be related to increases in phosphoinositide 3-kinase/Akt and mitogen-activated protein kinases/extracellular signal-regulated kinases
*lipid-P↓, Reduced lipid peroxidation and DNA injury and restored thiol redox and antioxidant status
*Thiols↑,
*antiOx↑,
*AChE↓, restoring oxidative damage biomarkers including glutathion and lipid peroxidation as well as modulating the activities of acetylcholinesterase (AChE) and monoamine oxidase (MAO)
*MAOA↝,
*SIRT1↑, up-regulate the SIRT1/PGC-1α pathway.
*PGC-1α↑,
*Ach↑, increases synaptic acetylcholine levels
*BChE↓, newly designed hybrid of galantamine (GAL) and curcumin (CCN) (compound 4b) decreases the activity of BChE in murine brain homogenates.
*AChE↓, Galantamine (GAL) is a natural alkaloid : It functions as an AChE inhibitor, enhancing the
levels of acetylcholine in the brain, which are important for memory and cognitio
*Ach↑,
*cognitive↑,
*memory↑,
*ROS↓, CCN is its ability to neutralize free radicals and reduce oxidative stress
*Inflam↓, CCN inhibits key enzymes and signaling pathways involved in inflammation, such as NF-kB and COX-2, making it valuable in managing inflammatory
conditions like arthritis
*NF-kB↓,
*COX2?,
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain
bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments
caused marked increase in ChAT positive cells.
*p‑tau↓, EGCG decreased the hyperphosphorylation of Tau in hippocampus
*BACE↓, BACE1 expression and activity as well as the expression of Aβ1-42 were suppressed by EGCG.
*Aβ↓,
*Ach↑, Moreover, EGCG promoted Ach content by diminishing the activity of AchE.
*AChE↓,
*antiOx↑, to improve the antioxidant system and learning and memory function of rats with AD.
*memory↑,
*hepatoP↑, notable components found in coffee have been shown to exert anti-diabetic and hepatoprotective functions
*ROS↓, EGCG Improved the Antioxidant System and Scavenged Free Radicals in AD Rats
*GPx↑, Compared with the AD rats, GPx and T-SOD activities were enhanced in the AD rats with EGCG treatment, especially in the AD rats treated with 250 mg/kg EGCG.
*SOD↑,
*cognitive↑, Consequently, only the three-ingredient group exhibited a significant improvement in cognitive function compared to the control group
*IL1β↓, significant decrease in IL-1β and an increasing trend in acetylcholine were observed. In the Cur group, significant decreases in Aβ and phosphorylated tau and an increasing trend in BDNF were observed
*Ach↑,
*Aβ↓,
*p‑tau↓,
*BDNF↑,
*APP↓, FA inhibits AB production via down-regulation of APP and β-secretase,6) inhibits AB aggregation, 8) and protects nerve cells from Aβ-induced neurotoxicity
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*BDNF↑, honokiol treatment led to an improvement in plasma BDNF levels.
*hepatoP↑, prevented liver damage by reducing transaminase levels (ALT and AST), liver OS, and TNF-α activity in mice challenged with LPS.
*ALAT↓,
*AST↓,
*TNF-α↓,
*SIRT3↑, 0.5, 1, 2, 5, 10 and 20 μM Enhanced SIRT3 expression, reduced Aβ levels
*Aβ↓,
*Apoptosis↓, Honokiol exhibited a dose-dependent reduction in hippocampal neural apoptosis, ROS generation, and decline in the membrane potential of mitochondria caused by AβO
*ROS↓,
*MMP↑,
*Ca+2↓, Dose-dependent reduction of ROS, suppression of intracellular Ca elevation, and inhibition of caspase-3 activity
*Casp3↓,
*Ach↑, Increased extracellular acetylcholine release to 165.5 ± 5.78% of the basal level
*PPARγ↑, Increased the expression of PPARγ and PGC1α
*PGC-1α↑,
*motorD↑, Improvement of motor dysfunction due to reversal of nigrostriatal dopaminergic neuronal loss
*TNF-α↓, Attenuated the levels of ROS, TNF-α, and IL-1β in both the in vivo and in vitro
*IL1β↓,
*neuroP↑, Several studies have reported both cholinergic and non-cholinergic effects of this compound on AD with significant neuroprotective properties.
*AChE↓, Hup A is a potent reversible inhibitor of AChE. By its action on AChE, it enhances the ACh levels which enhances learning and memory.
*Ach↑,
*memory↑,
*NGF↑, Increased levels of ACh augments NGF/BDNF and M1mAChR mediated sAPPα levels which further provides neuroprotection.
*BDNF↑,
*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,
*antiOx↑, antioxidant and nootropic activities of Moringa oleifera, the enhancement of spatial memory and neuroprotection of M. oleifera leaves extract in animal model of age-related dementia was determined
*memory↑,
*neuroP↑,
*MDA↓, decreased MDA level and AChE activity but increased SOD and CAT activities
*AChE↓,
*SOD↑,
*Catalase↑,
*cognitive↑, potential cognitive enhancer and neuroprotectant
*ROS↓, mechanism might occur partly via the decreased oxidative stress and the enhanced cholinergic function
*Ach↑,
*memory↑, treatment with MO-SD attenuated loss of spatial memory function via significant decrease in escape latency
*ROS↓, MO-SD significantly ameliorated oxido-inflammatory stress, restored cholinergic transmission via acetylcholinesterase inhibition and maintains neuronal integrity in the mice brain at both phases.
*Ach↑,
*AChE↓,
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*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.
*Inflam↓, Commonly recognized as an anti-inflammatory agent, quercetin not only limits capillary vessel permeability by inhibiting hyaluronidase but also blocks cyclooxygenases and lipoxygenases.
*COX2↓,
*5LO↓,
*antiOx↑, well-known antioxidant (recognized as one of the most potent antioxidant flavonoids, considered to be stronger than vitamin C or tocopherols
*BioAv↝, Quercetin-Loaded Nanocarriers—New Delivery to Better Availability
*GPx↑, Que at two higher doses improved the antioxidant enzymes (glutathione peroxidase, superoxide dismutase (SOD), Na+/K+-ATPase) supplies and elevated the levels of ACh
*SOD↑,
*Ach↑,
*4-HNE↓, whereas the levels of peroxidation product, 4-HNE, were reduced in the striatum
*CREB↑, A recent study showed a positive influence on the expression of the hippocampal FoxG1/CREB/BDNF signaling pathway [93]
*BDNF↑,
*ROS↓, quercetin exerted antioxidant (reducing ROS, increasing SOD, GST, GSH activity) as well as anti-inflammatory activity (suppressing IL-1β, IL-6, TNF-α, COX-2, microglial activation) [
*GSH↑,
*IL1β↓,
*IL6↓,
*TNF-α↓,
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*memory↑, It could be utilized to treat drug misuse or dependence, and those with memory and cognitive impairment
*cognitive↑,
*ROS↓, TQ protects brain cells from oxidative stress, which is especially pronounced in memory-related regions.
*Inflam↓, TQ’s antioxidant and anti-inflammatory properties protect brain cells from damage and inflammation.
*antiOx↑,
*TLR1↓, TQ’s role in inhibiting Toll-like receptors (TLRs) and some inflammatory mediators, leading to reduced inflammation and neurotoxicity.
*AChE↓, TQ has been shown in clinical studies to block acetylcholinesterase (AChE) activity, which increases acetylcholine (ACh).
*MMP↑, TQ ameliorates and prevents Aβ-induced neurotoxicity and mitochondrial membrane depolarization by inhibiting ROS formation and reducing oxidative stress by antioxidant properties.
*neuroP↑, TQ has an essential role in the neuroprotective impact on hippocampal cells after cerebral ischemia through the inhibition of lipid peroxidation
*lipid-P↓,
*SOD↑, This effect is due to the antioxidant activity of TQ on the levels of the superoxide dismutase (SOD) and GSH activities.
*GSH↑,
*Ach↑, TQ has been shown in clinical studies to block acetylcholinesterase (AChE) activity, which increases acetylcholine (ACh).
*memory↑, TQ enhanced the memory performance of Aβ1-42 infused rats
*BAX↓, expression profiles of mir29c and Bax which significantly upregulated in the Aβ1-42-infused animals were attenuated by TQ
*Aβ↓, administration of TQ decreased the expressions of Aβ, phosphorylated-tau, and BACE-1 proteins. removing Aβ plaques and by restoring neuron viability
*p‑tau↓,
*AChE↓, a decrease of AChE level was noted in the Aβ+TQ group compared to that of the Aβ group
*p‑Akt↓, Q treatment decreased the phosphorylation of AKT
*Ach↑, When the degradation of acetylcholine by AChE enzyme decreases, increment in
acetylcholine concentration leads to an improvement in memory
*Inflam↓, The healing effect of TQ on the reduction of the Aβ accumulation may be due to its anti-inflammatory
effect
*cognitive↑, TQ significantly improved cognition
*SOD↑, TQ significantly increased SOD and TAC and decreased AChE activities.
*TAC↑,
*AChE↓,
*MDA↓, It also decreased MDA and NO levels as well as TNF-α immunoreactivity and increased BDNF and Bcl-2 levels as well as ACh immunoreactivity.
*NO↓,
*TNF-α↓,
*Bcl-2↑,
*Ach↑,
*neuroP↑, These results indicate that TQ holds potential for neuroprotection and may be a promising approach for the treatment of neurodegenerative disorders.
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*Risk↓, Pantothenic acid was significantly decreased in the cerebellum (p = 0.008), substantia nigra (p = 0.02), and medulla (p = 0.008) of PDD cases.
*other↝, These findings have raised the question as to whether there may be common pathogenic insults present across multiple neurodegenerative diseases contributing to these similarities in presentation
*other↝, including widespread urea [12,13,14,15] and glucose increases [13,16,17,18], dysregulation of glucose and purine metabolism pathways [13,16,17,19,20], and decreases in the essential nutrient pantothenic acid [21,22], also known as vitamin B5.
*Ach↑, Pantothenic acid is essential for the synthesis of coenzyme A (CoA), a molecule with extensive roles in metabolism including in the tricarboxylic acid (TCA) cycle, fatty acid metabolism, and acetylcholine and myelin synthesis,
*Aβ↑, Interestingly though, an increased dietary intake of pantothenic acid has been associated with increased amyloid-β burden in individuals with cognitive impairment
*other?, This may indicate that pantothenic acid deficiencies in the brain cannot be counteracted by an increased dietary intake.
*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 measured metabolic perturbations in HD-human brain in a case-control study, identifying pervasive lowering of vitamin B5
*neuroP↑, Pantothenate deficiency could lead to neurodegeneration/dementia in HD that might be preventable by treatment with vitamin B5.
*other?, Vitamin B5 is an essential trace nutrient that exists in the brain at concentrations of up to 50-fold those in plasma
*Ach↑, vitamin B5 participates via acetyl-CoA in the production of steroid hormones and acetylcholine in the brain
*other↝, resemble dementia or psychiatric disorders. Examples include deficiency of water soluble (B-group) vitamins including: thiamine (vitamin B1) [32]; niacin (vitamin B3) [33]; vitamin B6; folate (vitamin B9); [34] and cyanocobalamin (vitamin B12) [35]
*eff↓, However, treatment of common age-related dementias, such as that caused by AD, with preparations containing B-vitamins (folate and vitamin B12) has proven ineffectual [39].
*other↝, Our results point to a possible defect in the mechanism of cerebral uptake and/or storage of vitamin B5, consistent with its lowered concentrations in affected regions of HD brain.
*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.
*BDNF↑, Vitamin K2 helps to restore hippocampal BDNF levels and reduced the amyloid β accumulation in AlCl3-administered animals.
*Aβ↓,
*cognitive↑, Vitamin K2 could partially reverse AlCl3-mediated cognitive decline.
*Ach↑, It increases acetylcholine and BDNF levels while reducing oxidative stress, neuroinflammation, and β-amyloid deposition, thus protecting the hippocampal neurons from AlCl3-mediated damage.
*Inflam↓,
Showing Research Papers: 1 to 37 of 37
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 37
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
OXPHOS↓, 1, ROS↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 2, FDG↓, 1, PDH↑, 1,
Cell Death ⓘ
Apoptosis↑, 1,
Transcription & Epigenetics ⓘ
other↑, 1,
Proliferation, Differentiation & Cell State ⓘ
mTOR↓, 1, TumCG↓, 1,
Migration ⓘ
TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
EGFR↓, 1, EGR4↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↝, 1, Half-Life↓, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1,
Total Targets: 17
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
4-HNE↓, 1, antiOx↑, 15, Catalase↑, 4, GPx↑, 8, GSH↑, 9, HO-1↑, 4, HO-2↓, 1, lipid-P↓, 7, MDA↓, 3, MDA↑, 1, NRF2↑, 7, ROS↓, 25, ROS↑, 1, SIRT3↑, 1, SOD↑, 11, TAC↑, 1, Thiols↑, 2, VitC↑, 1, VitE↑, 1,
Metal & Cofactor Biology ⓘ
Ferritin↑, 1, IronCh↑, 6,
Mitochondria & Bioenergetics ⓘ
ATP↑, 3, MMP↑, 3, PGC-1α↑, 2,
Core Metabolism/Glycolysis ⓘ
Acetyl-CoA↑, 4, ALAT↓, 1, cAMP↑, 1, CREB↑, 1, p‑CREB↑, 1, GlucoseCon↑, 5, LDL↓, 1, PDH↑, 1, PDKs↓, 1, PPARγ↑, 2, SIRT1↑, 2,
Cell Death ⓘ
Akt↑, 2, p‑Akt↓, 2, p‑Akt↑, 1, Apoptosis↓, 1, BAD↓, 1, BAX↓, 2, Bcl-2↑, 2, Casp3↓, 4, Casp9↓, 1, iNOS↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
Ach↑, 37, other?, 2, other↓, 1, other↝, 6,
Protein Folding & ER Stress ⓘ
HSPs↝, 1,
Proliferation, Differentiation & Cell State ⓘ
cFos↑, 1, Choline↑, 1, GSK‐3β↓, 1, mTOR↓, 1, p‑mTOR↑, 1, PI3K↑, 2,
Migration ⓘ
5LO↓, 2, APP↓, 2, Ca+2?, 1, Ca+2↓, 3, MMP-10↓, 1, MMP1↓, 1, MMP9↓, 1, TIMP1↑, 1, TIMP2↑, 1, VCAM-1↓, 2, β-catenin/ZEB1↑, 1,
Angiogenesis & Vasculature ⓘ
Hif1a↑, 1, NO↓, 1, VEGF↑, 1,
Barriers & Transport ⓘ
BBB↑, 6, GLUT3↑, 1, GLUT4↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2?, 1, COX2↓, 3, IL1↓, 1, IL1β↓, 8, IL2↓, 1, IL6↓, 4, INF-γ↓, 1, Inflam↓, 20, NF-kB↓, 5, PGE2↓, 2, TLR1↓, 1, TLR4↓, 1, TNF-α↓, 9,
Synaptic & Neurotransmission ⓘ
5HT↑, 3, AChE↓, 18, BChE↓, 2, BDNF↑, 9, ChAT↑, 11, GABA↑, 1, MAOA↓, 1, MAOA↝, 1, NGF↑, 2, tau↓, 3, p‑tau↓, 5, TrkB↑, 2,
Protein Aggregation ⓘ
Aβ↓, 18, Aβ↑, 1, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 4, BioAv↝, 4, BioEnh↑, 1, Dose↑, 2, eff↓, 1, eff↑, 4, Half-Life↓, 3,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 1, Ferritin↑, 1, IL6↓, 4,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↑, 1, cardioP↑, 1, cognitive↑, 24, hepatoP↑, 3, memory↑, 23, motorD↑, 1, neuroP↑, 24, Risk↓, 3, Sleep↑, 1, toxicity↓, 1, Weight↓, 1,
Total Targets: 128
Scientific Paper Hit Count for: Ach, Acetylcholine
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
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