MAOA Cancer Research Results

MAOA, Monoamine Oxidase A: Click to Expand ⟱
Source:
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
Scientific Papers found: Click to Expand⟱
4280- Api,    Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms
- Review, AD, NA - Review, Park, NA
*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

5425- ASTX,    Multiple roles of fucoxanthin and astaxanthin against Alzheimer's disease: Their pharmacological potential and therapeutic insights
- in-vivo, AD, NA
*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

3677- BBR,    Berberine: A Potential Multipotent Natural Product to Combat Alzheimer’s Disease
- Review, AD, NA
*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

3684- BBR,    Neuroprotective effects of berberine in animal models of Alzheimer’s disease: a systematic review of pre-clinical studies
- Review, AD, NA
*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

3637- Cro,    Investigation of the neuroprotective action of saffron (Crocus sativus L.) in aluminum-exposed adult mice through behavioral and neurobiochemical assessment
- NA, AD, NA
*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.

1616- CUR,  EA,    Kinetics of Inhibition of Monoamine Oxidase Using Curcumin and Ellagic Acid
- in-vitro, Nor, NA
*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)

140- CUR,    Curcumin inhibits cancer-associated fibroblast-driven prostate cancer invasion through MAOA/mTOR/HIF-1α signaling
- in-vitro, Pca, PC3
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↓,

3943- Shank,    Protective Mechanisms of Nootropic Herb Shankhpushpi (Convolvulus pluricaulis) against Dementia: Network Pharmacology and Computational Approach
- Review, AD, NA
*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

4876- Uro,    Urolithin A in Health and Diseases: Prospects for Parkinson’s Disease Management
- Review, Park, NA - Review, AD, NA
*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 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   mTOR↓, 1,  

Migration ⓘ

CAFs/TAFs↓, 1,  

Angiogenesis & Vasculature ⓘ

HIF-1↓, 1,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   IL6↓, 1,  

Synaptic & Neurotransmission ⓘ

MAOA↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose?, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 2,   antiOx↑, 3,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 3,   GSR↑, 1,   HO-1↑, 2,   lipid-P↓, 3,   MDA↓, 2,   NRF2↑, 3,   RNS↓, 1,   ROS↓, 6,   SOD↑, 3,  

Core Metabolism/Glycolysis ⓘ

LDL↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   iNOS↓, 1,   MAPK↓, 2,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 2,   PI3K↓, 1,   PI3K↑, 1,  

Migration ⓘ

APP↓, 2,  

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 3,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 2,   Inflam↓, 3,   Inflam↑, 1,   NF-kB↓, 2,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

5HT↑, 1,   AChE↓, 6,   BChE↓, 2,   BDNF↑, 1,   ChAT↑, 1,   GABA↑, 1,   MAOA↓, 8,   tau↓, 1,   p‑tau↓, 2,   TrkB↓, 1,   TrkB↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 4,   BACE↓, 2,   MAOB↓, 3,   NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 1,   Dose∅, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   cognitive∅, 1,   memory↑, 4,   Mood↑, 1,   neuroP↑, 5,   Risk↓, 1,   toxicity↓, 1,  
Total Targets: 63

Scientific Paper Hit Count for: MAOA, Monoamine Oxidase A
2 Berberine
2 Curcumin
1 Apigenin (mainly Parsley)
1 Astaxanthin
1 Crocetin
1 Ellagic acid
1 Shankhpushpi
1 Urolithin
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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