NRF2 Cancer Research Results

NRF2, nuclear factor erythroid 2-related factor 2: Click to Expand ⟱
Source: TCGA
Type: Antiapoptotic
Nrf2 is responsible for regulating an extensive panel of antioxidant enzymes involved in the detoxification and elimination of oxidative stress. Thought of as "Master Regulator" of antioxidant response.
-One way to estimate Nrf2 induction is through the expression of NQO1.
NQO1, the most potent inducer:
SFN 0.2 μM,
quercetin (2.5 μM),
curcumin (2.7 μM),
Silymarin (3.6 μM),
tamoxifen (5.9 μM),
genistein (6.2 μM ),
beta-carotene (7.2μM),
lutein (17 μM),
resveratrol (21 μM),
indol-3-carbinol (50 μM),
chlorophyll (250 μM),
alpha-cryptoxanthin (1.8 mM),
and zeaxanthin (2.2 mM)

1. Raising Nrf2 enhances the cell's antioxidant defenses and ↓ROS. This strategy is used to decrease chemo-radio side effects.
2. Downregulating Nrf2 lowers antioxidant defenses and ↑ROS. In cancer cells this leads to DNA damage, and cell death.
3. However there are some cases where increasing Nrf2 paradoxically causes an increase in ROS (cancer cells). Such as cases of Mitochondial overload, signal crosstalk, reductive stress

-In some cases, Nrf2 is overexpressed in cancer cells, which can lead to the activation of genes involved in cell proliferation, angiogenesis, and metastasis. This can contribute to the development of resistance to chemotherapy and targeted therapies.
-Increased Nrf2 expression: Lung, Breast, Colorectal, Prostrate.
Decreased Nrf2 expression: Skine, Liver, Pancreatic.
-Nrf2 is a cytoprotective transcription factor which demonstrated both a negative effect as well as a positive effect on cancer
- "promotes Nrf2 translocation from the cytoplasm to the nucleus," means facilitates the movement of Nrf2 into the nucleus, thereby enhancing the cell's antioxidant and cytoprotective responses. -Major regulator of Nrf2 activity in cells is the cytosolic inhibitor Keap1.

Nrf2 Inhibitors and Activators
Nrf2 Inhibitors: Brusatol, Luteolin, Trigonelline, VitC, Retinoic acid, Chrysin
Nrf2 Activators: SFN, OPZ EGCG, Resveratrol, DATS, CUR, CDDO, Api
- potent Nrf2 inducers from plants include sulforaphane, curcumin, EGCG, resveratrol, caffeic acid phenethyl ester, wasabi, cafestol and kahweol (coffee), cinnamon, ginger, garlic, lycopene, rosemany

Nrf2 plays dual roles in that it can protect normal tissues against oxidative damage and can act as an oncogenic protein in tumor tissue.
– In healthy tissues, NRF2 activation helps protect cells from oxidative damage and maintains cellular homeostasis.
– In many cancers, constitutive activation of NRF2 (often through mutations in NRF2 itself or loss-of-function mutations in KEAP1) leads to an enhanced antioxidant capacity.
– This upregulation can promote tumor cell survival by enabling cancer cells to thrive under oxidative stress, resist chemotherapeutic agents, and sustain metabolic reprogramming.
– Elevated NRF2 levels have been implicated in promoting tumor growth, metastasis, and resistance to therapy in various malignancies.
– High or sustained NRF2 activity is frequently associated with aggressive tumor phenotypes, poorer prognosis, and decreased overall survival in several cancer types.
– While its activation is essential for protecting normal cells from oxidative stress, aberrant or sustained NRF2 activation in tumor cells can lead to enhanced survival, therapeutic resistance, and tumor progression.

NRF2 inhibitors: (to decrease antioxidant defenses and increase cell death from ROS).
-Brusatol: most cited natural inhibitors of Nrf2.
-Luteolin: luteolin can reduce Nrf2 activity in specific cancer models and may enhance cell sensitivity to chemotherapy. However, luteolin is also known as an antioxidant, and its influence on Nrf2 can sometimes be context dependent.
-Apigenin: certain studies to down‑regulate Nrf2 in cancer cells: Dose and context dependent .
-Oridonin:
-Wogonin: although its effects might be cell‑ and dose‑specific.
- Withaferin A

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).
- AD models and human tissue studies show an imbalance toward mitochondrial fission, involving increased DRP1 and FIS1 and reduced fusion proteins such as MFN1, MFN2, and OPA1. Usually increased or overactive in AD-like pathology
-↓ Reduced miR-106b-5p has been reported in peripheral blood from Alzheimer's disease patients and has been investigated as a potential circulating biomarker.
-Glutaminyl cyclase (QC/QPCT)↑ : because it can increase formation of pyroglutamate Aβ
-GFAP↑ : Elevated GFAP is observed in affected brain regions and increased circulating GFAP is strongly associated with cerebral amyloid pathology and progression toward cognitive impairment.
-ODC1↑ : Experimental inhibition of astrocytic ODC1 reduces aberrant GABA production, improves memory deficits, and can markedly reduce hippocampal Aβ plaque burden in APP/PS1 models.
-H₂S signaling in Alzheimer’s disease: Generally ↓. AD is associated with reduced brain H₂S production, ↓ CSE/CTH expression, and particularly ↓ protein persulfidation. Reduced GSK3β persulfidation increases GSK3β activity and favors Tau hyperphosphorylation.
-↓ Reduced synaptophysin is a well-established marker of presynaptic and synaptic loss in Alzheimer's disease.
-↑ Increased 3-nitrotyrosine(3-NT) and protein tyrosine nitration are well-established indicators of oxidative and nitrosative stress in Alzheimer's disease.
-↑ Increased peroxynitrite formation (ONOO) and nitrosative stress are associated with Alzheimer's disease.
- salivary lactoferrin tends to be decreased in AD in several studies

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).
-↓ SYN3 expression has been reported in hippocampal CA1 pyramidal neurons in mild cognitive impairment and Alzheimer's disease

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
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Acetyl-L-carnitine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">ALA, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Apigenin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Anthocyanins Blueberrys, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Aromatherapy, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Artemisinin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ashwagandha,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">β-carotene(vitamin A), NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Bacopa monnieri, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Baicalein, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Baicalin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Berberine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Betulinic acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Boron, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Boswellia (frankincense),
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Caffeic acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Caffeine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Capsaicin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Carnosine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Carnosic acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Chlorogenic acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Choline (note U shaped dose curve-target 350mg/day), NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Chrysin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Cinnamon, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">CoQ10, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Crocetin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Curcumin,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">dietMed, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">dietMet, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">dietSTF, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">EGCG, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ellagic acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Exercise, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ferulic Acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Fisetin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Flav, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">FLS, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Folic Acid (5-MTHF, L-methylfolate)-reduce homocysteine,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Galantamine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ginger, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ginkgo biloba, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ginseng,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Honokiol, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Huperzine A, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">hydrogen gas, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lactoferrin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lecithin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Licochalcone A, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lutein, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Luteolin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lycopene,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">M-Blu, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Moringa oleifera, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Mushroom Lion’s Mane, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">MSM, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">MCToil, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">NAD, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Naringenin,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">PEMF, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Piperine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Phenylbutyrate, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Phosphatidylserine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Piperlongumine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Potassium, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">probiotics, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Propolis, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Pterostilbene,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Quercetin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Resveratrol, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Rivastigmine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Rosmaric Acid(reduce copper-induced neurotoxicity), NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Rutin,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Safflower yellow, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Sage, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">SAMe, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">selenium, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Serotonin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Shankhpushpi, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Shikonin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Shilajit/Fulvic Acid, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">silicon(reduce Alum bioavialability), NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Silymarin (Milk Thistle) silibinin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Sulforaphane,
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Taurine, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">TQ, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ursolic Acid
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B1, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B2, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B3, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B5, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B6, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B12, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin E, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin D, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin K2
NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Zeaxanthin, NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">zinc,

NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">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
11 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
12 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
13 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
14 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
15 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
16 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
21 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
22 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
23 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
24 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
31 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
32 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
33 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
41 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
42 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
43 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
44 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
51 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
52 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
53 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
61 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
62 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
63 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⟱
6461- 1,8-Cin,    1,8-cineole (eucalyptol): A versatile phytochemical with therapeutic applications across multiple diseases
- Review, AD, NA - Review, Var, NA
*Inflam↓, *antiOx↑, *neuroP↑, *BioAv↑, *Half-Life↝, *toxicity↓, *PGE2↓, *TNF-α↓, *IL1β↓, *NO↓, *NF-kB↓, *PPARγ↓, COX2/PTGS2↓, *ROS↓, *SOD↑, *Catalase↑, *TAC↑, *MDA↓, *lipid-P↓, *NRF2↑, *HO-1↑, *NADPH↑, *GPx↑, *AntiBio↑, *eff↑, *AntiFungal↑, *AntiViral↑, *TRPA1↑, eff↑, TumCCA↑, ROS↑, MAPK↝, mTOR↝, Apoptosis↑, survivin↓, Akt↓, p38↑, cl‑PARP↑, cl‑Casp3⇅, P53↑, BAX↑, Cyt‑c↑, Casp9↑, Dose↝, *Aβ↓, *tau↓, *GSK‐3β↓, *BACE/β-secretase↓, *cardioP↑, MFN2↑,
2657- AL,    Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases
- Review, CardioV, NA - Review, AD, NA
*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, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*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/PTGS2↓, *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/KDR/Flk1↓, p‑FAK↓,
3271- ALA,    Decrypting the potential role of α-lipoic acid in Alzheimer's disease
- Review, AD, NA
*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↑,
3272- ALA,    Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential
- Review, AD, NA
*antiOx↑, *glucose↑, *eNOS↑, *NRF2↑, *MMP9↓, *VCAM-1↓, *NF-kB↓, *cardioP↑, *cognitive↑, *eff↓, *BBB↑, *IronCh↑, *GSH↑, *PKCδ↑, *ERK↑, *p38↑, *MAPK↑, *PI3K↑, *Akt↑, *PTEN↓, *AMPK↑, *GLUT4↑, *GLUT1↑, *Inflam↓,
3438- ALA,    The Potent Antioxidant Alpha Lipoic Acid
- Review, NA, NA - Review, AD, NA
*antiOx↑, *cardioP↑, *cognitive↑, *AntiAge↑, *Inflam↓, *AntiCan↑, *neuroP↑, *IronCh↑, *ROS↑, *Weight↓, *Ach↑, *ROS↓, *GSH↑, *lipid-P↓, *memory↑, *NRF2↑, *ChAT↑, *GlucoseCon↑, *Acetyl-CoA↑,
3449- ALA,    Alpha-Lipoic Acid Downregulates IL-1β and IL-6 by DNA Hypermethylation in SK-N-BE Neuroblastoma Cells
- in-vitro, AD, SK-N-BE
*antiOx↑, *NRF2↑, *NF-kB↓, *IL1β↓, *IL6↓, neuroP↑,
3539- ALA,    Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential
- Review, AD, NA
*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↝,
3550- ALA,    Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer's Disease?
- Review, AD, NA
*antiOx↑, *Inflam↓, *PGE2↓, *COX2/PTGS2↓, *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↑,
4280- Api,    Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms
- Review, AD, NA - Review, Park, NA
*neuroP↑, *antiOx↑, *ROS↓, *Inflam↓, *TNF-α↓, *IL1β↓, *PI3K↑, *Akt↑, *BBB↑, *NRF2↑, *SOD↑, *GPx↑, *MAPK↓, *Catalase↑, *HO-1↑, *COX2/PTGS2↓, *PGE2↓, *PPARγ↑, *TLR4↓, *GSK‐3β↓, *Aβ↓, *NLRP3↓, *BDNF↑, *TrkB↑, *GABA↑, *AChE↓, *Ach↑, *5HT↑, *cognitive↑, *MAOA↓,
4804- ASTX,    Astaxanthin in cancer therapy and prevention (Review)
- Review, Var, NA - Review, AD, NA
*antiOx↑, *Inflam↓, ChemoSen⇅, chemoP↑, BioAv↑, TumCP↑, ROS⇅, Apoptosis↑, PI3K↑, Akt↑, GSK‐3β↑, NRF2↑, AntiCan↑, *neuroP↑, eff↑, AntiTum↑,
5425- ASTX,    Multiple roles of fucoxanthin and astaxanthin against Alzheimer's disease: Their pharmacological potential and therapeutic insights
- in-vivo, AD, NA
*neuroP↑, *antiOx↑, *Inflam↑, *AChE↓, *BACE/β-secretase↓, *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, NA - Review, Park, NA - Review, AD, NA
*neuroP↑, *antiOx↑, *Inflam↓, *BioAv↝, *BioAv↑, *Half-Life↝, *TLR4↓, *NF-kB↓, *iNOS↓, *COX2/PTGS2↓, *TNF-α↓, *12LOX↓, *NLRP3↓, *ROS↓, *IL1β↓, *IL6↓, *GSK‐3β↓, *NRF2↑, *BBB↑, *SOD↑, *GPx↑, *MDA↓,
2626- Ba,    Molecular targets and therapeutic potential of baicalein: a review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
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/PTGS2↓, *PGE2↓, *NRF2↑, *p‑AMPK↑, *Ferroptosis↓, *lipid-P↓, *ALAT↓, *AST↓, *Fas↓, *BAX↓, *Apoptosis↓,
3678- BBR,    Network pharmacology study on the mechanism of berberine in Alzheimer’s disease model
- Review, AD, NA
*APP↓, *PPARγ↑, *NF-kB↓, *Aβ↓, *cognitive↑, *antiOx↑, *Inflam↓, *Apoptosis↓, *BioAv↑, *BioAv↝, *BBB↑, *motorD↑, *NRF2↑, *HO-1↑, *ROS↓, *p‑Akt↑, *p‑ERK↑,
5633- BCA,    Mechanisms Behind the Pharmacological Application of Biochanin-A: A review
- Review, Var, NA - Review, AD, NA
*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/β-secretase↓, *memory↑, *BioAv↓,
6511- BCP,    Improvement of Oxidative Stress and Mitochondrial Dysfunction by β-Caryophyllene: A Focus on the Nervous System
- Review, AD, NA
*CB2 / CNR2↑, *Bacteria↓, *antiOx↑, *Inflam↓, *NP/CIPN↓, *neuroP↑, AntiCan↑, *ROS↓, *mtDam↓, *GSH↑, *SOD↑, *Catalase↑, *lipid-P↓, *IL1β↓, *IL6↓, *TNF-α↓, *COX2/PTGS2↓, *iNOS↓, *NRF2↑, *HO-1↑, *AChE↓,
6515- BCP,  Xan,    Advancing Brain Health Naturally: β-Caryophyllene and Xanthohumol as Neuroprotective Agents
- Review, AD, NA
*neuroP↑, *BioAv↝, *CB2 / CNR2↑, *Inflam↓, *iNOS↓, *IL1β↓, *IL6↓, *TNF-α↓, *NF-kB↓, *COX1↓, *COX2/PTGS2↓, *PPARα↑, *PPARγ↑, *ROS↓, *tau↓, *NRF2↑, *HO-1↑, *AChE↓, *BChE↓, *BioAv↓,
6507- BCP,    Exploring β-caryophyllene: a non-psychotropic cannabinoid's potential in mitigating cognitive impairment induced by sleep deprivation
- Review, AD, NA
*cognitive↑, *Inflam↓, *ROS↓, *TLR4↓, *NF-kB↓, *NLRP3↓, *MAPK↓, *NRF2↑, *HO-1↑, *PI3K↑, *Akt↑, *cAMP↑, *PKA↑, *CREB↑,
3866- Bos,    Mechanistic role of boswellic acids in Alzheimer's disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, *Inflam↓, *AChE↓, *Ach↑, *NRF2↑, *NF-kB↓, *Aβ↓,
2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, ER Stress↑, TumCG↓, Apoptosis↑, Inflam↓, ChemoSen↑, Casp↑, ERK↓, cl‑PARP↑, AR↓, cycD1/CCND1↓, VEGFR2/KDR/Flk1↓, CXCR4↓, radioP↑, NF-kB↓, VEGF↓, P21↑, Wnt↓, β-catenin/ZEB1↓, Cyt‑c↑, MMP2↓, MMP1↓, MMP9↓, PI3K↓, MAPK↓, JNK↑, *5LO↓, *NRF2↑, *HO-1↑, *MDA↓, *SOD↑, *hepatoP↑, *ALAT↓, *AST↓, *LDH↑, *CRP↓, *COX2/PTGS2↓, *GSH↑, *ROS↓, *Imm↑, *Dose↝, *eff↑, *neuroP↑, *cognitive↑, *IL6↓, *TNF-α↓,
2768- Bos,    Boswellic acids as promising agents for the management of brain diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, *ROS↓, *cognitive↓, TumCP↓, TumCMig↓, TumMeta↓, angioG↓, Apoptosis↑, *Inflam↓, IL1↓, IL2↓, IL4↓, IL6↓, TNF-α↓, P53↑, Akt↓, NF-kB↓, DNAdam↑, Casp↑, COX2/PTGS2↓, MMP9↓, CXCR4↓, VEGF↓, *SOD↑, *Catalase↑, *GPx↑, *NRF2↑,
2772- Bos,    Mechanistic role of boswellic acids in Alzheimer’s disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, *Inflam↓, *AChE↓, *Choline↑, *NRF2↑, *NF-kB↑, *BBB↑, *BioAv↑, *Half-Life↓, *Dose↝, *PGE2↓, *ROS↓, *cognitive↑, *antiOx↑, 5LO↓, *TNF-α↓, *IL6↓, *HO-1↑,
4263- CA,    Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action
- Review, AD, NA
*neuroP↑, *ROS↓, *NO↓, *COX2/PTGS2↓, *MAPK↓, *NRF2↑, *GSH↑, *HO-1↑, *5HT↑, *BDNF↑, *PI3K↑, *Akt↑, *NF-kB↑, *BBB↑, *SIRT1↑, *memory↑, *Aβ↓, *NLRP3↓,
7516- CA,    Caffeic Acid, a Polyphenolic Micronutrient Rescues Mice Brains against Aβ-Induced Neurodegeneration and Memory Impairment
- in-vivo, AD, NA
*neuroP↑, *antiOx↑, *memory↑, *Learn↑, *cognitive↑, *ROS↓, *lipid-P↓, *NRF2↑, *HO-1↑, *Aβ↓, *BACE/β-secretase↓,
5768- CAPE,    Neuroprotective Potential of Caffeic Acid Phenethyl Ester (CAPE) in CNS Disorders: Mechanistic and Therapeutic Insights
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*antiOx↑, *Inflam↑, *AntiCan↑, *NRF2↑, *GSK‐3β↑, *Akt↑, *PI3K↑, *ROS↓, *SOD↑, *GSH↑, *MDA↓, *tau↓, *neuroP↑, *memory↑, *AChE↓, *other↝, *lipid-P↓,
7520- CAPE,    Neuroprotective Effect of Caffeic Acid Phenethyl Ester in A Mouse Model of Alzheimer's Disease Involves Nrf2/HO-1 Pathway
- in-vivo, AD, NA
*ROS↓, *NRF2↑, *HO-1↑, *Apoptosis↓, *Inflam↓, *Learn↑, *memory↑, *cognitive↑, *neuroP↑, *p‑GSK‐3β↓, GFAP↓,
5926- CAR,    An Updated Review of Research into Carvacrol and Its Biological Activities
- Review, Nor, NA - Review, AD, NA - Review, Asthma, NA
*Inflam↓, *antiOx↑, *neuroP↑, *BioAv↑, *toxicity↓, *Pain↓, *TRPV3↑, *NRF2↑, *Ca+2↑, *ATP↑, *5LO↓, *COX2/PTGS2↓, PGE2↓, *hepatoP↑, *AntiAg↑, *Diar↓, *cardioP↑, *other↝, *chemoPv↑, *cognitive↑, *AChE↓, *GastroP↑, *eff↑, *BChE↓, *CRP↓,
5925- CAR,    Neuroprotective effects of carvacrol against Alzheimer’s disease and other neurodegenerative diseases: A review
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, *antiOx↑, *AChE↓, *BBB↑, *cardioP↑, *neuroP↑, *memory↑, *TAC↑, *ROS↓, *lipid-P↓, *MDA↓, *SOD↑, *Catalase↑, *NRF2↑, *cognitive↑, *IL1β↓, *COX2/PTGS2↓, *TNF-α↓, *TLR4↓, *BDNF↑, *PKCδ↑, *5LO↓, *TRPM7↓, *GSH↑, *other↑, *Ferroptosis↓, *GPx4↑,
6638- Cen,    Prolonged Treatment with Centella asiatica Improves Memory, Reduces Amyloid-β Pathology, and Activates NRF2-Regulated Antioxidant Response Pathway in 5xFAD Mice
- in-vivo, AD, NA
*memory↑, *Aβ↓, *NRF2↑, *toxicity↓, *neuroP↑, *ROS↓, *mtDam↓, *cognitive↑, NQO1↑, HO-1↑,
6636- Cen,    Pharmacokinetics and Pharmacodynamics of Key Components of a Standardized Centella asiatica Product in Cognitively Impaired Older Adults: A Phase 1, Double-Blind, Randomized Clinical Trial
- Trial, AD, NA
*cognitive↑, *NRF2↑, *Dose↝, *memory↑, *ROS↓, *mitResp↑, *neuroP↑, *Half-Life↝, *Half-Life↝, *Half-Life↝,
6650- Cen,    Therapeutic Potential of Centella asiatica and Its Triterpenes: A Review
- Review, AD, NA
*BioAv↝, *BioAv↝, *MDA↓, *GSH↑, *SOD↑, *AChE↓, *memory↑, *Ki-67↑, *Catalase↑, *PI3K↑, *BDNF↑, *NGF↑, *ROS↓, *NRF2↑, *HO-1↑, *NQO1↑, *ATP↑, *OCR↑, *TNF-α↓, *PP2A↑, *GSK‐3β↓, *Bcl-2↑, *TrkB↑, *NOTCH1↑, *SOX2↑, *Nestin↑, *MDA↓, *MAOA↓, *MAOB↓, *GPx↑, *cognitive↑, *ROS↓, *neuroP↑, *glucose↓, *ALAT↓, *AST↓, *PFK↓, *Weight↓, *Inflam↓, *AntiDiabetic↑, *Obesity↓, *Wound Healing↑, *cardioP↑, *GutMicro↑, *Sepsis↓, *BioAv↑,
6002- CGA,    Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials
- Review, Var, NA - Review, Diabetic, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, *Inflam↓, *antiOx↑, *cardioP↑, *NRF2↑, *AMPK↑, *SOD↑, *Catalase↑, *GSH↑, *GPx↑, *ROS↓, *TNF-α↓, *IL6↓, *NF-kB↓, *COX2/PTGS2↓, *glucose↓, *TRPC1↓, *Ca+2↓, *HO-1↑, *NF-kB↓, *PPARα↝, *Hif1a↓, *JNK↓, *BP↓, *AntiDiabetic↑, *hepatoP↑, *TLR4↓, *NRF2↑, *Casp↓, *neuroP↑, *Aβ↓, *LDH↓, *MDA↓, *memory↑, *AChE↓, *eff↑, EMT↝, N-cadherin↓, E-cadherin↑, TumCCA↑, ROS↑, p‑P53↑, HO-1↑, NRF2↑, ChemoSen↑, mtDam↑, Casp3↑, Casp9↑, PARP↑, Bax:Bcl2↑, TumCG↓, cycD1/CCND1↓, cMyc↓, CDK2↓, mitResp↓, Glycolysis↓, Hif1a↓, PCNA↓, p‑GSK‐3β↓, VEGF↓, PI3K↓, Akt↓, mTOR↓, OS↑,
6040- CGA,    Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway
- in-vivo, AD, NA
*neuroP↑, *Dose↝, *GSK‐3β↓, *tau↓, *β-catenin/ZEB1↑, *Wnt↑, *memory↑, *cognitive↑, *NRF2↑, *ROS↓,
6001- Chit,    Recent advances in engineering chitosan-based nanoplatforms in biotherapeutic multi-delivery for multi-targeted disease treatments: Promises and outlooks
- Review, Var, HepG2 - Review, AD, NA
TumVol↓, toxicity↓, Half-Life↑, eff↑, selectivity↑, Dose↝, *BDNF↑, *NRF2↑, *ROS↓, *neuroP↑, *memory↑, *cognitive↑, *Obesity↓,
6128- CHr,    Chrysin: A Comprehensive Review of Its Pharmacological Properties and Therapeutic Potential
- Review, Nor, NA - Review, Var, NA - Review, AD, NA
*antiOx↑, *Inflam↓, AntiCan↑, *neuroP↑, *ROS↓, *BioAv↓, *BioAv↑, *cardioP↑, *COX2/PTGS2↓, *TNF-α↓, *IL1β↓, *NF-kB↓, *lipid-P↓, *Apoptosis↓, *NRF2↑, *HO-1↑, *MDA↓, *GSH↑, *SOD↑, *GPx↑, *GSR↑, *Catalase↑, *5HT↑, *Casp3↓, *Casp9↓, TumCCA↑, MAPK↓, PI3K↓, Akt↓, TumCP↓, TET1↑, TLR4↓, HER2/EBBR2↓, HK2↓, Glycolysis↓, glucose↓, lactateProd↓, ROS↑, mTOR↓, TumAuto↑, tumCV↓, ER Stress↑, UPR↑, PERK↑, ATF4↑, eIF2α↑, BioAv↑,
6624- Cic,    Chicoric acid supplementation ameliorates cognitive impairment induced by oxidative stress via promotion of antioxidant defense system
- in-vivo, AD, NA - in-vivo, Park, NA
*neuroP↑, *TNF-α↓, *IL1β↓, *MDA↓, *Catalase↑, *GSH↑, *NRF2↑, *mtDam↓, *Inflam↓, *Apoptosis↓, *ROS↓, *cognitive↑, *Aβ↓, *BDNF∅, *APP↓, *BACE/β-secretase↓,
5798- CRMs,    Caloric restriction mimetics improve gut microbiota: a promising neurotherapeutics approach for managing age-related neurodegenerative disorders
- Review, Nor, NA - Review, AD, NA
*GutMicro↑, *neuroP↑, *eff↑, *Dose↝, *AMPK↑, *SIRT1↑, *mTOR↓, *NRF2↑, *p‑tau↓,
6185- Cuc,    Cucurbitacin B: A review of its pharmacology, toxicity, and pharmacokinetics
- Review, Var, NA - Review, Arthritis, NA - Review, AD, NA
*Inflam↓, *antiOx↑, *hepatoP↑, *neuroP↑, *AntiCan↑, *toxicity↝, *BioAv↓, *HO-1↑, *NRF2↑, *NLRP3↑, *SOD↑, *SOD1↑, *ROS↓, *AntiAge↑, *ARE↑, *STAT↓, *NF-kB↓, *neuroG↑, *memory↑, ROS↑, NLRP3↑, CIP2A↓, Akt↓, STAT3↑, VEGFR2/KDR/Flk1↓, DNMTs↓, MAPK↓, YAP/TEAD↓, PI3K↓, Wnt↓, NOTCH↓, TumCCA↑, TumCG↓, TumCP↓, FAK↑, MMP9↓, TumAuto↑, toxicity↝, BioAv↓, Half-Life↝, BioAv↑, selectivity∅,
3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,
3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, *Inflam↓, *AntiAge↑, *AMPK↑, *SIRT1↑, *NF-kB↓, *mTOR↓, *NLRP3↓, *NADPH↓, *ROS↓, *COX2/PTGS2↓, *MCP1/CCL2↓, *IL1β↓, *IL17↓, *IL23↓, *TNF-α↓, *MPO↓, *IL10↑, *lipid-P↓, *SOD↑, *Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *TXNIP↓, *NRF2↑, *NQO1↑, *HO-1↑, *OS↑, *memory↑, *BDNF↑, *neuroP↑, *BACE/β-secretase↓, *AChE↓, *LDL↓,
3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, *Inflam↓, *BBB↑, *NRF2↑, *NF-kB↓, *cognitive↑, *ROS↓, *MDA↓, *SOD↑, *Catalase↑, *INF-γ↓, *IL4↓, *memory↑, *TNF-α↓, *IL1β↓,
3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, *antiOx↑, *memory↑, *Aβ↓, *BBB↑, *cognitive↑, *tau↓, *LDL↓, *AChE↓, *IL1β↓, *IronCh↑, *neuroP↑, *BioAv↝, *PI3K↑, *Akt↑, *NRF2↑, *HO-1↑, *Ferritin↑, *HO-2↓, *ROS↓, *Ach↑, *GSH↑, *Bcl-2↑, *ChAT↑,
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, NA
*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *cognitive↑, *cardioP↑, other↑, *COX2/PTGS2↓, *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↑,
6259- Cyste,    Therapeutic Applications of Cysteamine and Cystamine in Neurodegenerative and Neuropsychiatric Diseases
- Review, AD, NA - Review, Park, NA
*ROS↓, *neuroP↑, *BDNF↑, *NRF2↑, *BBB↑, *HSPs↑, *GSH↑, *TG2/TGase↓, Aβ↓,
4333- Cyste,    Cystamine protects from 3-nitropropionic acid lesioning via induction of nf-e2 related factor 2 mediated transcription
- vitro+vivo, AD, NA
*NRF2↑, *ARE↑, *neuroP↑, *BDNF↑, *GSH↑,
6828- EMD,    Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling in U251 cells and APP/PS1 mice
- in-vitro, AD, U251
*MMP↑, *ROS↓, *NRF2↑, *HO-1↑, *SOD↑, *Bcl-2↑, *Catalase↑, *BAX↓, *memory↑, *ANXi↓, *Aβ↓, *antiOx↑, *MDA↓,
3714- FA,    Recent Advances in the Neuroprotective Properties of Ferulic Acid in Alzheimer's Disease: A Narrative Review
- Review, AD, NA
*antiOx↑, *Inflam↓, *neuroP↑, *NF-kB↓, *NLRP3↓, *iNOS↓, *COX2/PTGS2↓, *TNF-α↓, *IL1β↓, *VCAM-1↓, *ICAM-1↓, *p‑MAPK↓, *p38↓, *JNK↓, *IL6↓, *IL8↓, *hepatoP↑, *RenoP↑, *Catalase↑, *PPARγ↑, *ROS↓, *Fenton↓, *IronCh↑, *SOD↑, *MDA↓, *lipid-P↓, *NRF2↑, *HO-1↑, *ARE↑, *Bil↑, *radioP↑, *GCLC↑, *GCLM↑, *NQO1↑, *Half-Life↝, *GutMicro↑, *Aβ↓, *BDNF↑, *Ca+2↓, *lipid-P↓, *PGE2↓, *cognitive↑, *ChAT↑, *memory↑, *Dose↝, *toxicity↓,
3778- FA,    Recent Advances in the Neuroprotective Properties of Ferulic Acid in Alzheimer’s Disease: A Narrative Review
- Review, AD, NA
*neuroP↑, *Aβ↓, *antiOx↑, *Inflam↓, *ROS↓, *NF-kB↓, *NLRP3↓, *iNOS↓, *COX2/PTGS2↓, *TNF-α↓, *IL1β↓, *VCAM-1↓, *ICAM-1↓, *p‑MAPK?, *hepatoP↑, *TLR4↓, *PPARγ↑, *NRF2↑, *Fenton↓, *IronCh↑, *MDA↓, *HO-1↑, *Bil↑, *GCLC↑, *GCLM↑, *NQO1↑, *GutMicro↑, *SOD↑, *Ca+2↓, *lipid-P↓, *PGE2↓,
6907- FIS,    Fisetin stimulates autophagic degradation of phosphorylated tau via the activation of TFEB and Nrf2 transcription factors
- in-vitro, AD, NA
*p‑tau↓, *NRF2↑, *mTORC1↓, *neuroP↑, *memory↑, *Inflam↓, *memory↑, *TFEB↑, *mTOR↓,

Showing Research Papers: 1 to 50 of 120
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 120

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0)

GFAP↓, 1,  

Redox & Oxidative Stress(tgid=1)

GSH↓, 1,   HO-1↑, 2,   MFN2↑, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↑, 8,   ROS⇅, 1,  

Mitochondria & Bioenergetics(tgid=3)

mitResp↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

cMyc↓, 2,   glucose↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,  

Cell Death(tgid=5)

Akt↓, 5,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 5,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Bcl-2↑, 1,   Casp↑, 2,   Casp1↑, 1,   Casp12↑, 1,   Casp3↑, 3,   cl‑Casp3⇅, 1,   Casp8↑, 1,   Casp9↑, 3,   Cyt‑c↑, 3,   Fas↑, 1,   JNK↑, 1,   MAPK↓, 3,   MAPK↝, 1,   p38↑, 2,   survivin↓, 1,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction(tgid=6)

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7)

other↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8)

eIF2α↑, 1,   ER Stress↑, 2,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9)

BNIP3↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair(tgid=10)

CHK1↓, 1,   DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 3,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11)

CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↑, 1,   P21↑, 3,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State(tgid=12)

CIP2A↓, 1,   EMT↝, 1,   ERK↓, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   p‑GSK‐3β↓, 1,   mTOR↓, 3,   mTOR↝, 1,   NOTCH↓, 1,   PI3K↓, 5,   PI3K↑, 1,   STAT3↓, 1,   STAT3↑, 1,   TumCG↓, 3,   Wnt↓, 2,  

Migration(tgid=13)

5LO↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 1,   FAK↑, 1,   p‑FAK↓, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP9↓, 4,   MMPs↓, 1,   N-cadherin↓, 1,   TET1↑, 1,   TumCMig↓, 2,   TumCP↓, 3,   TumCP↑, 1,   TumMeta↓, 2,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 1,   ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 4,   VEGF↓, 6,   VEGFR2/KDR/Flk1↓, 3,  

Immune & Inflammatory Signaling(tgid=16)

COX2/PTGS2↓, 2,   CXCR4↓, 2,   IL1↓, 1,   IL2↓, 1,   IL4↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 1,   NF-kB↓, 4,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19)

Aβ↓, 1,   NLRP3↑, 1,  

Hormonal & Nuclear Receptors(tgid=20)

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↓, 1,   BioAv↑, 3,   ChemoSen↑, 3,   ChemoSen⇅, 1,   Dose↝, 2,   eff↑, 4,   Half-Life↑, 1,   Half-Life↝, 1,   RadioS↑, 1,   selectivity↑, 1,   selectivity∅, 1,  

Clinical Biomarkers(tgid=22)

AR↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23)

AntiCan↓, 1,   AntiCan↑, 4,   AntiTum↑, 1,   chemoP↑, 2,   neuroP↑, 1,   OS↑, 1,   radioP↑, 1,   toxicity↓, 1,   toxicity↝, 1,   TumVol↓, 1,  
Total Targets: 139

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

AntiBio↑, 1,   Learn↑, 2,   TRPA1↑, 1,  

Redox & Oxidative Stress(tgid=1)

antiOx↑, 30,   ARE↑, 3,   Bil↑, 2,   Catalase↑, 14,   Fenton↓, 2,   Ferroptosis↓, 2,   GCLC↑, 2,   GCLM↑, 2,   GPx↑, 10,   GPx4↑, 1,   GSH↑, 20,   GSR↓, 1,   GSR↑, 1,   GSTs↑, 1,   H2O2↓, 1,   H2O2∅, 1,   HO-1↑, 24,   HO-2↓, 1,   Keap1↓, 1,   lipid-P↓, 15,   MDA↓, 18,   MPO↓, 3,   NQO1↑, 4,   NRF2↑, 52,   ROS↓, 43,   ROS↑, 1,   SOD↑, 25,   SOD1↑, 1,   TAC↑, 2,   TBARS↓, 2,  

Metal & Cofactor Biology(tgid=2)

Ferritin↑, 1,   IronCh↑, 8,  

Mitochondria & Bioenergetics(tgid=3)

AIF↓, 1,   ATP↑, 3,   mitResp↑, 1,   MMP↑, 1,   mtDam↓, 3,   mtDam↑, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

12LOX↓, 1,   Acetyl-CoA↑, 1,   ALAT↓, 4,   AMPK↑, 5,   p‑AMPK↑, 1,   cAMP↑, 2,   CREB↑, 1,   glucose↓, 2,   glucose↑, 1,   GlucoseCon↑, 3,   H2S↑, 1,   LDH↓, 4,   LDH↑, 1,   LDL↓, 2,   NADPH↓, 1,   NADPH↑, 1,   PDH↑, 1,   PDKs↓, 1,   PFK↓, 1,   PPARα↑, 1,   PPARα↝, 1,   PPARγ↓, 1,   PPARγ↑, 6,   SIRT1↑, 4,  

Cell Death(tgid=5)

Akt↓, 1,   Akt↑, 7,   p‑Akt↑, 1,   Apoptosis↓, 6,   BAX↓, 2,   Bcl-2↑, 3,   Casp↓, 1,   Casp3↓, 3,   Casp9↓, 3,   Fas↓, 1,   Ferroptosis↓, 2,   iNOS↓, 11,   JNK↓, 2,   MAPK↓, 3,   MAPK↑, 2,   p‑MAPK?, 1,   p‑MAPK↓, 1,   p38↓, 1,   p38↑, 1,  

Kinase & Signal Transduction(tgid=6)

TRPV3↑, 1,  

Transcription & Epigenetics(tgid=7)

Ach↑, 6,   other↑, 2,   other↝, 2,  

Protein Folding & ER Stress(tgid=8)

ER Stress↓, 1,   HSP70/HSPA5↑, 1,   HSPs↑, 1,  

Autophagy & Lysosomes(tgid=9)

TFEB↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

Choline↑, 1,   ERK↑, 2,   p‑ERK↑, 1,   GSK‐3β↓, 9,   GSK‐3β↑, 1,   p‑GSK‐3β↓, 1,   mTOR↓, 3,   mTORC1↓, 1,   Nestin↑, 1,   neuroG↑, 1,   NOTCH1↑, 1,   PI3K↓, 1,   PI3K↑, 8,   PTEN↓, 2,   SOX2↑, 1,   STAT↓, 2,   TRPM7↓, 1,   Wnt↑, 1,  

Migration(tgid=13)

5LO↓, 3,   AntiAg↑, 1,   APP↓, 2,   Ca+2↓, 4,   Ca+2↑, 1,   CDK5↓, 2,   Ki-67↑, 1,   MMP9↓, 2,   PKA↑, 1,   PKCδ↑, 3,   TG2/TGase↓, 1,   TRPC1↓, 1,   TXNIP↓, 1,   VCAM-1↓, 6,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14)

eNOS↑, 1,   p‑eNOS↑, 1,   Hif1a↓, 1,   Hif1a↑, 1,   NO↓, 5,   VEGF↑, 1,  

Barriers & Transport(tgid=15)

BBB↑, 15,   GastroP↑, 1,   GLUT1↑, 1,   GLUT3↑, 1,   GLUT4↑, 3,  

Immune & Inflammatory Signaling(tgid=16)

CB2 / CNR2↑, 2,   COX1↓, 1,   COX2/PTGS2↓, 17,   CRP↓, 2,   ICAM-1↓, 3,   IL10↑, 1,   IL12↓, 1,   IL17↓, 1,   IL1β↓, 16,   IL2↓, 2,   IL23↓, 1,   IL4↓, 2,   IL4↑, 1,   IL6↓, 12,   IL8↓, 1,   Imm↑, 1,   INF-γ↓, 3,   Inflam↓, 34,   Inflam↑, 2,   MCP1/CCL2↓, 1,   NF-kB↓, 20,   NF-kB↑, 2,   PGE2↓, 9,   TLR4↓, 6,   TNF-α↓, 21,  

Synaptic & Neurotransmission(tgid=18)

5HT↑, 3,   AChE↓, 15,   BChE↓, 2,   BDNF↑, 9,   BDNF∅, 1,   ChAT↑, 6,   GABA↑, 1,   MAOA↓, 3,   NGF↑, 1,   tau↓, 5,   p‑tau↓, 5,   TrkB↑, 2,  

Protein Aggregation(tgid=19)

Aβ↓, 16,   BACE/β-secretase↓, 6,   MAOB↓, 1,   NLRP3↓, 7,   NLRP3↑, 1,   PP2A↑, 1,  

Hormonal & Nuclear Receptors(tgid=20)

CYP19↓, 1,   RAAS↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↓, 5,   BioAv↑, 8,   BioAv↝, 8,   Dose↝, 8,   eff↓, 1,   eff↑, 8,   Half-Life↓, 2,   Half-Life↝, 7,  

Clinical Biomarkers(tgid=22)

ALAT↓, 4,   ALP↓, 1,   AST↓, 5,   Bil↑, 2,   BP↓, 2,   BP↝, 1,   creat↓, 1,   CRP↓, 2,   Ferritin↑, 1,   GutMicro↑, 6,   IL6↓, 12,   Ki-67↑, 1,   LDH↓, 4,   LDH↑, 1,  

Functional Outcomes(tgid=23)

AntiAge↑, 3,   AntiCan↑, 3,   AntiDiabetic↑, 3,   AntiTum↑, 1,   ANXi↓, 1,   cardioP↑, 13,   chemoPv↑, 1,   cognitive↓, 1,   cognitive↑, 28,   hepatoP↑, 10,   memory↑, 25,   motorD↑, 1,   neuroP↑, 48,   NP/CIPN↓, 1,   Obesity↓, 3,   OS↑, 1,   Pain↓, 1,   radioP↑, 1,   RenoP↑, 2,   toxicity↓, 5,   toxicity↝, 1,   Weight↓, 2,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24)

AntiFungal↑, 1,   AntiViral↑, 1,   Bacteria↓, 2,   Diar↓, 1,   Sepsis↓, 1,  
Total Targets: 232

Scientific Paper Hit Count for: NRF2, nuclear factor erythroid 2-related factor 2
9 Sulforaphane (mainly Broccoli)
6 Alpha-Lipoic-Acid
6 Lycopene
5 Curcumin
5 Hydrogen Gas
5 Quercetin
4 Boswellia (frankincense)
4 Urolithin
3 Beta-Caryophyllene
3 Centella asiatica / Gotu kola → asiaticoside
3 Thymoquinone
2 Allicin (mainly Garlic)
2 Astaxanthin
2 Baicalein
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Carvacrol
2 Chlorogenic acid
2 Cysteamine
2 Ferulic acid
2 Ginseng
2 Honokiol
2 Isoliquiritigenin
2 isoorientin
2 Licochalcone A
2 Luteolin
2 Pterostilbene
2 Resveratrol
2 Rosmarinic acid
2 Silymarin (Milk Thistle) silibinin
2 Taurine
2 Vitexin
1 1,8-Cineole
1 Apigenin (mainly Parsley)
1 Berberine
1 Biochanin A
1 xanthohumol
1 Carnosic acid
1 Caffeic acid
1 chitosan
1 Chrysin
1 Cichoric acid / Chicoric acid
1 Calorie Restriction Mimetics
1 Cucurbitacin
1 Emodin
1 Fisetin
1 Formononetin
1 Gallic acid
1 Geraniol
1 hydrogen sulfide
1 Hyperoside
1 isoquercitrin
1 Kaempferol
1 Magnetic Fields
1 Methylsulfonylmethane
1 Nimbolide
1 Propolis -bee glue
1 Phenolic Acids
1 Hydroxycinnamic-acid
1 Piperine
1 Selenium NanoParticles
1 Vanillic Acid
1 Mung Bean Sprouts
1 Vitamin B1/Thiamine
1 Isovitexin
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#:226  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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