NO Cancer Research Results

NO, Nitric Oxide: Click to Expand ⟱

Source:

Type:

Once the cancer has begun, NO seems to play a protumoral role rather than antitumoral one as the concentration required to cause tumor cell cytotoxicity cannot be achieved by cancer cells.
The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, being both pro-and antitumorigenic, which complicates the development of cancer treatments based on the modulation of NO fluxes in tumors. At a fundamental level, low levels of NO drive oncogenic pathways, immunosuppression, metastasis, and angiogenesis, while higher levels lead to apoptosis and reduced hypoxia and also sensitize tumors to conventional therapies. However, clinical outcome depends on the type and stage of the tumor as well as the tumor microenvironment.
Nitric oxide is generated by three main nitric oxide synthase isoforms: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS).

– In many cancers, especially under inflammatory conditions, iNOS expression is upregulated. In contrast, eNOS levels may also be altered in cancers such as breast or prostate cancer.

• Expression Patterns in Tumors:
– Elevated iNOS expression is commonly observed in various tumor types (e.g., colon, breast, lung, and melanoma) and is often associated with an inflammatory microenvironment.

– Changes in eNOS and nNOS expression have also been reported and may contribute to angiogenesis and tumor blood flow regulation.

AD, Alzheimer's Disease: Click to Expand ⟱

In Alzheimer's disease (AD), cholinergic dysfunction (often with reduced acetylcholine tone and impaired choline metabolism) is linked with cortical dysfunction, memory deficit, abnormal cerebral blood flow, task learning difficulty, sleep-cycle disruption, and neurodevelopmental effects (context-dependent).
CORE HALLMARKS / HIGH-CONFIDENCE AXES:
- tau and Aβ, their accumulation in AD brains is known to be a major hallmark.
  In AD, PP2A↓ activity is decreased (reported), contributing to hyperphosphorylated tau accumulation.
  SIRT-1↓ levels in AD brains are associated with accumulation of Aβ and tau (reported).
- glucose metabolism↓ (brain glucose hypometabolism) occurs in AD long before significant clinical signs in many cohorts/models (reported).
- Neuroinflammation / lipid mediator tone (reported): 5-LOX↑ and PGE2↑ (model-/region-dependent).
- Synaptic vulnerability (reported): PSD95↓ in hippocampus and cortex; restoring PSD95 shows cognitive benefits in models.
- Clearance/transport imbalance (reported): IDE↓, NEP↓, LRP1↓, and AEP↑ protein levels in AD brains (reported).

COMMONLY REPORTED DIRECTIONAL CHANGES (model/region/compartment dependent):
- Monoamines (reported): concentrations of 5-HTP↓, 5-HT(seratonin)↓, and 5-HIAA↓ are lower in Alzheimer's patients (varies by region/study).
- Cholinergic system (clinical target): reduction in ACh↓ production; ChAT↓ activity reduced (synthesizes ACh).
- Four key enzymes frequently targeted in AD symptom/adjunct strategies: AChE, BChE, MAOA, MAOB (objective inhibit).
- Neurotrophic tone (reported): BDNF↓ in key regions.
  - Stress can decrease expression of brain-derived neurotrophic factor (BDNF).
- Kinase/protease stress (reported): CDK5↑ hyperactivation; calpain↑ overactivated by increased intracellular Ca²⁺ → p-tau and aggregation.
- Aβ-linked synaptic regulator (reported): STEP↑ upregulated largely due to Aβ oligomer accumulation.
- α-secretase axis (reported): ADAM10↓ downregulated in AD brains.
- Metabolic cofactors (reported): ALC↓ (ALCAR); Homocarnosine↓ (CSF declines with age); possible low Taurine↓ (age-related + dementia reports).
- Ion/glutamate handling (reported): impaired glutamate clearance + depressed Na+/K+ ATPase → cellular ion imbalance risk.
- Aging reduces NAD⁺↓ (in AD depletion may be more severe).
- Mitochondrial capacity axis (reported): PGC-1↓ decreased in Alzheimer’s brains.
- Innate immune DNA-sensing axis (animal): cGAS–STING↑ elevation observed in AD mice and normalized by NR treatment.
- Vascular/structure (reported): a profound change in BBB permeability; progressive brain shrinkage (atrophy).
- Glycation axis (reported): AGEs↑ and RAGE↑ expression.
- cerebrospinal fluid (CSF) TMAO is higher in individuals with MCI and AD dementia compared to cognitively-unimpaired individuals. (gut microbes enzymatically generate trimethylamine (TMA) from choline or l-carnitine).

HOMOCYSTEINE / B-VITAMIN AXIS:
- Raised plasma total homocysteine (tHcy)↑ associated with cognitive impairment, AD, or vascular dementia (epidemiology).
  - Homocysteine can build up if vitamin B6, B12, or folate levels are low.
  - Homocysteine and B-vitamin in Cognitive Impairment (VITACOG) study.
  - Vit B6 might be an important B vitamin (often discussed along with B12 and folate).
- Thiamine↓ deficiency produces a cholinergic deficit (well-aligned with AD features).
- Decreased thiamine (B1) in AD may exacerbate Aβ deposition, tau hyperphosphorylation, and oxidative stress (reported).

MICRONUTRIENTS / CAROTENOIDS (reported; compartment-dependent):
- vitamin A↓ and β-carotene↓ lower in some AD cohorts; excess retinol may contribute to osteoporosis risk.
- Diminished circulating vitamin E↓ reported in AD.
- Vitamin B5↓ in multiple brain regions (reported).
- Trace elements: patients with AD reported lower serum Se, Cu, and Zn↓ (serum findings vary by study).
- Brain metals: some studies report higher brain copper↑ and iron↑ in specific regions/structures; compartment and region matter.
  Rosmarinic acid reported to reduce copper-induced neurotoxicity in vitro/in vivo and may interfere with amyloid–copper interactions (preclinical).
- SAMe↓ concentrations in CSF reported in AD.
- MPOD often reduced in AD patients.
- AD brains reported lower levels of lutein↓, zeaxanthin↓, anhydrolutein↓, (VitA)retinol↓, lycopene↓, alpha-tocopherol↓.

RISK CONTEXT:
- Apolipoprotein E4 (ApoE4) genotype is the strongest known genetic risk factor for late-onset AD.
  - One copy of ApoE4: ~3–4× increased risk (range varies by cohort).
  - Two copies: ~8–12× increased risk (range varies).
  - VitK lower in circulating blood of APOE4 carriers (reported).
- Type 2 diabetes, traumatic brain injury, stroke, diet, and above all, aging is the number ONE risk factor.

Treatments / Strategy Targets (high-level):
- Early intervention tends to have a greater positive effect than interventions during middle or late stages.
- BOLD fMRI imaging can be used to observe brain activity via blood oxygen/flow changes.
- Reduce ROS and inflammation in the brain (context-dependent; avoid over-suppressing adaptive signaling).
- Inhibiting acetylcholinesterase (AChE) (which breaks down ACh), e.g., donepezil, rivastigmine.
- Natural AChE inhibitors include: Berberine, Luteolin, Crocetin(saffron), Querctin, TQ
- Natural AChE inhibitors in database (check BBB pass potential).
- MAOB inhibitors, APP inhibitors, PGE2 inhibitors, NLRP3 inhibitors, BACE inhibitors
- BDNF activators, PSD95 activator
- STEP, ADAM10
- Diets with an adequate ratio (5:1) of omega-6:3 (Mediterranean diet).
- Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects (general nutrition framing).
- Antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin).
- Fiber may promote gut microbiome diversity influencing brain health.
- Supplementing with NAD⁺ precursors (NR or NMN) improves cognition and reduces amyloid/tau pathologies in AD mice (animal evidence).
- "It is advisable to consume diets with an adequate ratio (5:1) of omega-6:3 fatty acids (Mediterranean diet) ... antioxidants ... role in oxidative stress ... cognition." Nutrition Strategies
- Reduction of cognitive decline may be achieved by following a healthy dietary pattern limiting added sugars while maximizing fish, fruits, vegetables, nuts, seeds.

SeNPs may also be useful as a Drug Delivery System.

Related Pathways to research in this database (products that modulate them):
- neuroprotective, cognitive, memory
- Aβ aggregation, Tau↓, AChE↓, ACh↑, ChAT↑, acetyl-CoA↑, BDNF↑, BACE↓, NLRP3↓, PSD95↑, PGE2↓, homoC↓
- Increasing AntiOxidants: Catalase↑, GSH↑, SOD↑, HO-1↑, to decrease ROS↓
- Lower Inflammation: TNF-α↓, IL1β↓, IL6↓

Natural Products that may benefit AD.
-Some key pathways are highlighted in RED in the following links
Acetyl-L-carnitine, ALA, Apigenin, Anthocyanins Blueberrys, Aromatherapy, Artemisinin, Ashwagandha,
β-carotene(vitamin A), Bacopa monnieri, Baicalein, Baicalin, Berberine, Betulinic acid, Boron, Boswellia (frankincense),
Caffeic acid, Caffeine, Capsaicin, Carnosine, Carnosic acid, Chlorogenic acid, Choline (note U shaped dose curve-target 350mg/day), Chrysin, Cinnamon, CoQ10, Crocetin, Curcumin,
dietMed, dietMet, dietSTF, EGCG, Ellagic acid, Exercise, Ferulic Acid, Fisetin, Flav, FLS, Folic Acid (5-MTHF, L-methylfolate)-reduce homocysteine,
Galantamine, Ginger, Ginkgo biloba, Ginseng,
Honokiol, Huperzine A, hydrogen gas, Lecithin, Lutein, Luteolin, Lycopene,
M-Blu, Moringa oleifera, Mushroom Lion’s Mane, MSM, MCToil, NAD, Naringenin,
PEMF, Piperine, Phenylbutyrate, Phosphatidylserine, Piperlongumine, Potassium, probiotics, Propolis, Pterostilbene,
Quercetin, Resveratrol, Rivastigmine, Rosmaric Acid(reduce copper-induced neurotoxicity), Rutin,
Safflower yellow, Sage, SAMe, selenium, Serotonin, Shankhpushpi, Shikonin, Shilajit/Fulvic Acid, silicon(reduce Alum bioavialability), Silymarin (Milk Thistle) silibinin, Sulforaphane,
Taurine, TQ, Ursolic Acid
Vitamin B1, Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B6, Vitamin B12, Vitamin E, Vitamin D, Vitamin K2
Zeaxanthin, zinc,

Aluminium has a negative impact on cognition but silicon can decrease Alumunium bioavailability, and Vitamin K2 may provide some protection. Example So does RMF

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⟱

3972-

ACNs,

Recent Research on the Health Benefits of Blueberries and Their Anthocyanins

Review,

AD,

Review,

Park,

*cardioP↑, *neuroP↑, *Inflam↓, *antiOx↓, *GutMicro↑, *Half-Life↑, *LDL↓, *adiP↓, *HDL↑, *CRP↓, *IL1β↓, *Risk↓, *Risk↓, *cognitive↑, *memory↑, *other↑, *BOLD↑, *NO↓, *MDA↓, *GSH↑, *VitC↑, *SOD↑, *GPx↑, *eff↓, *eff↓, *eff↓, *eff↝, *Risk↓,

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↓,

3552-

ALA,

The dietary fatty acids α-linolenic acid (ALA) and linoleic acid (LA) selectively inhibit microglial nitric oxide production

in-vitro,

AD,

BV2

*NO↓, *cognitive↑,

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?,

3544-

ALA,

Alpha lipoic acid for dementia

Review,

AD,

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

3886-

Api,

Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease

in-vitro,

AD,

*Inflam↓, *neuroP↑, *NO↓, *Apoptosis↓,

3665-

ART/DHA,

Artemisinin B Improves Learning and Memory Impairment in AD Dementia Mice by Suppressing Neuroinflammation

Review,

AD,

*Inflam↓, *NO↓, *IL1β↓, *IL6↓, *TNF-α↓, *MyD88↓, *NF-kB↓, *TLR4↓, *memory↑,

2626-

Ba,

Molecular targets and therapeutic potential of baicalein: a review

Review,

Var,

Review,

AD,

Review,

Stroke,

AntiCan↓, *neuroP↑, *cardioP↑, *hepatoP↑, *RenoP↑, TumCCA↑, CDK4↓, cycD1/CCND1↓, cycE/CCNE↑, BAX↑, Bcl-2↓, VEGF↓, Hif1a↓, cMyc↓, NF-kB↓, ROS↑, BNIP3↑, *neuroP↑, *cognitive↑, *NO↓, *iNOS↓, *COX2↓, *PGE2↓, *NRF2↑, *p‑AMPK↑, *Ferroptosis↓, *lipid-P↓, *ALAT↓, *AST↓, *Fas↓, *BAX↓, *Apoptosis↓,

5656-

BNL,

Role of borneol as enhancer in drug formulation: A review

Review,

Nor,

Review,

Stroke,

Review,

AD,

*eff↑, BBB↑, ChemoSen↑, *Inflam↓, *NO↓, *TNF-α↓, *IL6↓, *Bacteria↓, *eff↑, *Aβ↓, *SOD↑, *neuroP↑, *EPR↑, toxicity↓, P-gp↓, eff↑, other↝,

3514-

Bor,

CUR,

Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta

in-vivo,

AD,

rat

*DNAdam↓, *MDA↓, *AChE↓, *neuroP↑, *ROS↓, *NO↓,

4263-

CA,

Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action

Review,

AD,

*neuroP↑, *ROS↓, *NO↓, *COX2↓, *MAPK↓, *NRF2↑, *GSH↑, *HO-1↑, *5HT↑, *BDNF↑, *PI3K↑, *Akt↑, *NF-kB↑, *BBB↑, *SIRT1↑, *memory↑, *Aβ↓, *NLRP3↓,

5927-

CAR,

Neuroprotective Potential and Underlying Pharmacological Mechanism of Carvacrol for Alzheimer’s and Parkinson’s Diseases

Review,

AD,

Review,

Park,

*memory↑, *cognitive↑, *ROS↓, *Inflam↓, *motorD↑, *toxicity↓, *TRPV3↑, *other↓, *antiOx↑, *LDL↓, *COX2↓, *PPARα↑, *NO↓, *AChE↓, *eff↑, *SOD↑, *Catalase↑, *neuroP↑, *BioAv↝, *BBB↑, *BioAv↑,

3872-

Carno,

Carnosine Protects Macrophages against the Toxicity of Aβ1-42 Oligomers by Decreasing Oxidative Stress

in-vitro,

AD,

*antiOx↑, *Inflam↓, *Aβ↓, *neuroP↑, *ROS↓, *NO↓,

2818-

CUR,

Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways

Review,

AD,

*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *cognitive↑, *cardioP↑, other↑, *COX2↓, *IL1β↓, *TNF-α↓, NF-kB↓, *PGE2↓, *iNOS↓, *NO↓, *IL2↓, *IL4↓, *IL6↓, *INF-γ↓, *GSK‐3β↓, *STAT↓, *GSH↑, *MDA↓, *lipid-P↓, *SOD↑, *GPx↑, *Catalase↑, *GSR↓, *LDH↓, *H2O2↓, *Casp3↓, *Casp9↓, *NRF2↑, *AIF↓, *ATP↑,

3723-

Gb,

Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies

Review,

AD,

*memory↑, *antiOx↑, *Casp3↓, *APP↓, *AChE↓, *Aβ↓, *5HT↑, *SOD↓, *MDA↓, *NO↓, *GSH↑, *Bcl-2↑, *BAX↑, *TNF-α↓, *IL1β↑, *iNOS↓, *IL10↓, *p‑tau↓, *ROS↓, *MAOB↓, *cognitive↑, *neuroP↑, *Apoptosis↓,

3768-

H2,

Effects of Hydrogen Gas Inhalation on Community-Dwelling Adults of Various Ages: A Single-Arm, Open-Label, Prospective Clinical Trial

Trial,

AD,

*ROS↓, *NO↓, *BACE↓, *BDNF↑, *VEGF↑, *p‑tau↓, *MCP1↓, *IL6↓, *cognitive↑, *toxicity∅,

3770-

H2,

Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases

Review,

AD,

Review,

Park,

*antiOx↑, *NRF2↑, *HO-1↑, *Inflam↓, *neuroP↑, *cardioP↑, *other↓, *ROS↓, *NADPH↓, *Catalase↑, *GPx1↑, *NO↓, *mt-ROS↓, *SIRT3↑, *SIRT1↑, *TLR4↓, *mTOR↓, *cognitive↑, *Sepsis↓, *PTEN↓, *Akt↓, *NLRP3↓, *AntiAg↑, *IL6↓, *TNF-α↓, *IL1β↓, *MDA↓, *memory↑, *FOXO3↑, TumCG↓, *LDL↓,

3764-

H2,

Therapeutic Effects of Hydrogen Gas Inhalation on Trimethyltin-Induced Neurotoxicity and Cognitive Impairment in the C57BL/6 Mice Model

in-vivo,

AD,

mice

*memory↑, *Aβ↓, *p‑tau↓, *BAX↓, *ROS↓, *NO↓, *Ca+2↓, *MDA↓, *Catalase↓, *GPx↓, *TNF-α↓, *Bcl-2↑, *VEGF↑, *Inflam↓, *cognitive↑,

3767-

H2,

The role of hydrogen therapy in Alzheimer's disease management: Insights into mechanisms, administration routes, and future challenges

Review,

AD,

*Inflam↓, *neuroP↑, *toxicity↓, *antiOx↑, *ROS↓, *NLRP3↓, *IL1β↓, *mtDam↓, *ATP↑, *AMPK↑, *FOXO3↑, *SOD1↑, *Catalase↑, *NRF2↑, *NO↓, *MDA↓, *lipid-P↓, *memory↑, *ER(estro)↓, *BDNF↑, *cognitive↑, *APP↓, *BACE↓, *Aβ↓, *BP∅, *BBB↑,

2916-

LT,

Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies

Review,

Var,

Review,

AD,

Review,

Park,

proCasp9↓, CDC2↓, CycB/CCNB1↓, Casp9↑, Casp3↑, Cyt‑c↑, cycA1/CCNA1↑, CDK2↓, APAF1↑, TumCCA↑, P53↑, BAX↑, VEGF↓, Bcl-2↓, Apoptosis↑, p‑Akt↓, p‑EGFR↓, p‑ERK↓, p‑STAT3↓, cardioP↑, Catalase↓, SOD↓, *BioAv↓, *antiOx↑, *ROS↓, *NO↓, *GSTs↑, *GSR↑, *SOD↑, *Catalase↑, *lipid-P↓, PI3K↓, Akt↓, CDK2↓, BNIP3↑, hTERT/TERT↓, DR5↑, Beclin-1↑, TNF-α↓, NF-kB↓, IL1↓, IL6↓, EMT↓, FAK↓, E-cadherin↑, MDM2↓, NOTCH↓, MAPK↑, Vim↓, N-cadherin↓, Snail↓, MMP2↓, Twist↓, MMP9↓, ROS↑, MMP↓, *AChE↓, *MMP↑, *Aβ↓, *neuroP↑, Trx1↑, ROS↓, *NRF2↑, NRF2↓, *BBB↑, ChemoSen↑, GutMicro↑,

3528-

Lyco,

The Importance of Antioxidant Activity for the Health-Promoting Effect of Lycopene

Review,

Nor,

Review,

AD,

Review,

Park,

*antiOx↑, *ROS↓, *BioAv↝, *Half-Life↑, *BioAv↓, *BioAv↑, *cardioP↑, *neuroP↑, *H2O2↓, *VitC↑, *VitE↑, *GPx↑, *GSH↑, *MPO↓, *GSTs↓, *SOD↑, *NF-kB↓, *IL1β↓, *IL6↓, *IL10↑, *MAPK↓, *Akt↓, *COX2↓, *TNF-α↓, *TGF-β1↑, *NO↓, *GSR↑, *NRF2↑, *HO-1↑, *TAC↑, *Inflam↓, *BBB↑, *neuroP↑, *memory↑,

3264-

Lyco,

Pharmacological potentials of lycopene against aging and aging‐related disorders: A review

Review,

Var,

Review,

AD,

Review,

Stroke,

*antiOx↑, *ROS↓, *SOD↑, *Catalase↑, *GSH↑, *GSTs↑, *MDA↓, *lipid-P↓, *NRF2↑, *HO-1↑, *iNOS↓, *NO↓, *TAC↑, *NOX4↓, *Inflam↓, *IL1↓, *IL6↓, *IL8↓, *IL1β↓, *TNF-α↓, *TLR2↓, *TLR4↓, *VCAM-1↓, *ICAM-1↓, *STAT3↓, *NF-kB↓, *ERK↓, *BP↓, ROS↓, PGE2↓, cardioP↑, *neuroP↑, *creat↓, *RenoP↑, *CRM↑,

4105-

MF,

Extremely low frequency electromagnetic fields stimulation modulates autoimmunity and immune responses: a possible immuno-modulatory therapeutic effect in neurodegenerative diseases

Review,

AD,

*Inflam↓, *neuroP↑, *NO↑, *ROS↓, *NO↓, *MCP1↑, *HSP70/HSPA5↑, *antiOx↑, *NRF2↑, *NF-kB↓,

204-

MFrot,

MF,

Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization

in-vivo,

AD,

 0.2T, 4Hz

 reduced aluminum deposition in the brains of AD mice

*NF-kB↓, *MAPK↓, *TLR4↓, *memory↑, *cognitive↑, *TGF-β1↑, *ARG↑, *IL4↑, *IL10↑, *IL6↓, *IL1↓, *TNF-α↓, *iNOS↓, *ROS↓, *NO↓, *MyD88↓, *p‑IKKα↓, *p‑IκB↓, *p‑p65↓, *p‑JNK↓, *p‑p38↓, *ERK↓, *neuroP↑, *Aβ↓,

3814-

mushLions,

Lion's Mane (Hericium erinaceus) Exerts Anxiolytic Effects in the rTg4510 Tau Mouse Model

in-vitro,

AD,

mouse

*neuroP↑, *cognitive↑, *cognitive∅, *BBB↑, *NGF↑, *BDNF↑, *NO↓, *memory↑, *Aβ↓,

3251-

PBG,

The Antioxidant and Anti-Inflammatory Effects of Flavonoids from Propolis via Nrf2 and NF-κB Pathways

Review,

AD,

Review,

Diabetic,

Review,

Var,

in-vitro,

Nor,

H9c2

To induce oxidative stress, H9c2 cells were exposed to multiple H2O2 concentrations (0, 50, 100, 150, 200, and 250 μM) for 1 h

*antiOx↑, *Inflam↓, *ROS↓, *SOD↑, *Catalase↑, *HO-1↑, *NO↓, *NOS2↓, *NF-kB↓, *NRF2↑, *hepatoP↑, *MDA↓, *mtDam↓, *GSH↑, *p65↓, *TNF-α↓, *IL1β↓, *NRF2↑, *NRF2↓, *ROS⇅, *BioAv↓, *BioAv↑,

3918-

PTS,

Pterostilbene inhibits amyloid-β-induced neuroinflammation in a microglia cell line by inactivating the NLRP3/caspase-1 inflammasome pathway

in-vitro,

AD,

BV2

*IL6↓, *IL1β↓, *TNF-α↓, *NLRP3↓, *Inflam↓, *NO↓, *iNOS↓,

3380-

QC,

Quercetin as a JAK–STAT inhibitor: a potential role in solid tumors and neurodegenerative diseases

Review,

Var,

Review,

Park,

Review,

AD,

JAK↓, STAT↓, Inflam↓, NO↓, COX2↓, CRP↓, selectivity↑, *neuroP↑, STAT3↓, cycD1/CCND1↓, MMP2↓, STAT4↓, JAK2↓, TumCP↓, Diff↓, *eff↑, *IL6↓, *TNF-α↓, *IL1β↓, *Aβ↓,

3099-

RES,

Resveratrol and cognitive decline: a clinician perspective

Review,

Nor,

NA,

AD,

*antiOx↑, *ROS↓, *cognitive↑, *neuroP↑, *SIRT1↑, *AMPK↑, *GPx↑, *HO-1↑, *GSK‐3β↑, *COX2↓, *PGE2↓, *NF-kB↓, *NO↓, *Casp3↓, *MMP3↓, *MMP9↓, *MMP↑, *GSH↑, *other↑, *BioAv↑, *memory↑, *GlutMet↑, *BioAv↓, *Half-Life↓, *toxicity∅,

3616-

RosA,

Therapeutic effects of rosemary (Rosmarinus officinalis L.) and its active constituents on nervous system disorders

Review,

AD,

*Inflam↓, *memory↑, *toxicity↓, *ROS↓, *Catalase↑, *SOD↑, *NRF2↑, *Aβ↓, *AChE↓, *Ca+2↓, *NO↓, *IL2↓, *COX2↓, *PGE2↓, *MMPs↓, *TNF-α↓, *iNOS↓, *TLR4↓, *cognitive↑, *cortisol↓, *lipid-P↓,

3660-

SFN,

Sulforaphane - role in aging and neurodegeneration

Review,

AD,

*antiOx↑, *Inflam↓, *NRF2↑, *NF-kB↓, *HDAC↓, *DNMTs↓, *neuroP↑, *AntiAge↑, *DNMT1↓, *DNMT3A↓, *memory↑, *HO-1↑, *ROS↓, *NO↓, *GSH↑, *NF-kB↓, *TNF-α↓, *IL10↑,

3320-

SIL,

Neuroprotective Potential of Silymarin against CNS Disorders: Insight into the Pathways and Molecular Mechanisms of Action

Review,

AD,

*hepatoP↑, *neuroP↑, *ROS↓, *β-Amyloid↓, *Inflam↓, *Aβ↓, *NF-kB↓, *TNF-α↓, *TNF-β↓, *iNOS↓, *NO↓, *COX2↓,

3318-

SIL,

Pharmaceutical prospects of Silymarin for the treatment of neurological patients: an updated insight

Review,

AD,

Review,

Park,

*hepatoP↑, *neuroP↑, *TLR4↓, *TNF-α↓, *IL1β↓, *NF-kB↓, *memory↑, *cognitive↑, *NRF2↑, *HO-1↑, *ROS↓, *Akt↑, *mTOR↑, *SOD↑, *Catalase↑, *GSH↑, *IL10↑, *IL6↑, *NO↓, *MDA↓, *AChE↓, *MAPK↓, *BDNF↑,

3558-

TQ,

Behavioral and histological study on the neuroprotective effect of thymoquinone on the cerebellum in AlCl3-induced neurotoxicity in rats through modulation of oxidative stress, apoptosis, and autophagy

in-vivo,

AD,

Rats

*MDA↓, *NO↓, *GSH↑, *neuroP↑, *cognitive↑,

3560-

TQ,

Protective effects of thymoquinone on D-galactose and aluminum chloride induced neurotoxicity in rats: biochemical, histological and behavioral changes

in-vivo,

AD,

orally TQ (20 mg/kg/dose) dissolved in corn oil
daily for 14 consecutive days

Forty Sprague Dawley male albino rats

*cognitive↑, *SOD↑, *TAC↑, *AChE↓, *MDA↓, *NO↓, *TNF-α↓, *Bcl-2↑, *Ach↑, *neuroP↑,

5904-

TV,

Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development

Review,

Var,

Review,

Stroke,

Review,

Diabetic,

Review,

Obesity,

Review,

AD,

Review,

Arthritis,

*antiOx↑, *ROS↓, *Inflam↓, *Bacteria↓, AntiTum↑, IronCh↑, *HDL↑, *LDL↓, *BioAv↝, *Half-Life↝, *BioAv↑, *SOD↑, *GPx↑, *GSTs↑, *eff↑, radioP↑, *MDA↓, *other↑, *COX1↓, *COX2↓, *AntiAg↑, *RNS↓, *NO↓, *H2O2↓, *NOS2↓, *NADH↓, *Imm↑, Apoptosis↑, TumCP↓, angioG↓, TumCMig↓, Ca+2↑, TumCCA↑, DNAdam↑, BAX↑, Casp9↑, Casp8↑, Casp3↑, cl‑PARP↑, AIF↑, i-ROS↑, MMP↓, Cyt‑c↑, APAF1↑, Ca+2↑, MMP9↓, MMP2↓, PKCδ↓, ERK↓, H2O2↑, BAX↑, Bcl-2↓, DNAdam↑, lipid-P↑, ChemoSen↑, chemoP↑, *cardioP↑, *SOD↑, *Catalase↑, *GPx↑, *GSH↑, *BP↓, *AntiDiabetic↑, *Obesity↓, RenoP↑, *GastroP↑, hepatoP↑, *AChE↓, *cognitive↑, *BChE↓, *other↓, *BioAv↑,

Showing Research Papers: 1 to 36 of 36

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 36

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 16, Catalase↓, 1, Catalase↑, 10, Ferroptosis↓, 1, GPx↓, 1, GPx↑, 6, GPx1↑, 1, GSH↑, 14, GSR↓, 1, GSR↑, 2, GSTs↓, 1, GSTs↑, 4, H2O2↓, 3, HDL↑, 2, HO-1↑, 8, Keap1↓, 1, lipid-P↓, 7, MDA↓, 14, MPO↓, 2, NADH↓, 1, NOX4↓, 1, NRF2↓, 1, NRF2↑, 15, RNS↓, 1, ROS↓, 26, ROS⇅, 1, mt-ROS↓, 1, SIRT3↑, 1, SOD↓, 1, SOD↑, 14, SOD1↑, 1, TAC↑, 3, TBARS↓, 1, VitC↑, 3, VitE↑, 2,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Mitochondria & Bioenergetics ⓘ

AIF↓, 1, ATP↑, 2, MMP↑, 2, mtDam↓, 2,

Core Metabolism/Glycolysis ⓘ

adiP↓, 1, adiP↑, 1, ALAT↓, 2, AMPK↑, 2, p‑AMPK↑, 1, cAMP↑, 1, CRM↑, 1, GlutMet↑, 1, H2S↑, 1, LDH↓, 3, LDL↓, 4, NADPH↓, 1, PPARα↑, 1, SIRT1↑, 3,

Cell Death ⓘ

Akt↓, 3, Akt↑, 3, Apoptosis↓, 4, BAX↓, 2, BAX↑, 1, Bcl-2↑, 3, Casp3↓, 3, Casp6↓, 1, Casp9↓, 2, Fas↓, 1, Ferroptosis↓, 1, iNOS↓, 10, JNK↓, 1, p‑JNK↓, 1, MAPK↓, 4, p‑p38↓, 1,

Kinase & Signal Transduction ⓘ

TRPV3↑, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1, other↓, 3, other↑, 4, other↝, 2,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1, DNMT1↓, 1, DNMT3A↓, 1, DNMTs↓, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 2, ERK↑, 1, FOXO3↑, 2, GSK‐3β↓, 1, GSK‐3β↑, 1, HDAC↓, 1, mTOR↓, 1, mTOR↑, 1, PI3K↓, 1, PI3K↑, 1, PTEN↓, 1, STAT↓, 1, STAT3↓, 1,

Migration ⓘ

AntiAg↑, 2, APP↓, 2, ARG↑, 1, Ca+2↓, 2, MMP3↓, 1, MMP9↓, 1, MMPs↓, 1, TGF-β1↑, 2, VCAM-1↓, 1,

Angiogenesis & Vasculature ⓘ

EPR↑, 1, NO↓, 35, NO↑, 1, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↑, 9, GastroP↑, 1,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 11, CRP↓, 1, ICAM-1↓, 1, p‑IKKα↓, 1, IL1↓, 2, IL10↓, 1, IL10↑, 4, IL1β↓, 12, IL1β↑, 1, IL2↓, 2, IL4↓, 1, IL4↑, 1, IL6↓, 12, IL6↑, 1, IL8↓, 1, Imm↑, 1, INF-γ↓, 1, Inflam↓, 21, p‑IκB↓, 1, MCP1↓, 1, MCP1↑, 1, MyD88↓, 2, NF-kB↓, 12, NF-kB↑, 1, p‑NF-kB↓, 1, p65↓, 1, p‑p65↓, 1, PGE2↓, 5, TLR2↓, 1, TLR4↓, 6, TNF-α↓, 19, TNF-β↓, 1,

Synaptic & Neurotransmission ⓘ

5HT↑, 2, AChE↓, 8, BChE↓, 1, BDNF↑, 5, NGF↑, 1, p‑tau↓, 3,

Protein Aggregation ⓘ

Aβ↓, 13, BACE↓, 2, MAOB↓, 1, NLRP3↓, 4, β-Amyloid↓, 1,

Hormonal & Nuclear Receptors ⓘ

cortisol↓, 1, ER(estro)↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 4, BioAv↑, 6, BioAv↝, 4, eff↓, 3, eff↑, 6, eff↝, 1, Half-Life↓, 1, Half-Life↑, 2, Half-Life↝, 2,

Clinical Biomarkers ⓘ

ALAT↓, 2, AST↓, 2, BP↓, 4, BP∅, 1, creat↓, 2, CRP↓, 1, GutMicro↑, 2, IL6↓, 12, IL6↑, 1, LDH↓, 3, NOS2↓, 2,

Functional Outcomes ⓘ

AntiAge↑, 2, AntiDiabetic↑, 1, BOLD↑, 1, cardioP↑, 7, cognitive↑, 20, cognitive∅, 1, hepatoP↑, 5, memory↑, 18, motorD↑, 1, neuroP↑, 31, Obesity↓, 1, RenoP↑, 2, Risk↓, 3, toxicity↓, 3, toxicity∅, 2,

Infection & Microbiome ⓘ

Bacteria↓, 2, Sepsis↓, 1,
Total Targets: 192

Scientific Paper Hit Count for: NO, Nitric Oxide

4 Hydrogen Gas
3 Alpha-Lipoic-Acid
2 Curcumin
2 Lycopene
2 Magnetic Fields
2 Silymarin (Milk Thistle) silibinin
2 Thymoquinone
1 Anthocyanins
1 Allicin (mainly Garlic)
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Baicalein
1 borneol
1 Boron
1 Carnosic acid
1 Carvacrol
1 Carnosine
1 Ginkgo biloba
1 Luteolin
1 Magnetic Field Rotating
1 Mushroom Lion’s Mane
1 Propolis -bee glue
1 Pterostilbene
1 Quercetin
1 Resveratrol
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Thymol-Thymus vulgaris

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#:563  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

NO Cancer Research Results

Brain Energy Systems Matrix (AD)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

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 ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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