MAOA Cancer Research Results
MAOA, Monoamine Oxidase A: Click to Expand ⟱
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| Type: gene/enzyme |
Also known as MAO-A, or "Warrior Gene"(associated with increased aggression and impulsivity).
This enzyme plays a crucial role in the breakdown of various neurotransmitters, such as serotonin, dopamine, and norepinephrine.
MAOA is commonly overexpressed in prostate cancer, and others.
-MAO-A inhibitors have been proven to be effective antidepressantn
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Scientific Papers found: Click to Expand⟱
*neuroP↑, Preclinical studies have suggested several pharmacological effects for anethole including neuroprotective properties.
*antiOx↓, Anethole's principal anti-oxidant abilities are due to three mechanisms: increased antioxidant enzyme activity, free radical scavenging, and metal ion chelation
*ROS↓,
*Inflam↓, Anti-inflammatory properties of Anethole
*TNF-α↓, TA decreased inflammatory edema by reducing the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukine (IL)-1β, and IL-6
*IL1β↓,
*IL6↓,
*motorD↑, TA has been found to protect against cerebral ischemia, improve motor coordination, lower brain water content, and attenuate excitatory mediators.
*MAOA↓, potentially by inhibiting brain MAO-A activity and the reduction of oxidative stress
*memory↑, The effect of fennel has been studies on memory function in rodents. In this regards, various studies have determined that this plant, which is rich in anethole, improved memory
*AChE↑, investigation revealed that fennel extract strongly suppressed acetylcholinesterase.
*PI3K↑, anethole boosted the expression of phosphoinositide 3-kinases (PI3K), protein kinase B (PKB), also known as AKT, and the mammalian target of rapamycin (mTOR) genes in the hippocampus.
*Akt↑,
*mTOR↑,
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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
*neuroP↑, fucoxanthin and astaxanthin, natural carotenoids abundant in algae, has shown to possess neuroprotective properties through antioxidant, and anti-inflammatory characteristics in modulating the symptoms of AD.
*antiOx↑,
*Inflam↑,
*AChE↓, Fucoxanthin and astaxanthin exhibit anti-AD activities by inhibition of AChE, BuChE, BACE-1, and MAO, suppression of Aβ accumulation.
*BACE↓,
*MAOA↓,
*Aβ↓,
*memory↑, Recently, Che, Li (Che et al., 2018) reported that astaxanthin possessed memory enhancement.
*MDA↓, Astaxanthin, as an antioxidant, helps to reduce oxidative stress by lowering malondialdehyde (MDA) levels and increasing SOD activity by activation of the NrF2/HO-1 pathway
*SOD↑,
*NRF2↑,
*HO-1↑,
*NF-kB↓, astaxanthin showed NFκB inhibitory activity which caused the downregulation of BACE-1 expression, resulting in Aβ reduction
*GSK‐3β↓, astaxanthin dose-dependently attenuated the GSK-3β activity
*ChAT↑, astaxanthin could reduce neuroinflammation via reducing iNOS expression and spine loss on the hippocampal CA1 pyramidal neurons, and restoring the ChAT expression in the medial septal nucleus
*iNOS↓,
*ROS↓, astaxanthin treatment decreased the ROS production and enhanced the cell growth.
*BBB↑, Astaxanthin can attenuate neurological dysfunction because of its unique chemical structure and can cross the BBB to enter the brain tissue
*antiOx↑, multiple activities of berberine, including antioxidant, acetylcholinesterase and butyrylcholinesterase inhibitory,
*AChE↓, inhibit AChE with an IC50 of 0.44 μM
*BChE↓, BChE inhibitor and the corresponding IC50 was estimated to be 3.44 μM
*MAOA↓, inhibitory activity on MAO-A with an IC50 value of 126 μM
*Aβ↓, monoamine oxidase inhibitory, amyloid-b peptide level-reducing and cholesterol-lowering activities.
*LDL↓, effectively reduce serum cholesterol and LDL-cholesterol levels in hyperlipidemic hamsters and human hypercholesterolemic patients
*ROS↓, First, it was reported that berberine can scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS)
*RNS↓,
*lipid-P↓, Secondly, berberine can inhibit lipid peroxidation
*Dose↝, berberine can inhibit AChE with an IC50 of 0.44 μM
*MAOB↓, inhibition of berberine against MAO-B: IC50 was estimated to be 98.4 μM
*memory↑, beneficial effect of berberine in ameliorating memory dysfunction in a rat model of streptozotocin-induced diabetes
*toxicity↓, Berberine is generally considered to be non-toxic at doses used in clinical situations and lacks genotoxic, cytotoxic or mutagenic activity
*BBB↑, Berberine can be administered orally [67] and pass through the blood-brain barrier
*Inflam↓, berberine showed significant memory-improving activities with multiple mechanisms, such as anti-inflammation, anti-oxidative stress, cholinesterase (ChE) inhibition and anti-amyloid effects.
*antiOx↓,
*AChE↓,
*BChE↓, berberine exerts inhibitory effects on the four key enzymes in the pathogenesis of AD: acetylcholinesterase, butyrylcholinesterase, monoamine oxidase A, and monoamine oxidase B
*MAOA↓,
*MAOB↓,
*lipid-P↓, Fig3
*GSH↑,
*ROS↓,
*APP↓,
*BACE↓,
*p‑tau↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*MAPK↓,
*PI3K↓,
*Akt↓,
*neuroP↑, neuroprotective effects of berberine have been extensively studied
*memory↑, berberine displayed significant effects in preventing memory impairment in these mechanistically different animal models, suggesting an over-all improvement of memory function by berberine
*cognitive∅, Although saffron extract co-administration had no effect on cognitive performance of mice,
*MAOA↓, reversed significantly the Al-induced changes in MAO activity and the levels of MDA and GSH.
*MDA↓,
*GSH↑,
*AChE↓, AChE activity was further significantly decreased in cerebral tissues of Al+saffron group.
*MAOA↓, MAO activity was inhibited by curcumin and ellagic acid
*Dose∅, however, higher half maximal inhibitory concentrations of curcumin (500.46 nM) and ellagic acid (412.24 nM)
Dose?, MAO-B by curcumin (IC50 500.46 nM) and ellagic acid (IC50 412.24 nM)
CAFs/TAFs↓, curcumin abrogated CAF-induced invasion and EMT, and inhibited ROS production and CXCR4 and IL-6 receptor expression in prostate cancer cells
EMT↓,
ROS↓, We found that curcumin abolished the CAF-derived CM-induced ROS production and CXCR4 and IL-6 receptor expression in PC3 cells
CXCR4↓,
IL6↓,
MAOA↓, inhibiting MAOA/mTOR/HIF-1α signaling, thereby supporting the therapeutic effect of curcumin in prostate cancer.
mTOR↓,
HIF-1↓,
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*Inflam↓, EUG shows remarkable anti-inflammatory, antioxidant, analgesic, and antimicrobial properties and has a significant effect on human health.
*Bacteria↓,
ChemoSen↑, In an in vitro study, use of little quantity of EUG in combination with gemcitabine potentiates the effects of the drug with no side effects on healthy cells
*selectivity↑, EUG shows a synergistic effect when used with some chemoinhibitory drug leading to a great reduction in drug toxicity on healthy cells
ROS⇅, EUG behaves as an antioxidant at lower concentrations by minimizing ROS-mediated oxidative stress, but on the contrary, EUG at higher concentrations acts as a prooxidant to enhance the production of the ROS
TumCG↓, 40% reduction was reported in tumor size by the action of EUG
MMP↓, mitochondrial membrane potential loss were much enhanced in combination treatment in contrast to single drug exposure
antiOx⇅, EUG has been reported to pose both prooxidant and antioxidant effects when applied to the cancer cells in a concentration-dependent fashion
*antiOx↑, the antioxidant behaviour of EUG is greater than most of the known or standard antioxidants such as Trolox
*BBB↑, The hydrophobic property of EUG makes it efficient in penetrating the blood-brain barrier for its entry into the brain and performs its action in vivo [
*neuroP↑, EUG shows a neuroprotective potential on hippocampal tissues owing to its power reduce brain-derived neurotrophic factor (BDNF),
*BDNF↑, (note ref has it increasing, so it has been corrected here)
*Aβ↓, and retardation of amyloid-β peptide (A-β) induced cell death through the abnormal blockage of Ca2+ (resulted from A-β) [130].
*Ca+2↓,
*5LO↓, The inhibitory action of EUG has been reported on 5-lipoxygenase, in addition to an improved action in response to excitotoxic and ROS-injured neuron cells [
*MAOA↓, It also retards monoamine oxidase A (MAO-A) and sometimes reverts back monoamines that are reduced in the brains of depressed patients [129].
other↑, EUG has been proved useful against stress-induced irritable bowel syndrome (IBS) [136].
*eff↑, Isoeugenol derivatives have become a popular subject of research due to their fungicidal and insecticidal properties, because they exhibit greater antimicrobial activity than eugenol
*BioAv↝, Eugenol is a clear to pale yellow liquid with an oily consistency and a spicy aroma. It is sparingly soluble in water and well soluble in organic solvents.
*BioAv↝, Eugenol has low chemical stability and is sensitive to oxidation and various chemical interactions. When orally administered, it is rapidly absorbed by various organs and metabolized in the liver.
*BioAv↑, encapsulation of eugenol seems to be the best solution to prevent early absorption, improve its water solubility, and, thus, increase its activity. eugenol delivered increases at least sixfold in infected cells when delivered as solid lipid NPs
*antiOx↑, Eugenol has demonstrated various antioxidant, analgesic, antimutagenic, anti-platelet, antiallergic, anti-swelling, and anti-inflammatory properties.
*AntiAg↑,
*Inflam↓,
*AntiBio↑, It has also displayed antimicrobial effects against many human pathogens, including a wide group of Gram-positive and Gram-negative bacteria and fungi and a number of parasites
*MAOA↓, Eugenol is a popular antioxidant and monoamine oxidase (MAO) inhibitor, and it is also known to exhibit neuroprotective properties
*neuroP↑,
*ROS↓, Eugenol is known to scavenge free radicals, inhibit the generation of reactive oxygen species, prevent the production of reactive forms of nitrogen
*RNS↓,
*eff↑, The study on eugenol showed that this compound has synergistic activity with various antibiotics, such as vancomycin, penicillin, ampicillin, and erythromycin, and the combination of these compounds allowed a reduction in MIC values of 5–1000 times
NF-kB↓, killing cancer cells. The molecular mechanism is believed to include various stages: inhibiting NF-κB activation, downregulating prostaglandin synthesis, reducing cyclooxygenase-2 activity,
PGE2↓,
COX2↓,
TumCCA↑, inducing cell cycle arrest in the S phase, and causing apoptotic cell death by lowering inflammatory cytokine levels
Apoptosis↑,
TumCMig↓, even a low dose of eugenol interfered with the migration and invasion of carcinogenic cells, inhibited lung cancer cell viability,
TumCI↓,
tumCV↓,
PI3K↓, blocking the PI3K/Akt pathway (an intracellular signaling pathway involved in cell cycle regulation) and inhibiting MMP (matrix metalloproteinase) activity
Akt↓,
MMPs↓,
ChemoSen↑, eugenol is believed to enhance the inhibition of breast cancer stem cells by cisplatin by inhibiting the activity of aldehyde dehydrogenases (ALDH)
ALDH↓,
*Pain↓, Eugenol is a popular painkiller and anesthetic used in dental practice.
*VGSC↓, It has been found to inhibit voltage-gated sodium channels (VGSC) in the primary supply neurons of the teeth in various studies, including one based on a rat model
*IL1β↓, It is also known to be an inhibitor of pro-inflammatory mediators, including IL-1β and IL-6, tumor necrosis factor alpha (TNF-α), prostaglandin E2 (PGE2), expression of inducible oxide nitrate synthase (iNOS)
*IL6↓,
*TNF-α↓,
*iNOS↓,
*5LO↓, nuclear factor kappa B (NF-κB), and leukotriene C4 and 5-lipoxygenase (5-LOX)
*chemoPv↑, eugenol dimers have shown chemopreventive properties by inhibiting cytokine expression in macrophages
Apoptosis↓, Eugenol’s multitargeted action encompasses apoptosis induction, cell cycle arrest, suppression of inflammatory pathways, and inhibition of metastatic progression.
TumCCA↓,
Inflam↓,
TumMeta↓,
BioAv↑, nanotechnological encapsulation strategies have been explored to enhance bioavailability and pharmacokinetic stability.
eff↓, The compound is susceptible to oxidation when exposed to light, atmospheric oxygen, and elevated temperatures[2].
Half-Life↓, eugenol undergoes rapid absorption across the gastrointestinal epithelium, entering the systemic circulation within 30-60 minutes[3]. The swift absorption profile, while ensuring bioavailability, paradoxically limits it therapeutic effectiveness
*ROS↓, eugenol inhibits the endogenous production of reactive oxygen species (ROS) and reactive nitrogen species (RNS)
*RNS↓,
*SOD↓, Eugenol augments the body’s intrinsic antioxidant defense mechanisms, elevating expression of cytoprotective enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferases (GSTs)
*Catalase↑,
*GSTs↑,
*MAOA↓, Through monoamine oxidase (MAO) inhibition, eugenol modulates neurotransmitter homeostasis in the central nervous system, offering neuroprotective benefit
*neuroP↑,
*DNAdam↓, By eliminating reactive molecular species and preventing accumulation of damaged DNA and proteins, eugenol reduces the likelihood of mutations
Apoptosis↑, Multiple investigations have demonstrated eugenol’s capacity to induce apoptosis in diverse colon cancer cell lines, including HT-29, HCT-116,
Caco-2, and SW-620
ROS↑, In human promyelocytic leukemia cells (HL-60) and colorectal cancer models, eugenol triggers elevated intracellular ROS accumulation
selectivity↑, This pro-oxidant activity in cancer cells contrasts sharply with eugenol’s cytoprotective antioxidant effects in normal cells, illustrating its selective anticancer action
MMP↓, Loss of mitochondrial membrane integrity triggers cytochrome c release into the cytosol, activating the caspase-9/caspase-3 cascade and culminating in programmed cell death
Cyt‑c↓,
Casp3↑,
Casp9↑,
TumCD↑,
BAX↑, Eugenol enhances expression of the tumor suppressor protein p53, which transactivates pro-apoptotic genes (BAX, BAD, APAF-1) while suppressing anti-apoptotic genes (BCL-2, BCL-XL)
BAD↑,
APAF1↑,
Bcl-2↓,
Bcl-xL↓,
P53↑,
cl‑PARP↑, eugenol activates executioner caspases-3 and -7, facilitating cleavage of critical substrates (PARP, DFF45) and morphological manifestations of apoptosis
TumCCA↑, Eugenol-treated cancer cells exhibit accumulation at the G2/M phase transition, accompanied by downregulation of cell cycle-promoting proteins (cyclin D1, cyclin B1, CDK2, CDK4) and upregulation of CDK inhibitors (p21, p27)
cycD1/CCND1↓,
CycB/CCNB1↓,
CDK2↓,
CDK4↓,
P21↑,
p27↑,
NF-kB↓, Eugenol inhibits IκB-α phosphorylation, preventing NF-κB nuclear translocation and transcriptional activity[
COX2↓, Eugenol downregulates COX-2 expression, reducing pro-tumorigenic prostaglandin production and associated inflammation[3]
PGE2↓,
MAPK↓, Suppression of MAPK cascade reduces cancer cell proliferation and survival
PI3K↓, PI3K/Akt/mTOR Pathway Blockade
Akt↓,
mTOR↓,
MMPs↓, Eugenol suppresses MMP expression and activity, reducing tumor cell invasive capacity
EMT↓, Eugenol suppresses EMT-promoting transcription factors (Snail, Slug, ZEB1), maintaining E-cadherin expression and cellular adhesion[5].
Snail↓,
Slug↓,
Zeb1↓,
E-cadherin↑,
ChemoSen↑, Emerging evidence suggests eugenol enhances anticancer efficacy of conventional
chemotherapeutic agents[5][6].
*neuroP↑, Experimental evidence suggests various neuroactive potentials of CP such as memory-enhancing, neuroprotective, and antiepileptic.
*memory↑,
*other↝, analysis predicted a total of five druglike phytochemicals from CP constituents, namely, scopoletin, 4-hydroxycinnamic acid, kaempferol, quercetin, and ayapanin
*AChE↓, scopoletin showed the highest binding affinity with PTGS1, NOS3, PPARG, ACHE, MAOA, MAOB, and TRKB
*MAOA↓,
*MAOB↓,
*TrkB↓,
*tau↓, CP treatment prevented protein and mRNA expressions of tau and amyloid precursor protein (APP) in scopolamine-induced rat brain
*APP↓,
*ROS↓, Scopoletin, a coumarin of CP, attenuated oxidative stress-mediated loss of dopaminergic neurons and increased the efficacy of dopamine in PD model
*Mood↑, In addition, CP improved anxiety, depression, and epileptic seizure
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*Inflam↓, its anti-inflammatory, anti-oxidant, and anti-apoptotic properties.
*antiOx↓,
*neuroP↑, potential applications of UA in neuroprotective strategies
*p‑tau↓, mainly in AD and ischemic neuronal injury resulting in improved cognition, reduced neuroinflammation, neuronal loss, tau phosphorylation, and amyloid plaques
*Aβ↓,
*eff↑, The bioavailability of ellagitannin is very low; however, their absorption may be increased by the co-intake of dietary fructooligosaccharides.
*BioAv↓, only 40% of individuals could naturally convert the polyphenolic precursors to UA
*BioAv↑, administration of UA is proposed to be an answer for urolithin non-producers, which could allow for the exploration of its health benefits
*GSH↑, UA administration protected against the cisplatin-induced depletion of the renal GSH pool, the inhibition of GPx and superoxide dismutase (SOD) activity
*SOD↑,
*lipid-P↓, declined lipid peroxidation and protein nitration were observed
*Catalase↑, UA not only enhanced the cellular antioxidant mechanism attributed to increased CAT, SOD, glutathione reductase (GR), and GPx activity, but also inhibited oxidizing enzymes contributing to reactive oxygen species (ROS)
*GSR↑,
*GPx↑,
*ROS↓,
*NRF2↑, Beneficial effects of UA, including antioxidant activity, are believed to be mediated through the activation of the Nrf2/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway
*GutMicro↑, enhancing the gut barrier integrity caused by the UA administration
*Risk↓, Urine UA elevation was reported to also be associated with decreased age-related hippocamp atrophy—a biomarker of neurodegeneration and cognitive decline
*BBB↓, free form of UA crossing the blood–brain barrier (BBB) in animal model studies
*NLRP3↓, UA downregulated NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome-mediated inflammation,
*MAOA↓, Another aspect of the role of UA in PD management is its inhibitory effects on monoamine oxidase (MAO).
Showing Research Papers: 1 to 13 of 13
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx⇅, 1, ROS↓, 1, ROS↑, 1, ROS⇅, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 2,
Cell Death ⓘ
Akt↓, 2, APAF1↑, 1, Apoptosis↓, 1, Apoptosis↑, 2, BAD↑, 1, BAX↑, 1, Bcl-2↓, 1, Bcl-xL↓, 1, Casp3↑, 1, Casp9↑, 1, Cyt‑c↓, 1, MAPK↓, 1, p27↑, 1, TumCD↑, 1,
Transcription & Epigenetics ⓘ
other↑, 1, tumCV↓, 1,
DNA Damage & Repair ⓘ
P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
ALDH↓, 1, EMT↓, 2, mTOR↓, 2, PI3K↓, 2, TumCG↓, 1,
Migration ⓘ
CAFs/TAFs↓, 1, E-cadherin↑, 1, MMPs↓, 2, Slug↓, 1, Snail↓, 1, TumCI↓, 1, TumCMig↓, 1, TumMeta↓, 1, Zeb1↓, 1,
Angiogenesis & Vasculature ⓘ
HIF-1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CXCR4↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 2, PGE2↓, 2,
Synaptic & Neurotransmission ⓘ
MAOA↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, ChemoSen↑, 3, Dose?, 1, eff↓, 1, Half-Life↓, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Total Targets: 59
Pathway results for Effect on Normal Cells:
NA, unassigned ⓘ
AntiBio↑, 1,
Redox & Oxidative Stress ⓘ
antiOx↓, 3, antiOx↑, 5, Catalase↑, 3, GPx↑, 2, GSH↑, 3, GSR↑, 1, GSTs↑, 1, HO-1↑, 2, lipid-P↓, 3, MDA↓, 2, NRF2↑, 3, RNS↓, 3, ROS↓, 9, SOD↓, 1, SOD↑, 3,
Core Metabolism/Glycolysis ⓘ
LDL↓, 1, PPARγ↑, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 2, iNOS↓, 2, MAPK↓, 2,
Transcription & Epigenetics ⓘ
Ach↑, 1, other↝, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 2, mTOR↑, 1, PI3K↓, 1, PI3K↑, 2, VGSC↓, 1,
Migration ⓘ
5LO↓, 2, AntiAg↑, 1, APP↓, 2, Ca+2↓, 1,
Barriers & Transport ⓘ
BBB↓, 1, BBB↑, 4,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1β↓, 4, IL6↓, 2, Inflam↓, 6, Inflam↑, 1, NF-kB↓, 2, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission ⓘ
5HT↑, 1, AChE↓, 6, AChE↑, 1, BChE↓, 2, BDNF↑, 2, ChAT↑, 1, GABA↑, 1, MAOA↓, 12, tau↓, 1, p‑tau↓, 2, TrkB↓, 1, TrkB↑, 1,
Protein Aggregation ⓘ
Aβ↓, 5, BACE↓, 2, MAOB↓, 3, NLRP3↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 2, Dose↝, 1, Dose∅, 1, eff↑, 3, selectivity↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1, IL6↓, 2,
Functional Outcomes ⓘ
chemoPv↑, 1, cognitive↑, 1, cognitive∅, 1, memory↑, 5, Mood↑, 1, motorD↑, 1, neuroP↑, 9, Pain↓, 1, Risk↓, 1, toxicity↓, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 81
Scientific Paper Hit Count for: MAOA, Monoamine Oxidase A
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#:472 State#:% Dir#:1
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