ROS Cancer Research Results

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



ROS">Copper (ionic / nano)
+++ ↓ [Fe][F] ROS-dominant
Fenton-type redox chemistry



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



ROS">Alpha-lipoic acid (ALA)
± ↑ [D][M] NRF2-dominant
Antioxidant at low dose



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



ROS">Quercetin
± ↑/↓ [D][Fe] NRF2-dominant
GSH-dependent cycling



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

AD, Alzheimer's Disease: Click to Expand ⟱

Brain Energy Systems Matrix (AD)

Tier 1–2 as “core metabolic cofactors / redox pools”
Tier 4 as “alternative fuels / bypass strategies”
Tier 5–6 as “capacity + delivery constraints” (often explains why supplements don’t translate)

Tier	Rank	Node / Lever	What it Supports (Bioenergetic Role)	Key Enzymes / Targets	AD-Relevant Mechanism	TSF	Evidence	Common Constraints / Gotchas
1	1	Thiamine (B1) / TPP	Glucose → acetyl-CoA entry + TCA throughput + NADPH support	PDH, α-KGDH, Transketolase (PPP)	Addresses cerebral glucose hypometabolism; improves mitochondrial flux; PPP→NADPH supports redox	R, G	Mechanistic + small clinical	Benefit strongest if low status; standard thiamine vs lipophilic derivatives differ
1	2	Benfotiamine	Higher-bioavailability B1 strategy	Transketolase ↑; glycation axis ↓	AGE/RAGE burden reduction + metabolic support (model/trial dependent)	G	Small clinical + mechanistic	Not a “rapid” effect; mostly longer-term metabolic/toxicity load reduction
1	3	Riboflavin (B2) / FAD, FMN	ETC redox enzymes + mitochondrial dehydrogenases	Complex I/II flavoproteins; many oxidoreductases	Supports electron handling; can be limiting in mitochondrial enzyme insufficiency	R, G	Mechanistic	Direct AD cognitive trial support limited; “helps” mostly when deficient or enzyme-limited
1	4	Niacin forms (B3) → NAD pool	NAD+/NADH redox + signaling + repair	NAD salvage; sirtuins; PARP substrate	NAD decline is an aging/inflammation theme; supports mitochondrial redox capacity	R, G	Emerging human + mechanistic	Different forms behave differently; NAD raising ≠ guaranteed clinical cognition benefit
1	5	Pantothenic acid (B5) → CoA	Acetyl-CoA formation; lipid metabolism; TCA entry	CoA biosynthesis; acetylation capacity	Foundational for fuel oxidation and acetylation balance	G	Mechanistic	Often overlooked; deficiency uncommon but suboptimal intake can matter in frailty
1	6	Magnesium	ATP handling (Mg-ATP) + enzyme kinetics	ATP-dependent enzymes; synaptic function	Supports neuronal energy usage + plasticity; deficiency can worsen excitotoxic vulnerability	R, G	Supportive human + mechanistic	Form/absorption variability; renal constraints for supplementation in some patients
2	1	NAD+ precursors (NR/NMN/NA/NAM)	Restores NAD+ availability for redox + signaling	NAMPT salvage; sirtuins; PARPs; CD38	Supports mitochondrial function; may improve resilience under oxidative/repair load	R, G	Animal > human (emerging)	NAD “sinks” (CD38/PARP) can dominate; response varies by inflammation/age
2	2	Alpha-lipoic acid (ALA)	Mitochondrial redox cofactor + antioxidant recycling	PDH/α-KGDH cofactor; GSH recycling support	Improves redox tone and mitochondrial efficiency (signals strongest in metabolic/oxidative phenotypes)	R, G	Small AD trials + mechanistic	“Antioxidant” framing can be misleading—main value is mitochondrial/redox coupling support
2	3	Glutathione system support	Detox + peroxide handling	GSH, GPx, GR, NADPH supply (PPP)	Reduces oxidative damage load that impairs mitochondria/synapses	R, G	Mechanistic	GSH depends on substrates + NADPH; pushing one component may not fix system
2	4	Selenium (GPx capacity)	Peroxide detox via selenoenzymes	Glutathione peroxidases	Supports antioxidant enzyme capacity (context-dependent)	G	Mixed human	Narrower safety margin; avoid “more is better” mindset
3	1	CoQ10 (ubiquinone)	ETC electron carrier (I/II→III) + membrane redox	Complex I/II→III transfer	Supports OXPHOS efficiency; may reduce electron leak under some conditions	R, G	Limited AD-specific	Bioavailability/formulation matters; AD cognition data not robust
3	2	Cardiolipin / mitochondrial membranes (support axis)	ETC supercomplex stability; cristae integrity	Inner mitochondrial membrane architecture	Membrane integrity affects ETC efficiency and ROS leak	G	Mechanistic	Hard to “target” nutritionally in a clean way; effects indirect
3	3	Iron / copper homeostasis (burden control)	Prevents metal-catalyzed oxidative damage	Fenton chemistry burden; metal transport/storage	Metal dyshomeostasis can amplify ROS and mitochondrial injury	R, G	Mechanistic + mixed human	“Chelation” is not casually safe; needs careful framing and evidence
4	1	Ketone utilization (BHB/acetoacetate axis)	Alternative brain fuel bypassing glucose bottlenecks	MCT1/2 transport; ketolysis enzymes	Addresses brain glucose hypometabolism by providing alternate substrate	R, G	Moderate (human MCI/AD signals exist)	GI tolerance and adherence; response varies by genotype/metabolic status
4	2	Creatine / phosphocreatine shuttle	ATP buffering and rapid energy stabilization	Creatine kinase system	May stabilize energy during stress; supports muscle/functional reserve that impacts cognition indirectly	G	Limited AD	CNS benefit uncertain; stronger for muscle/functional outcomes
4	3	Acetyl-L-carnitine (ALCAR)	Fatty acid oxidation support + acetyl group handling	Carnitine shuttle; acetyl-CoA support	May support mitochondrial energy and neuronal function (mixed clinical results)	R, G	Mixed human	Benefits heterogeneous; not a universal cognitive improver
4	4	Medium-chain triglycerides (MCT oil → ketones)	Rapid ketone support strategy	Hepatic ketogenesis; brain ketone uptake	Practical ketone-raising approach for some phenotypes	R, G	Moderate human	GI effects; calorie load; titration matters
5	1	AMPK → PGC-1α biogenesis axis	Mitochondrial number/quality regulation	AMPK, PGC-1α, SIRT1	Supports long-term mitochondrial capacity and stress resistance	G	Mechanistic	Most effects are slow; many “activators” are indirect and context-dependent
5	2	Mitophagy / autophagy quality control	Removes damaged mitochondria	PINK1/Parkin axis; autophagy machinery	Damaged mitochondria drive ROS and energy failure; quality control is protective in theory	G	Mechanistic	Autophagy modulation is double-edged; oversimplified “more autophagy = good” is risky
5	3	Exercise signaling (the “master cofactor”)	Improves vascular + mitochondrial + neurotrophic tone	BDNF; insulin sensitivity; AMPK/PGC-1α	Most evidence-backed multi-pathway energy intervention for aging brain	R, G	Strong (human)	Adherence/ability constraints; must be individualized
6	1	Cerebral perfusion / vascular health	Fuel + oxygen delivery and waste clearance support	Neurovascular unit; endothelial function	Vascular dysfunction worsens hypometabolism and inflammation	R, G	Strong (human)	Often upstream of “supplement” efficacy; if delivery is poor, cofactors underperform
6	2	Sleep / glymphatic clearance	Waste clearance & metabolic recovery	Glymphatic system; circadian regulation	Supports clearance of metabolic byproducts; indirectly supports energy balance	G	Strong (human)	Often neglected; impacts cognition and inflammation strongly
6	3	Oxygen utilization context (respiratory capacity)	Oxidative metabolism support	OXPHOS dependence	If oxygen delivery/usage is limited, pushing mitochondrial cofactors won’t fully translate	R, G	Supportive	More about system constraints than a “node to supplement”

TSF (Time-Scale Flag): P = 0–30 min, R = 30 min–3 hr, G = >3 hr (adaptation/phenotype). Evidence: "Strong (human)" = consistent clinical/epidemiologic support; "Moderate" = mixed but plausible human signals; "Emerging" = early-stage human; "Mechanistic" = preclinical/biochemical rationale.

Scientific Papers found: Click to Expand⟱

5296-

5-HTP,

Serotonergic Regulation in Alzheimer’s Disease

Review,

AD,

*Risk↓, *5HT↓, *ROS↓, *MDA↓, *Apoptosis↓, *Mood↑, *other↑, *other↑,

5289-

5-HTP,

5-Hydroxytryptophan (5-HTP): Natural Occurrence, Analysis, Biosynthesis, Biotechnology, Physiology and Toxicology

Review,

AD,

Review,

Arthritis,

*5HT↑, *Inflam↓, *memory↑, *Sleep↑, *Weight↓, *DNAdam↓, *ROS↓, *toxicity↝,

3970-

ACNs,

Anthocyanin-rich blueberry extracts and anthocyanin metabolite protocatechuic acid promote autophagy-lysosomal pathway and alleviate neurons damage in in vivo and in vitro models of Alzheimer's disease

in-vivo,

AD,

 150 mg/kg BBE daily for 16 wk.

 APP/PS1 mice

*cognitive↑, *LDH↓, *ROS↓, *neuroP↑,

3969-

ACNs,

Blueberry Supplementation in Midlife for Dementia Risk Reduction

Human,

AD,

Freeze-Dried Blueberry, 0.5 c whole-fruit equivalent administered once each day

Thirty-three participants

*memory↑, *cognitive↑, *ROS↓,

3864-

ACNs,

Anthocyanins Potentially Contribute to Defense against Alzheimer’s Disease

Review,

AD,

*antiOx↑, *Aβ↓, *ROS↓, *cognitive↑, *APP↓, *BBB↑, *Ca+2↓, *ATP↑, *BACE↓, *p‑NF-kB↓, *TNF-α↓, *iNOS↓,

2558-

AL,

Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment

Review,

AD,

*AntiCan↑, *antiOx↑, *cardioP↑, *neuroP↑, cognitive↑, *ROS↓, *NOX↓, *TLR4↓, *NF-kB↓, *JNK↓, *AntiAg↑, *H2S↑, *BP↓, Telomerase↓, *Insulin↑, BioAv↝, *GSH↑, *Catalase↑,

2657-

AL,

Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases

Review,

CardioV,

Review,

AD,

*Inflam↓, *antiOx↑, *neuroP↑, *cardioP↑, *AntiTum↑, *mtDam↑, *HSP70/HSPA5↑, *NRF2↑, *RAAS↓, *cognitive↑, *SOD↑, *ROS↓, *NRF2↑, *ER Stress↓, *neuroP↑, *memory↑, *TBARS↓, *MPO↓, *SOD↑, *GSH↑, *iNOS↓, *p‑eNOS↑, *HO-1↑,

2660-

AL,

Allicin: A review of its important pharmacological activities

Review,

AD,

Review,

Var,

Review,

Park,

Review,

Stroke,

*Inflam↓, AntiCan↑, *antiOx↑, *cardioP↑, *hepatoP↑, *BBB↑, *Half-Life↝, *H2S↑, *BP↓, *neuroP↑, *cognitive↑, *neuroP↑, *ROS↓, *GutMicro↑, *LDH↓, *ROS↓, *lipid-P↓, *antiOx↑, *other↑, *PI3K↓, *Akt↓, *NF-kB↓, *NO↓, *iNOS↓, *PGE2↓, *COX2↓, *IL6↓, *TNF-α↓, *MPO↓, *eff↑, *NRF2↑, *Keap1↓, *TBARS↓, *creat↓, *LDH↓, *AST↓, *ALAT↓, *MDA↓, *SOD↑, *GSH↑, *GSTs↑, *memory↑, chemoP↑, IL8↓, Cyt‑c↑, Casp3↑, Casp8↑, Casp9↑, Casp12↑, p38↑, Fas↑, P53↑, P21↑, CHK1↓, CycB/CCNB1↓, GSH↓, ROS↑, TumCCA↑, Hif1a↓, Bcl-2↓, VEGF↓, TumCMig↓, STAT3↓, VEGFR2↓, p‑FAK↓,

3270-

ALA,

Alpha-lipoic acid as a new treatment option for Alzheimer's disease--a 48 months follow-up analysis

Trial,

AD,

600mg alpha-lipoic acid was given daily to nine patients

 43 AD
patients treated with a-lipoic acid for periods up to 4 years
were analyzed.

*cognitive↑, *other↝, *neuroP↑, *IronCh↑, *ROS↓, *GSH↑,

3271-

ALA,

Decrypting the potential role of α-lipoic acid in Alzheimer's disease

Review,

AD,

*antiOx↑, *memory↑, *neuroP↑, *Inflam↓, *IronCh↑, *NRF2↑, *BBB↑, *GlucoseCon↑, *Ach↑, *ROS↓, *p‑tau↓, *Aβ↓, *cognitive↑, *Hif1a↑, *Ca+2↓, *GLUT3↑, *GLUT4↑, *HO-1↑, *VEGF↑, *PDKs↓, *PDH↑, *VCAM-1↓, *GSH↑, *NRF2↑, *hepatoP↑, *ChAT↑,

3438-

ALA,

The Potent Antioxidant Alpha Lipoic Acid

Review,

NA,

Review,

AD,

*antiOx↑, *cardioP↑, *cognitive↑, *AntiAge↑, *Inflam↓, *AntiCan↑, *neuroP↑, *IronCh↑, *ROS↑, *Weight↓, *Ach↑, *ROS↓, *GSH↑, *lipid-P↓, *memory↑, *NRF2↑, *ChAT↑, *GlucoseCon↑, *Acetyl-CoA↑,

3440-

ALA,

Protective effects of alpha lipoic acid (ALA) are mediated by hormetic mechanisms

Review,

AD,

*ROS↓, *neuroP↑, *Aβ↓, *cardioP?,

3443-

ALA,

Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention

Review,

Var,

Review,

AD,

*antiOx↑, *ROS↓, *IronCh↑, *cognitive↑, *cardioP↓, AntiCan↑, *neuroP↑, *Inflam↓, *BioAv↓, *AntiAge↑, *Half-Life↓, *BioAv↝, other↝, EGFR↓, Akt↓, ROS↓, TumCCA↑, p27↑, PDH↑, Glycolysis↓, ROS↑, *eff↑, *memory↑, *motorD↑, *GutMicro↑,

3447-

ALA,

Redox Active α-Lipoic Acid Differentially Improves Mitochondrial Dysfunction in a Cellular Model of Alzheimer and Its Control Cells

in-vitro,

AD,

SH-SY5Y

*ATP↑, *MMP↑, *ROS↓, *GlucoseCon↑, *GSH↑, *neuroP↑, *cognitive↑, *Ach↑, *Inflam↓, *Aβ↓, OXPHOS↓,

3539-

ALA,

Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential

Review,

AD,

*ROS↓, *IronCh↑, *GSH↑, *antiOx↑, *NRF2↑, *MMP9↓, *VCAM-1↓, *NF-kB↓, *cognitive↑, *Inflam↓, *BioAv↝, *BioAv↝, *BBB↑, *H2O2∅, *neuroP↑, *PKCδ↑, *ERK↑, *MAPK↑, *PI3K↑, *Akt↑, *PTEN↓, *AMPK↑, *GLUT4↑, *GlucoseCon↑, *BP↝, *eff↑, *ICAM-1↓, *VCAM-1↓, *Dose↝,

3543-

ALA,

The Effect of Lipoic Acid Therapy on Cognitive Functioning in Patients with Alzheimer's Disease

Study,

AD,

600 mg/day

 126 patients (75 women and 51 men) with AD

*cognitive↑, *antiOx↑, *Inflam↓, *neuroP↑, *Ach↑, *ROS↓, *GlucoseCon↑, *lipid-P↓, *GSH↑, *Acetyl-CoA↑,

3550-

ALA,

Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer's Disease?

Review,

AD,

*antiOx↑, *Inflam↓, *PGE2↓, *COX2↓, *iNOS↓, *TNF-α↓, *IL1β↓, *IL6↓, *BioAv↓, *Ach↑, *ROS↓, *cognitive↑, *neuroP↑, *BBB↑, *Half-Life↓, *BioAv↑, *Casp3↓, *Casp9↓, *ChAT↑, *cognitive↑, *eff↑, *cAMP↑, *IL2↓, *INF-γ↓, *TNF-α↓, *SIRT1↑, *SOD↑, *GPx↑, *MDA↓, *NRF2↑,

3549-

ALA,

Important roles of linoleic acid and α-linolenic acid in regulating cognitive impairment and neuropsychiatric issues in metabolic-related dementia

Review,

AD,

*Inflam↓, *other↝, *other↝, *neuroP↑, *BioAv↝, *adiP↑, *BBB↑, *Casp6↓, *Casp9↓, *TNF-α↓, *IL6↓, *IL1β↓, *ROS↓, *NO↓, *iNOS↓, *COX2↓, *JNK↓, *p‑NF-kB↓, *Aβ↓, *BP↓, *memory↑, *cAMP↑, *ERK↑, *Akt↑, cognitive?,

3548-

ALA,

How Alpha Linolenic Acid May Sustain Blood–Brain Barrier Integrity and Boost Brain Resilience against Alzheimer’s Disease

Review,

AD,

*BBB↑, *other↑, *other↑, *DHA↑, *neuroP↑, *ROS↓, *other?,

3546-

ALA,

Cognitive and Mood Effect of Alpha-Lipoic Acid Supplementation in a Nonclinical Elder Sample: An Open-Label Pilot Study

Study,

AD,

fifteen elder patients (mean age: 84.5 ± 5.77) received ALA at a daily dose of 600 mg/day for 12 weeks.

*antiOx↑, *ROS↓, *cognitive∅, *lipid-P↓, *memory↑, *ChAT↑, *Acetyl-CoA↑, *Aβ↓, *BioAv↑, *BBB↑, *toxicity∅,

3545-

ALA,

Potential therapeutic effects of alpha lipoic acid in memory disorders

Review,

AD,

*neuroP↑, *Inflam↓, *VCAM-1↓, *5HT↑, *memory↑, *BioAv↝, *Half-Life↓, *NF-kB↓, *antiOx↑, *IronCh↑, *ROS↓, *ATP↑, *ChAT↑, *Ach↑, *cognitive↑, *lipid-P↓, *VitC↑, *VitE↑, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *Aβ↓,

3544-

ALA,

Alpha lipoic acid for dementia

Review,

AD,

*antiOx↑, *BBB↑, *VitC↑, *VitE↑, *GSH↑, *IronCh↑, *neuroP↑, *NO↓, *cognitive↑, *AntiAge↑, *memory↑, *ROS↓,

297-

ALA,

Insights on the Use of α-Lipoic Acid for Therapeutic Purposes

Review,

BC,

SkBr3

Review,

neuroblastoma,

SK-N-SH

Review,

AD,

PDH↑, TumCG↓, ROS↑, AMPK↑, EGR4↓, Half-Life↓, BioAv↝, *GSH↑, *IronCh↑, *ROS↓, *antiOx↑, *neuroP↑, *Ach↑, *lipid-P↓, *IL1β↓, *IL6↓, TumCP↓, FDG↓, Apoptosis↑, AMPK↑, mTOR↓, EGFR↓, TumCI↓, TumCMig↓, *memory↑, *BioAv↑, *BioAv↝, *other↓, *other↝, *Half-Life↓, *BioAv↑, *ChAT↑, *GlucoseCon↑,

3859-

ALC,

Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer’s Disease Treatment

Review,

AD,

*ROS↓, *ADAM10↑,

4280-

Api,

Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms

Review,

AD,

Review,

Park,

*neuroP↑, *antiOx↑, *ROS↓, *Inflam↓, *TNF-α↓, *IL1β↓, *PI3K↑, *Akt↑, *BBB↑, *NRF2↑, *SOD↑, *GPx↑, *MAPK↓, *Catalase↑, *HO-1↑, *COX2↓, *PGE2↓, *PPARγ↑, *TLR4↓, *GSK‐3β↓, *Aβ↓, *NLRP3↓, *BDNF↑, *TrkB↑, *GABA↑, *AChE↓, *Ach↑, *5HT↑, *cognitive↑, *MAOA↓,

3887-

Api,

The flavonoid apigenin protects brain neurovascular coupling against amyloid-β₂₅₋₃₅-induced toxicity in mice

in-vivo,

AD,

mice

*Inflam↓, *ROS↓, *Aβ↓, *memory↑, *AChE↓, *Ach↑, *Dose↑, *BDNF↑, *TrkB↑, *p‑CREB↑, *BBB↑, *Ca+2?,

3884-

Api,

Neuroprotective, Anti-Amyloidogenic and Neurotrophic Effects of Apigenin in an Alzheimer’s Disease Mouse Model

in-vivo,

AD,

double transgenic AD mice

*memory↑, *Aβ↓, *BACE↓, *antiOx↑, *BDNF↑, *p‑CREB↑, *p‑ERK↑, *ROS↓, *SOD↑, *GPx↑, *neuroP↑,

3817-

Aroma,

Therapeutic potential of aromatic plant extracts in Alzheimer's disease: Comprehensive review of their underlying mechanisms

Review,

AD,

*BChE↓, *AChE↓, *other↓, *other?, *Ach?, *eff↑, *antiOx↑, *ROS↓, *cognitive↑, *Mood↑, *Sleep↑,

3821-

Aroma,

Neuroprotective and Anti-Aging Potentials of Essential Oils from Aromatic and Medicinal Plants

Review,

AD,

*cognitive↑, *AChE↓, *BChE↓, *ROS↓, *other↓, *other↓, *other↓, *other↓, *other↓, *memory↑, *BACE↓, *Mood↑, *motorD↑,

3666-

ART/DHA,

Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling

NA,

AD,

*Inflam↓, *neuroP↑, *TLR4↓, *NF-kB↓, *memory↑, *ROS↓, *iNOS↓, *COX2↓, *cognitive↑,

3670-

Ash,

Neurodegenerative diseases and Withania somnifera (L.): An update

Review,

AD,

Review,

Park,

*Apoptosis↓, *Inflam↓, *ROS↓, *neuroP↑,

3687-

Ash,

Role of Withaferin A and Its Derivatives in the Management of Alzheimer’s Disease: Recent Trends and Future Perspectives

Review,

AD,

*Aβ↓, *tau↓, *HSPs↝, *antiOx↑, *ROS↓, *Inflam↓, *neuroP↑, *cognitive↑, *NF-kB↓, *HO-1↑, *memory↑, *AChE↓, *BChE↓, *ChAT↑, *Ach↑,

4303-

Ash,

Ashwagandha (Withania somnifera)—Current Research on the Health-Promoting Activities: A Narrative Review

Review,

AD,

*neuroP↑, *Sleep↑, *Inflam↓, *cardioP↑, *cognitive↑, *Aβ↓, *TNF-α↓, *IL1β↓, *IL6↓, *MCP1↓, *lipid-P↓, *tau↓, *ROS↓, *BBB↑, *AChE↓, *GSH↑, *GSTs↑, *GSR↑, *GPx↑, *SOD↑, *Catalase↑, ChemoSen↑, *Strength↑,

4813-

ASTX,

Astaxanthin Prevents Oxidative Damage and Cell Apoptosis Under Oxidative Stress Involving the Restoration of Mitochondrial Function

in-vitro,

AD,

*antiOx↑, *Apoptosis↓, *AntiTum↑, *ROS↓, *MMP↑, *neuroP↑,

5425-

ASTX,

Multiple roles of fucoxanthin and astaxanthin against Alzheimer's disease: Their pharmacological potential and therapeutic insights

in-vivo,

AD,

*neuroP↑, *antiOx↑, *Inflam↑, *AChE↓, *BACE↓, *MAOA↓, *Aβ↓, *memory↑, *MDA↓, *SOD↑, *NRF2↑, *HO-1↑, *NF-kB↓, *GSK‐3β↓, *ChAT↑, *iNOS↓, *ROS↓, *BBB↑,

5508-

Ba,

Neuroprotective effects of baicalin and baicalein on the central nervous system and the underlying mechanisms

Review,

Stroke,

Review,

Park,

Review,

AD,

*neuroP↑, *antiOx↑, *Inflam↓, *BioAv↝, *BioAv↑, *Half-Life↝, *TLR4↓, *NF-kB↓, *iNOS↓, *COX2↓, *TNF-α↓, *12LOX↓, *NLRP3↓, *ROS↓, *IL1β↓, *IL6↓, *GSK‐3β↓, *NRF2↑, *BBB↑, *SOD↑, *GPx↑, *MDA↓,

2611-

Ba,

Baicalein as a potent neuroprotective agent: A review

Review,

Nor,

Review,

AD,

Review,

Park,

*neuroP↑, *ROS↓, *β-Amyloid↓,

2605-

Ba,

BA,

Potential therapeutic effects of baicalin and baicalein

Review,

Var,

Review,

Stroke,

Review,

IBD,

Review,

Arthritis,

Review,

AD,

Review,

Park,

cardioP↑, Inflam↓, cognitive↑, *hepatoP↑, *ROS?, *SOD↑, *GSH↑, *MMP↑, *GutMicro↑, ChemoSen↑, *TNF-α↓, *IL10↑, *IL6↓, *eff↑, *ROS↓, *COX2↓, *NF-kB↓, *STAT3↓, *PGE2↓, *MPO↓, *IL1β↓, *MMP2↓, *MMP9↓, *β-Amyloid↓, *neuroP↑, *Dose↝, *BioAv↝, *BioAv↝, *BBB↑, *BDNF↑,

2689-

BBR,

Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells

in-vitro,

Nor,

PC12

in-vitro,

AD,

in-vitro,

Stroke,

*ROS↓, *lipid-P↓, *DNAdam↓, *GSH↑, *SOD↑, *eff↑, *cl‑Casp3↓, *BAX↓, *neuroP↑, *Dose↝, *Ca+2↓,

2679-

BBR,

Berberine Improves Behavioral and Cognitive Deficits in a Mouse Model of Alzheimer’s Disease via Regulation of β-Amyloid Production and Endoplasmic Reticulum Stress

in-vivo,

AD,

*cognitive↑, PERK↓, *eIF2α↓, *neuroP↑, *ER Stress↓, *ROS↓,

3677-

BBR,

Berberine: A Potential Multipotent Natural Product to Combat Alzheimer’s Disease

Review,

AD,

0.44uM(AChEi)

*antiOx↑, *AChE↓, *BChE↓, *MAOA↓, *Aβ↓, *LDL↓, *ROS↓, *RNS↓, *lipid-P↓, *Dose↝, *MAOB↓, *memory↑, *toxicity↓, *BBB↑,

3678-

BBR,

Network pharmacology study on the mechanism of berberine in Alzheimer’s disease model

Review,

AD,

*APP↓, *PPARγ↑, *NF-kB↓, *Aβ↓, *cognitive↑, *antiOx↑, *Inflam↓, *Apoptosis↓, *BioAv↑, *BioAv↝, *BBB↑, *motorD↑, *NRF2↑, *HO-1↑, *ROS↓, *p‑Akt↑, *p‑ERK↑,

3679-

BBR,

Berberine alleviates Alzheimer's disease by activating autophagy and inhibiting ferroptosis through the JNK-p38MAPK signaling pathway

in-vivo,

AD,

5xFAD mice

*Beclin-1↑, *LC3B↑, *p62↓, *ROS↓, *lipid-P↓, *MDA↓, *Ferroptosis↓, *TfR1/CD71↓, *FTH1↑, *memory↑, *JNK↓, *p38↓, *Aβ↓, *Inflam↓,

3680-

BBR,

Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway

in-vivo,

AD,

3 × Tg AD mice

*Akt↑, *neuroP↑, *p‑ERK↑, *Aβ↓, *Inflam↓, *ROS↓, *BioAv↑, *BBB↑, *Half-Life↝, *memory↑, *cognitive↑, *HSP90↑, *APP↓, *mTOR↓, *P70S6K↓, *CD31↑, *VEGF↑, *N-cadherin↑, *Apoptosis↓,

3684-

BBR,

Neuroprotective effects of berberine in animal models of Alzheimer’s disease: a systematic review of pre-clinical studies

Review,

AD,

*Inflam↓, *antiOx↓, *AChE↓, *BChE↓, *MAOA↓, *MAOB↓, *lipid-P↓, *GSH↑, *ROS↓, *APP↓, *BACE↓, *p‑tau↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *MAPK↓, *PI3K↓, *Akt↓, *neuroP↑, *memory↑,

4299-

BBR,

Berberine attenuates cognitive impairment and ameliorates tau hyperphosphorylation by limiting the self-perpetuating pathogenic cycle between NF-κB signaling, oxidative stress and neuroinflammation

in-vivo,

AD,

AD mice

*memory↑, *p‑tau↓, *NF-kB↓, *GSH↑, *lipid-P↓, *cognitive↑, *ROS↓, *Inflam↓,

5631-

BCA,

Perspectives Regarding the Role of Biochanin A in Humans

Review,

Var,

Review,

AD,

*BioAv↓, *Inflam↓, AntiCan↑, *neuroP↑, chemoPv↑, Dose↝, *SOD↑, *MDA↓, *BAX↓, *HSP70/HSPA5↑, *AntiDiabetic↑, *Insulin↑, *TNF-α↓, *IL1β↓, *IL6↓, *iNOS↓, *COX2↓, *MMP9↓, *ROS↓, *PGE2↓, *BACE↓, *BioAv↑, P-gp⇅,

5633-

BCA,

Mechanisms Behind the Pharmacological Application of Biochanin-A: A review

Review,

Var,

Review,

AD,

*AntiDiabetic↑, *neuroP↑, *toxicity↓, *CYP19↓, p‑Akt↓, mTOR↓, TumCCA↑, P21↑, Casp3↑, Bcl-2↑, Apoptosis↑, E-cadherin↓, TumMeta↓, eff↑, GSK‐3β↓, β-catenin/ZEB1↓, RadioS↑, ROS↑, Casp1↑, MMP2↓, MMP9↓, EGFR↓, ChemoSen↑, PI3K↓, MMPs↓, Hif1a↓, VEGF↓, *ROS↓, *Obesity↓, *cardioP↑, *NRF2↑, *NF-kB↓, *Inflam↓, *lipid-P↓, *hepatoP↑, *AST↓, *ALP↓, *Bacteria↓, *neuroP↑, *SOD↑, *GPx↑, *AChE↓, *BACE↓, *memory↑, *BioAv↓,

2731-

BetA,

Betulinic Acid for Glioblastoma Treatment: Reality, Challenges and Perspectives

Review,

GBM,

Review,

Park,

Review,

AD,

BBB↑, *GSH↑, *Catalase↑, *motorD↑, *neuroP↑, *cognitive↑, *ROS↓, *antiOx↑, *Inflam↓, MMP↓, STAT3↓, NF-kB↓, Sp1/3/4↓, TOP1↓, EMT↓, Hif1a↓, VEGF↓, ChemoSen↑, RadioS↑, BioAv↓,

5561-

betaCar,

Carotenoid Supplementation for Alleviating the Symptoms of Alzheimer’s Disease

Review,

AD,

*ROS↓, *cognitive↑, *BBB↑, *lipid-P↓, *eff↑,

Showing Research Papers: 1 to 50 of 271
Page 1 of 6 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 271

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 25, Catalase↑, 5, Ferroptosis↓, 1, GPx↑, 7, GSH↑, 18, GSR↑, 1, GSTs↑, 2, H2O2∅, 1, HO-1↑, 6, Keap1↓, 1, lipid-P↓, 14, MDA↓, 7, MPO↓, 3, NRF2↑, 13, RNS↓, 1, ROS?, 1, ROS↓, 51, ROS↑, 1, SOD↑, 14, TBARS↓, 2, VitC↑, 2, VitE↑, 2,

Metal & Cofactor Biology ⓘ

FTH1↑, 1, IronCh↑, 8, TfR1/CD71↓, 1,

Mitochondria & Bioenergetics ⓘ

ATP↑, 3, Insulin↑, 2, MMP↑, 3, mtDam↑, 1,

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1, Acetyl-CoA↑, 3, adiP↑, 1, ALAT↓, 1, AMPK↑, 1, cAMP↑, 2, p‑CREB↑, 2, DHA↑, 1, GlucoseCon↑, 6, H2S↑, 2, LDH↓, 3, LDL↓, 1, PDH↑, 1, PDKs↓, 1, PPARγ↑, 2, SIRT1↑, 1,

Cell Death ⓘ

Akt↓, 2, Akt↑, 4, p‑Akt↑, 1, Apoptosis↓, 5, BAX↓, 2, Casp3↓, 1, cl‑Casp3↓, 1, Casp6↓, 1, Casp9↓, 2, Ferroptosis↓, 1, iNOS↓, 9, JNK↓, 3, MAPK↓, 2, MAPK↑, 1, p38↓, 1,

Transcription & Epigenetics ⓘ

Ach?, 1, Ach↑, 10, other?, 2, other↓, 7, other↑, 5, other↝, 4,

Protein Folding & ER Stress ⓘ

eIF2α↓, 1, ER Stress↓, 2, HSP70/HSPA5↑, 2, HSP90↑, 1, HSPs↝, 1,

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1, LC3B↑, 1, p62↓, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 2,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 2, p‑ERK↑, 3, GSK‐3β↓, 3, mTOR↓, 1, P70S6K↓, 1, PI3K↓, 2, PI3K↑, 2, PTEN↓, 1, STAT3↓, 1,

Migration ⓘ

AntiAg↑, 1, APP↓, 4, Ca+2?, 1, Ca+2↓, 3, CD31↑, 1, MMP2↓, 1, MMP9↓, 3, N-cadherin↑, 1, PKCδ↑, 1, VCAM-1↓, 4,

Angiogenesis & Vasculature ⓘ

p‑eNOS↑, 1, Hif1a↑, 1, NO↓, 3, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↑, 19, GLUT3↑, 1, GLUT4↑, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 8, ICAM-1↓, 1, IL10↑, 1, IL1β↓, 9, IL2↓, 1, IL6↓, 8, INF-γ↓, 1, Inflam↓, 27, Inflam↑, 1, MCP1↓, 1, NF-kB↓, 13, p‑NF-kB↓, 2, PGE2↓, 5, TLR4↓, 4, TNF-α↓, 11,

Cellular Microenvironment ⓘ

NOX↓, 1,

Synaptic & Neurotransmission ⓘ

5HT↓, 1, 5HT↑, 3, AChE↓, 10, ADAM10↑, 1, BChE↓, 5, BDNF↑, 4, ChAT↑, 8, GABA↑, 1, MAOA↓, 4, tau↓, 2, p‑tau↓, 3, TrkB↑, 2,

Protein Aggregation ⓘ

Aβ↓, 17, BACE↓, 7, MAOB↓, 2, NLRP3↓, 2, β-Amyloid↓, 2,

Hormonal & Nuclear Receptors ⓘ

CYP19↓, 1, RAAS↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 4, BioAv↑, 8, BioAv↝, 10, Dose↑, 1, Dose↝, 4, eff↑, 8, Half-Life↓, 4, Half-Life↝, 3,

Clinical Biomarkers ⓘ

ALAT↓, 1, ALP↓, 1, AST↓, 2, BP↓, 3, BP↝, 1, creat↓, 1, GutMicro↑, 3, IL6↓, 8, LDH↓, 3,

Functional Outcomes ⓘ

AntiAge↑, 3, AntiCan↑, 2, AntiDiabetic↑, 2, AntiTum↑, 2, cardioP?, 1, cardioP↓, 1, cardioP↑, 6, cognitive↑, 28, cognitive∅, 1, hepatoP↑, 4, memory↑, 24, Mood↑, 3, motorD↑, 4, neuroP↑, 39, Obesity↓, 1, Risk↓, 1, Sleep↑, 3, Strength↑, 1, toxicity↓, 2, toxicity↝, 1, toxicity∅, 1, Weight↓, 2,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 177

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

16 Curcumin
15 Alpha-Lipoic-Acid
15 Hydrogen Gas
10 Selenium NanoParticles
10 Resveratrol
10 Quercetin
9 Lycopene
8 Berberine
8 Bacopa monnieri
8 Ferulic acid
8 Magnetic Fields
8 Urolithin
7 Chlorogenic acid
7 Rosmarinic acid
7 Thymoquinone
5 Carnosine
5 Honokiol
5 Moringa oleifera
5 Sulforaphane (mainly Broccoli)
5 Silymarin (Milk Thistle) silibinin
4 Coenzyme Q10
4 Crocetin
4 EGCG (Epigallocatechin Gallate)
4 Magnetic Field Rotating
3 Anthocyanins
3 Allicin (mainly Garlic)
3 Apigenin (mainly Parsley)
3 Ashwagandha(Withaferin A)
3 Baicalein
3 Boswellia (frankincense)
3 Caffeic acid
3 Luteolin
3 Piperine
3 Rutin
3 Shankhpushpi
3 Vitamin K2
2 5-Hydroxytryptophan
2 Aromatherapy
2 Astaxanthin
2 Biochanin A
2 Boron
2 Carnosic acid
2 Capsaicin
2 Carvacrol
2 Celastrol
2 chitosan
2 Cinnamon
2 Vitamin E
2 Galantamine
2 Huperzine A/Huperzia serrata
2 Folic Acid, Vit B9
2 Ginkgo biloba
2 Potassium
2 MCToil
2 nicotinamide adenine dinucleotide
2 Propolis -bee glue
2 Radio Frequency
2 EMF
2 Ursolic acid
2 Vitamin B1/Thiamine
1 Acetyl-l-carnitine
1 Artemisinin
1 Baicalin
1 Betulinic acid
1 beta-carotene(VitA)
1 borneol
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Choline
1 Selenium
1 Rivastigmine
1 hydrogen sulfide
1 Juglone
1 Melatonin
1 Metformin
1 Methylsulfonylmethane
1 Mushroom Lion’s Mane
1 Vitamin B3,Niacin
1 Parthenolide
1 Pterostilbene
1 Salvia officinalis
1 Sesame seeds and Oil
1 Selenite (Sodium)
1 Taurine
1 Thymol-Thymus vulgaris
1 Vitamin B12
1 Vitamin B5,Pantothenic Acid
1 Vitamin C (Ascorbic Acid)
1 probiotics

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:38  Cells:%  prod#:%  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

ROS Cancer Research Results

Brain Energy Systems Matrix (AD)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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