toxicity Cancer Research Results

toxicity, toxicity: Click to Expand ⟱

Source:

Type:

Toxicity

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
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, Lactoferrin, Lecithin, Licochalcone A, 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⟱

6461-

1,8-Cin,

1,8-cineole (eucalyptol): A versatile phytochemical with therapeutic applications across multiple diseases

Review,

AD,

Review,

Var,

*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↑,

3677-

BBR,

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

Review,

AD,

0.44uM(AChEi)

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

5633-

BCA,

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

Review,

Var,

Review,

AD,

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

3690-

BM,

Neurocognitive Effect of Nootropic Drug Brahmi (Bacopa monnieri) in Alzheimer's Disease

Review,

AD,

*ROS↓, *5LO↓, *lipid-P↓, *GPx↑, *IronCh↑, *neuroP↑, *AChE↓, *memory↑, *toxicity↓, *SOD↑, *Catalase↑, *cognitive↑, *ChAT↑, *Ach↑, *BP↓,

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/ABCB1↓, eff↑, other↝,

6542-

BSB,

Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol

Review,

Var,

Review,

Park,

Review,

AD,

AntiCan↑, *neuroP↑, *cardioP↑, *AntiBio↑, *BioAv↑, *toxicity↓, *BioAv↑, *motorD↑, *SOD↑, *Catalase↑, *Keap1↑, *MDA↓, *GSH↑, *IL1β↓, *IL6↓, *TNF-α↓, *iNOS↓, *COX2/PTGS2↓, *lipid-P↓, *Cyt‑c↓, *ROS↓, *MMP↑, *antiOx↑, *AChE↓, *Apoptosis↓, *BAX↓, *Casp3↓, *Bcl-2↑, *BACE/β-secretase↓, *BChE↓, *eff↑, *Aβ↓, *ATP↑, RadioS↑, Cyt‑c↑, Casp3↑, Casp8↑, Casp9↑, Apoptosis↑, PARP↑, BAX↑, BID↑, NF-kB↑, Fas↑, EGFR↑, TIMP2↑, XIAP↓, COX2/PTGS2↓, Bak↓, Bcl-2↓, P53↑, HER2/EBBR2↓, FGF↓, CEA↓, Akt↓, TumCCA↑, *Imm↑, *CD4+↑, *CD8+↑, *BBB↑, *Pain↓, *cardioP↑, *TBARS↓, *SOD↑, *Catalase↑, *GSH↑, *AntiBio↑, *AntiFungal↑, *GastroP↑, *RenoP↑, *creat↓, *uricA↓, *Inflam↓, *iNOS↓, *COX2/PTGS2↓, *TNF-α↓, *IL6↑, *MMP13↓,

6556-

BSB,

A Comprehensive Study of Therapeutic Applications of Chamomile

Review,

Nor,

Review,

AD,

Review,

Park,

Review,

Stroke,

*Inflam↓, *antiOx↑, *AntiBio↑, *hepatoP↑, *AntiCan↑, *other↝, *toxicity↓, *Wound Healing↓, *Dose↝, *Dose↝, *eff↝, *ROS↓, *TNF-α↓, *IL6↓, *other↝, *AST↓, *ALAT↓,

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/PTGS2↓, *PPARα↑, *NO↓, *AChE↓, *eff↑, *SOD↑, *Catalase↑, *neuroP↑, *BioAv↝, *BBB↑, *BioAv↑,

5926-

CAR,

An Updated Review of Research into Carvacrol and Its Biological Activities

Review,

Nor,

Review,

AD,

Review,

Asthma,

*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↓,

3869-

Carno,

Carnosine, Small but Mighty—Prospect of Use as Functional Ingredient for Functional Food Formulation

Review,

AD,

Review,

Stroke,

*ROS↓, *IronCh↑, *AntiAge↑, *antiOx↑, *Inflam↓, *neuroP↑, *lipid-P↓, *toxicity↓, *NOX4↓, *SOD↑, *HNE↓, *IL6↓, *TNF-α↓, *IL1β↓, *Sepsis↓, *eff↑, *GABA↝, *Aβ↓, Glycolysis↓, AntiTum↑, p‑Akt↓, TumCCA↑, angioG↓, VEGFR2/KDR/Flk1↓, NF-kB↓,

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,

5xFAD mice

*memory↑, *Aβ↓, *NRF2↑, *toxicity↓, *neuroP↑, *ROS↓, *mtDam↓, *cognitive↑, NQO1↑, HO-1↑,

6043-

CGA,

SeNPs,

Enhanced Effect of Combining Chlorogenic Acid on Selenium Nanoparticles in Inhibiting Amyloid β Aggregation and Reactive Oxygen Species Formation In Vitro

in-vitro,

AD,

*ROS↓, *Aβ↓, *BioAv↝, *BioAv↑, *Dose↝, *ROS↓, *H2O2↓, *toxicity↓,

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,

TumVol↓, toxicity↓, Half-Life↑, eff↑, selectivity↑, Dose↝, *BDNF↑, *NRF2↑, *ROS↓, *neuroP↑, *memory↑, *cognitive↑, *Obesity↓,

3893-

Cin,

Cinnamon extract inhibits tau aggregation associated with Alzheimer's disease in vitro

Review,

AD,

*tau↓, *toxicity↓,

3892-

Cin,

Cinnamon from the selection of traditional applications to its novel effects on the inhibition of angiogenesis in cancer cells and prevention of Alzheimer's disease, and a series of functions such as antioxidant, anticholesterol, antidiabetes, antibacterial, antifungal, nematicidal, acaracidal, and repellent activities

Review,

AD,

Review,

Var,

*antiOx↑, *Inflam↓, *cardioP↑, angioG↓, VEGF↓, *LDL↓, COX2/PTGS2↓, Hif1a↓, *Aβ↓, *tau↓, *toxicity↓,

3575-

CUR,

The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse

in-vivo,

AD,

mice

*antiOx↑, *ROS↓, *IL1β↓, *Aβ↓, *Inflam↓, *toxicity↓,

6281-

DL,

Applications of Limonene in Neoplasms and Non-Neoplastic Diseases

Review,

Var,

Review,

AD,

Review,

Diabetic,

*antiOx↑, AntiTum↑, *AntiDiabetic↑, *neuroP↑, *GastroP↑, *ROS↓, *toxicity↓, *BioAv↑, ChemoSen↑, BAX↑, P53↓, Bcl-2↓, iNOS↓, COX2/PTGS2↓, eff↑, ROS↑, TumCCA↑, cycD1/CCND1↓, CycB/CCNB1↓, TumCMig↓, *lipid-P↓, *GSH↑, *SOD↑, *GPx↑, *hepatoP↑, *glucose↓, *AGEs↓, *Obesity↓, *Aβ↓, *AChE↓,

7209-

EGb 761,

Ginkgo biloba Extract EGb 761 in the Treatment of Patients with Mild Neurocognitive Impairment: A Systematic Review

Review,

AD,

*cognitive↑, *toxicity↓,

7202-

EGb 761,

Ginkgo biloba leaf extract EGb 761® for the treatment of various diseases: Overview of systematic reviews

Review,

AD,

*cognitive↑, *Tinn↓, *toxicity↓,

7196-

EGb 761,

Ginkgo biloba extract EGb 761 in patients with dementia and a history of cerebral infarction-meta-analysis of pooled data from randomised clinical trials

Review,

AD,

Review,

Stroke,

*neuroP↑, *cognitive↑, *Stroke↓, *toxicity↓, Dose↝,

7232-

EGb 761,

Efficacy and safety of Ginkgo biloba extract EGb 761 in mild cognitive impairment with neuropsychiatric symptoms: a randomized, placebo-controlled, double-blind, multi-center trial

Trial,

AD,

240 mg EGb 761 daily or placebo for a period of 24 weeks, 37 patients taking EGb 761 and 36 patients receiving placebo.

*cognitive↑, *toxicity↓,

7231-

EGb 761,

Efficacy and tolerability of Ginkgo biloba extract EGb 761® in dementia: a systematic review and meta-analysis of randomized placebo-controlled trials

Review,

AD,

 2,684 outpatients randomized to receive treatment for 22–26 weeks,

*toxicity↓, *eff↑, *cognitive↑, *other↑, *eff↑,

7229-

EGb 761,

Meta-analysis of the efficacy and safety of Ginkgo biloba extract for the treatment of dementia

Review,

AD,

*toxicity↓, *Dose↝, *ROS↓, *PAF↓, *memory↑, *BloodF↑, *antiOx↑, *Inflam↓, *Tinn↓,

7222-

EGb 761,

Ginkgo biloba extract EGb 761® in the symptomatic treatment of mild-to-moderate dementia: a profile of its use

Review,

AD,

*cognitive↑, *toxicity↓, *Dose↝, *BioAv↑, *Half-Life↑, *neuroP↑, *Half-Life↝, *Dose↝, *other↝, *eff↑,

6820-

EMD,

The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb—A Summary Update

Review,

Nor,

Review,

Arthritis,

Review,

AD,

*diuretic↑, *Bacteria↓, *Inflam↓, AntiCan↑, TumCP↓, TumCI↓, angioG↓, *toxicity↓, IFN-γ↑, IL12↑, ROS↑, TNF-α↓, TNF-α↓, TGF-β↓, MAPK↓, PKCδ↓, NF-kB↓, HER2/EBBR2↓, VEGF↓, DNAdam↑, Necroptosis↑, Glycolysis↓, GLUT1↓, PI3K↓, Akt↓, Casp9↑, Casp3↑, BAX↑, Bcl-2↓, eff↑, MMP2↓, MMP9↓, eff↑, ChemoSen↑, P-gp/ABCB1↓, SREBP2↓, eff↑, *other↝, *COX2/PTGS2↓, *Hif1a↓, *HDAC↓, *tau↓, *PKCδ↑, *ROS↓, *Inflam↓, AntiAg?,

6378-

Eug,

Effects of Eugenol on the Central Nervous System: Its Possible Application to Treatment of Alzheimer's Disease, Depression, and Parkinson's Disease

Review,

AD,

*other↑, *Aβ↓, *BDNF↑, *MAOA↑, *toxicity↓, *Ca+2↓, *antiOx↑, *ROS↓, *lipid-P↓, *neuroP↑, *PGE2↓, *COX2/PTGS2↓, *5LO↓,

3714-

FA,

Recent Advances in the Neuroprotective Properties of Ferulic Acid in Alzheimer's Disease: A Narrative Review

Review,

AD,

*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↓,

3717-

FA,

Neuroprotective Properties of Ferulic Acid in Preclinical Models of Alzheimer's Disease: A Systematic Literature Review

Review,

AD,

*toxicity↓, *BBB↑, *Aβ↓, *antiOx↑, *Inflam↓, *neuroP↑,

6933-

FLS,

AudGS,

Gamma sensory stimulation in mild Alzheimer's dementia: An open-label extension study

Trial,

AD,

*Dose↝, *toxicity↓, *cognitive↑,

6932-

FLS,

Safety, Feasibility, and Potential Clinical Efficacy of 40 Hz Invisible Spectral Flicker versus Placebo in Patients with Mild-to-Moderate Alzheimer's Disease: A Randomized, Placebo-Controlled, Double-Blinded, Pilot Study

Trial,

AD,

*toxicity↓,

6981-

Form,

Formononetin: a review of its source, pharmacology, drug combination, toxicity, derivatives, and drug delivery systems

Review,

Var,

Review,

AD,

Review,

PSA,

BioAv↝, *memory↑, *ROS↓, *AChE↓, *NF-kB↓, *Keap1↝, *NRF2↑, *Inflam↓, *PGC-1α↝, *HO-1↓, *p‑tau↓, *cognitive↑, *BDNF↑, *5HT↑, *Stroke↓, *PARP1↓, *AIF↓, *Casp3↓, NP/CIPN↓, *neuroP↑, *NGF↑, *TNF-α↓, *IL1β↓, *IL18↓, *IL6↓, *VCAM-1↓, *pol-M2 MC↑, *hepatoP↑, *AST↓, *ALAT↓, *LC3II↑, *Beclin-1/ATG6↑, *p62↑, *COX2/PTGS2↑, *MMP↑, *ATP↑, *GSH↑, *Catalase↑, *GPx↑, *MDA↓, *antiPs↑, *AntiDiabetic↑, *glucose↓, *Insulin↑, *GutMicro↑, *Obesity↓, COX2/PTGS2↓, cycD1/CCND1↓, TumCCA↑, EGFR↓, GSK‐3β↑, Mcl-1↓, *toxicity↓, TumCP↓, Hif1a↓, VEGF↓, ERK↓, LAMs↓, Cyt‑c↑, Casp9↑, Casp3↑, PARP↑, TumCD↑, mitA↑, BACH1↓, P53↓, ROS↑, PD-1↓, NF-kB↓, *Bacteria↓, *AntiViral↑, *mt-ROS?, *PI3K↓, *chemoP↑, ChemoSen↑, eff↑, *toxicity↓, *BioAv↑, *BioAv↑, *eff↑,

7080-

GABA,

The Effect of Oral GABA on the Nervous System: Potential for Therapeutic Intervention

Review,

AD,

*BBB↝, *cognitive↑, *Dose↝, *toxicity↓, *Stress↓, *Inflam↓, *iNOS↓, *COX2/PTGS2↓, *IL6↓, *IL1β↓, *TNF-α↓, *Sleep↑, *Pain↓, *neuroP↑, *eff↑, *Ach↑, *AST↓, *ALAT↓, *BP↓, *other↝,

7197-

GBE,

Ginkgo biloba for cognitive impairment and dementia

Review,

AD,

*cognitive↑, *toxicity↓,

7212-

GBE,

The Use of Ginkgo Biloba L. as a Neuroprotective Agent in the Alzheimer’s Disease

Review,

AD,

*antiOx↑, *ROS↓, *mitResp↑, *Casp9↓, *Casp3↓, *Apoptosis↓, *ATP↑, *neuroP↑, *IL1β↓, *IL6↓, *TNF-α↓, *PGE2↓, *memory↑, *cognitive↑, *BloodF↑, *lipid-P↓, *Aβ↓, *MAOA↓, *DA↑, *Dose↝, *toxicity↓,

7110-

GEN,

Genistein

Review,

AD,

*toxicity↓, *Dose↝, *cognitive↑,

7260-

Gink,

Ginkgetin: A natural biflavone with versatile pharmacological activities

Review,

Var,

Review,

Stroke,

Review,

AD,

*AntiCan↑, *Inflam↓, *AntiBio↑, *neuroP↑, *TumCCA↑, Apoptosis↑, TumAuto↑, iNOS↓, COX2/PTGS2↓, PGE2↓, NF-kB↓, PLA2↓, *neuroP↑, *Stroke↓, *AntiFungal↓, *Bacteria↓, Bcl-xL↓, Bcl-2↓, Casp9↑, Casp3↑, cl‑PARP↑, IL6↓, STAT3↓, JAK1↓, survivin↓, COX2/PTGS2↓, IAP1↓, MMP2↓, MMP9↓, PTEN↑, SHP1↑, eff↑, TumVol↓, TumW↓, *toxicity↓, *ROS↓,

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/β-secretase↓, *Aβ↓, *BP∅, *BBB↑,

7453-

HNK,

Determination of Potential Lead Compound from Magnolia officinalis for Alzheimer's Disease through Pharmacokinetic Prediction, Molecular Docking, Dynamic Simulation, and Experimental Validation

Study,

AD,

*BACE/β-secretase↓, *AChE↓, *QPCT/QC↓, *GSK‐3β↓, *toxicity↓,

7565-

HYP,

Potential Implications of Hyperoside on Oxidative Stress-Induced Human Diseases: A Comprehensive Review

Review,

AD,

*Inflam↓, *antiOx↑, *neuroP↑, *lipid-P↓, *ROS↓, *IL1β↓, *IL6↓, *IL8↓, *TNF-α↓, *MDA↓, *BAX↓, *Casp3↓, *Catalase↑, *SOD↑, *GSH↑, *BDNF↑, *TrkB↑, *NGF↑, *BDNF↑, *NF-kB↓, *AChE↓, *H2S↑, Casp3↑, Apoptosis↑, NF-kB↓, AMPK↑, HO-1↑, MAPK↑, cl‑Casp3↑, cl‑Casp9↑, BAX↑, SOD?, Catalase↓, NRF2↓, NQO1↓, HO-1↓, Bcl-2↓, TumCCA↑, FOXO1↑, TumAuto↑, Akt↓, mTOR↓, P70S6K↓, BMP7/OP1↓, *cardioP↑, *hepatoP↑, *antiCG↑, *AntiThr↑, *Diar↓, *AntiFungal↑, *CYP2D6↓, *PDGFR-BB↓, *PDGFRB↓, *toxicity↓, *Half-Life↑,

7560-

HYP,

Hyperoside: A Review of Its Structure, Synthesis, Pharmacology, Pharmacokinetics and Toxicity

Review,

Nor,

Review,

AD,

*RenoP↓, Casp3↑, Casp8↑, MDA↑, GSH↓, SOD↓, Catalase↓, VEGF↓, Bcl-2↓, TumCG↓, p‑Akt↓, PI3K↓, TumCCA↑, TumCP↓, BMP7/OP1↓, *ZO-1↑, *BBB↝, *p‑Akt↑, *GSK‐3β↑, *SOD↑, *Catalase↑, *GSH↑, *SIRT1↑, *NF-kB↓, *IL1β↓, *IL6↓, *IL8↓, *TNF-α↓, *ROS↓, *MDA↓, *BAX↓, *Casp3↓, *Bcl-2↑, *BDNF↑, *TrkB↑, *NGF↑, *Apoptosis↓, *cardioP↑, *AST↓, *hepatoP↑, *AST↓, *ALAT↓, *MDA↓, *BACH1↓, *neuroP↑, *Stroke↓, *ICAM-1↓, *VCAM-1↓, *TLR4↓, *COX2/PTGS2↓, *RenoP↑, *NLRP3↓, *Casp1↓, *ASC↓, *BioAv↓, *BioAv↑, *toxicity↓,

8219-

LCA,

Licochalcone A Ameliorates Cognitive Dysfunction in an Alzheimer's Disease Model by Inhibiting Endoplasmic Reticulum Stress-Mediated Apoptosis

in-vivo,

AD,

riple transgenic mouse AD models

*Dose↝, *cognitive↑, *Aβ↓, *ER Stress↓, *BioAv↑, *toxicity↓, *PERK↓, *eIF2α↓, *ATF4↓, *CHOP/DDIT3↓, *NRF2↑,

3905-

MCT,

Medium Chain Triglycerides induce mild ketosis and may improve cognition in Alzheimer's disease. A systematic review and meta-analysis of human studies

Review,

AD,

Twelve records (422 participants) were included

*cognitive↑, *KeyT↑, *eff↑, *other↑, *toxicity↓,

3927-

PTS,

Effects of Pterostilbene on Cardiovascular Health and Disease

Review,

AD,

Review,

Stroke,

*Inflam↓, *antiOx↑, *BioAv↑, *toxicity↓, *NADPH↓, *ROS↓, *Catalase↑, *GSH↑, *SOD↑, *TNF-α↓, *IL1β↓, *IL4↓, *MMPs↓, *COX2/PTGS2↓, *MAPK↝, *NF-kB↓, *IL8↓, *MCP1/CCL2↓, *E-sel↓, *lipid-P↓, *NRF2↑, *PPARα↑, *LDL↓, other↓,

3613-

RES,

Resveratrol for Alzheimer's disease

Review,

AD,

*SIRT1↑, *BioAv↝, *toxicity↓, *ROS↓, *antiOx↑, *Aβ↓, *MMP9↓, *TNF-α↓,

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/PTGS2↓, *PGE2↓, *MMPs↓, *TNF-α↓, *iNOS↓, *TLR4↓, *cognitive↑, *cortisol↓, *lipid-P↓,

4608-

SeNPs,

Selenium Nanoparticles for Biomedical Applications: From Development and Characterization to Therapeutics

Review,

Var,

NA,

AD,

*toxicity↝, *toxicity↓, *other↝, ROS↑, *Dose↝, *selenoP↑, AntiCan↑, AntiTum↑, *Bacteria↓, *radioP↑, *BioAv↑, *Inflam↓, *Imm↑, ChemoSen↑, *AntiAg↑, selectivity↑, eff↑, other↝, *eff↑, *Aβ↓, *eff↑,

3958-

Taur,

Evaluation of the neuroprotective effect of taurine in Alzheimer’s disease using functional molecular imaging

in-vivo,

AD,

5xFAD transgenic mice

*neuroP↑, *Aβ∅, *cognitive↑, *toxicity↓, *Ca+2↓, *memory↑,

6453-

TUR,

Pharmacological Profile, Bioactivities, and Safety of Turmeric Oil

Review,

Var,

Review,

AD,

Review,

Park,

*Dose↝, *BioEnh↑, *BBB↑, *ROS↓, *GSH↑, *SOD↑, *GSR↑, *NO↓, *P450↓, OS↑, TumCG↓, *GutMicro↑, *Pain↓, *neuroP↑, *AChE↓, *BDNF↑, *Bacteria↓, *AntiFungal↑, *toxicity↓,

4864-

Uro,

Therapeutic Potential of Mitophagy-Inducing Microflora Metabolite, Urolithin A for Alzheimer's Disease

Review,

AD,

*neuroP↑, *Half-Life↝, *BBB↑, *toxicity↓, *Inflam↓, *Strength↑, *BACE/β-secretase↓, *Aβ↓, *MitoP↑, *SIRT1↑, *SIRT3↑, *AMPK↑, *PGC-1α↑, *mTOR↓, *PARK2↑, *Beclin-1/ATG6↑, *ROS↓, *GutMicro↑, *Risk↓,

4861-

Uro,

Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions

in-vivo,

AD,

mice were treated with UA (200 mg/kg/day) by oral gavage for 5 months, ending at 17 months

three mouse models of AD

*memory↑, *Aβ↓, *toxicity↓, *BBB↑, *p‑tau↓, *eff↓, *IL1α↓, *MCP1/CCL2↓, *MIP‑1α/CCL3↓, *TNF-α↓, *IL2↓, *SIRT1↓, *DNAdam↓, *Dose↝, *Strength↑, *motorD↑, *CTSZ↓,

Showing Research Papers: 1 to 50 of 50

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 50

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 5, antiCG↑, 1, CYP2D6↓, 1, DA↑, 1, diuretic↑, 1, PAF↓, 1, QPCT/QC↓, 1, Stress↓, 1, Stroke↓, 4, Tinn↓, 2, TRPA1↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 19, ARE↑, 1, Bil↑, 1, Catalase↑, 12, Fenton↓, 1, GCLC↑, 1, GCLM↑, 1, GPx↑, 5, GSH↑, 8, GSR↑, 1, H2O2↓, 1, HNE↓, 1, HO-1↓, 1, HO-1↑, 2, Keap1↑, 1, Keap1↝, 1, lipid-P↓, 15, MDA↓, 8, NOX4↓, 1, NQO1↑, 1, NRF2↑, 11, PARK2↑, 1, RNS↓, 1, ROS↓, 29, mt-ROS?, 1, selenoP↑, 1, SIRT3↑, 1, SOD↑, 15, SOD1↑, 1, TAC↑, 1, TBARS↓, 1, uricA↓, 1,

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 3,

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1, ATP↑, 5, Insulin↑, 1, mitResp↑, 1, MMP↑, 2, mtDam↓, 2, PGC-1α↑, 1, PGC-1α↝, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 4, AMPK↑, 2, glucose↓, 2, H2S↑, 1, KeyT↑, 1, LDL↓, 4, NADPH↓, 1, NADPH↑, 1, PPARα↑, 2, PPARγ↓, 1, PPARγ↑, 1, SIRT1↓, 1, SIRT1↑, 3,

Cell Death(tgid=5) ⓘ

p‑Akt↑, 1, Apoptosis↓, 3, BAX↓, 3, Bcl-2↑, 2, Casp1↓, 1, Casp3↓, 5, Casp9↓, 1, Cyt‑c↓, 1, iNOS↓, 5, JNK↓, 1, MAPK↝, 1, p‑MAPK↓, 1, p38↓, 1,

Kinase & Signal Transduction(tgid=6) ⓘ

TRPV3↑, 2,

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 2, AntiThr↑, 1, other↓, 1, other↑, 3, other↝, 7,

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1, eIF2α↓, 1, ER Stress↓, 1, PERK↓, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 2, LC3II↑, 1, MitoP↑, 1, p62↑, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1, PARP1↓, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

FOXO3↑, 1, GSK‐3β↓, 2, GSK‐3β↑, 1, HDAC↓, 1, mTOR↓, 1, PDGFRB↓, 1, PI3K↓, 1,

Migration(tgid=13) ⓘ

5LO↓, 3, AntiAg↑, 2, APP↓, 1, BACH1↓, 1, Ca+2↓, 4, Ca+2↑, 1, E-sel↓, 1, MMP13↓, 1, MMP9↓, 1, MMPs↓, 2, PKCδ↑, 1, VCAM-1↓, 3, ZO-1↑, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1, EPR↑, 1, Hif1a↓, 1, NO↓, 6, PDGFR-BB↓, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 8, BBB↝, 2, GastroP↑, 3,

Immune & Inflammatory Signaling(tgid=16) ⓘ

ASC↓, 1, CD4+↑, 1, COX2/PTGS2↓, 11, COX2/PTGS2↑, 1, CRP↓, 1, CTSZ↓, 1, ICAM-1↓, 2, IL18↓, 1, IL1α↓, 1, IL1β↓, 12, IL2↓, 2, IL4↓, 1, IL6↓, 10, IL6↑, 1, IL8↓, 4, Imm↑, 2, Inflam↓, 24, pol-M2 MC↑, 1, MCP1/CCL2↓, 2, MIP‑1α/CCL3↓, 1, NF-kB↓, 7, PGE2↓, 5, TLR4↓, 2, TNF-α↓, 16,

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1, AChE↓, 12, BChE↓, 3, BDNF↑, 9, ChAT↑, 2, GABA↝, 1, MAOA↓, 2, MAOA↑, 1, NGF↑, 3, tau↓, 4, p‑tau↓, 2, TrkB↑, 2,

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1, Aβ↓, 21, Aβ∅, 1, BACE/β-secretase↓, 6, MAOB↓, 1, NLRP3↓, 3,

Hormonal & Nuclear Receptors(tgid=20) ⓘ

cortisol↓, 1, CYP19↓, 1, ER(estro)↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2, BioAv↑, 14, BioAv↝, 3, BioEnh↑, 1, Dose↝, 16, eff↓, 1, eff↑, 15, eff↝, 1, Half-Life↑, 2, Half-Life↝, 4, P450↓, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 4, ALP↓, 1, AST↓, 6, Bil↑, 1, BloodF↑, 2, BP↓, 2, BP∅, 1, creat↓, 1, CRP↓, 1, GutMicro↑, 4, IL6↓, 10, IL6↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↑, 3, antiPs↑, 1, cardioP↑, 8, chemoP↑, 1, chemoPv↑, 1, cognitive↑, 23, hepatoP↑, 8, memory↑, 14, motorD↑, 3, neuroP↑, 28, Obesity↓, 4, Pain↓, 4, radioP↑, 2, RenoP↓, 1, RenoP↑, 3, Risk↓, 1, Sleep↑, 1, Strength↑, 2, toxicity↓, 49, toxicity↝, 1, Wound Healing↓, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↓, 1, AntiFungal↑, 4, AntiViral↑, 2, Bacteria↓, 7, CD8+↑, 1, Diar↓, 2, Sepsis↓, 1,
Total Targets: 221

Scientific Paper Hit Count for: toxicity, toxicity

7 Ginkgo biloba-EGb 761
2 α-Bisabolol / Chamomile oil
2 Carvacrol
2 Selenium NanoParticles
2 Cinnamon
2 Ferulic acid
2 Flickering Light Stimulation
2 Ginkgo biloba
2 Hyperoside
2 Urolithin
1 1,8-Cineole
1 Berberine
1 Biochanin A
1 Bacopa monnieri
1 borneol
1 Carnosine
1 Centella asiatica / Gotu kola → asiaticoside
1 Chlorogenic acid
1 chitosan
1 Curcumin
1 D-limonene
1 Emodin
1 Eugenol
1 Auditory Gamma Stimulation / 40 Hz Auditory Stimulation
1 Formononetin
1 Gamma-aminobutyric acid
1 Genistein (soy isoflavone)
1 Ginkgetin
1 Hydrogen Gas
1 Honokiol
1 Licochalcone A
1 MCToil
1 Pterostilbene
1 Resveratrol
1 Rosmarinic acid
1 Taurine
1 Turmerones

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#:1025  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

toxicity Cancer Research Results

Brain Energy Systems Matrix (AD)

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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