MMP Cancer Research Results

MMP, ΔΨm, mitochondrial membrane potential: Click to Expand ⟱

Source:

Type:

Destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Mitochondria are organelles within eukaryotic cells that produce adenosine triphosphate (ATP), the main energy molecule used by the cell. For this reason, the mitochondrion is sometimes referred to as “the powerhouse of the cell”.
Mitochondria produce ATP through process of cellular respiration—specifically, aerobic respiration, which requires oxygen. The citric acid cycle, or Krebs cycle, takes place in the mitochondria.
The mitochondrial membrane potential is widely used in assessing mitochondrial function as it relates to the mitochondrial capacity of ATP generation by oxidative phosphorylation. The mitochondrial membrane potential is a reliable indicator of mitochondrial health.
In cancer cells, ΔΨm is often decreased, which can lead to changes in cellular metabolism, increased glycolysis, increased reactive oxygen species (ROS) production, and altered cell death pathways.

The membrane of malignant mitochondria is hyperpolarized (−220 mV) in comparison to their healthy counterparts (−160 mV), which facilitates the penetration of positively charged molecules to the cancer cells mitochondria.
The MMP is a critical indicator of mitochondrial function, directly reflecting the organelle's capacity to generate ATP through oxidative phosphorylation.

AD, Alzheimer's Disease: Click to Expand ⟱

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

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

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

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

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

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

SeNPs may also be useful as a Drug Delivery System.

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

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

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

Brain Energy Systems Matrix (AD)

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

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

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

Scientific Papers found: Click to Expand⟱

3447-

ALA,

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

in-vitro,

AD,

SH-SY5Y

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

4813-

ASTX,

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

in-vitro,

AD,

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

2605-

Ba,

BA,

Potential therapeutic effects of baicalin and baicalein

Review,

Var,

Review,

Stroke,

Review,

IBD,

Review,

Arthritis,

Review,

AD,

Review,

Park,

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

760-

Bor,

Therapeutic Efficacy of Boric Acid Treatment on Brain Tissue and Cognitive Functions in Rats with Experimental Alzheimer’s Disease

in-vivo,

AD,

rats

*memory↑, *ROS↓, *GSH↑, *Aβ↓, *Inflam↓, *MMP↑, *lipid-P↓, *Ca+2↓, *cognitive↑, *TOS↓,

5943-

Cela,

Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases

Review,

Arthritis,

Review,

IBD,

Review,

AD,

Review,

Park,

*other↝, *other↝, *CRP↓, *eff↝, *other↑, *CXCR4↓, *IL1β↓, *IL6↓, *IL17↓, *IL18↓, *TNF-α↓, *MMP9↓, *PGE2↓, *COX1↓, *COX2↓, *PI3K↓, *Akt↓, *other↑, TumCCA↑, Apoptosis↑, ROS↑, JNK↑, TumAuto↑, Hif1a↓, BNIP3↝, HSP90↓, Fas↑, FasL↑, ETC↓, VEGF↓, angioG↓, RadioS↑, *neuroP↑, *HSP70/HSPA5↑, *ROS↓, *MMP↑, *Cyt‑c↓, *Casp3↓, *Casp9↓, *MAPK↓, *Dose⇅, *HSPs↑, BioAv↓, Dose↝,

3831-

CUR,

Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease

Review,

AD,

*neuroP↑, *ROS↓, *Ca+2↓, *MMP↑,

3205-

EGCG,

The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas

Review,

Var,

Review,

AD,

Beclin-1↑, ROS↑, Apoptosis↑, ER Stress↑, *Inflam↓, *cardioP↑, *antiOx↑, *LDL↓, *NF-kB↓, *MPO↓, *glucose↓, *ROS↓, ATG5↑, LC3B↑, MMP↑, lactateProd↓, VEGF↓, Zeb1↑, Wnt↑, IGF-1R↑, Fas↑, Bak↑, BAD↑, TP53↓, Myc↓, Casp8↓, LC3II↑, NOTCH3↓, eff↑, p‑Akt↓, PARP↑, *Cyt‑c↓, *BAX↓, *memory↑, *neuroP↑, *Ca+2?, GRP78/BiP↑, CHOP↑, ATF4↑, Casp3↑, Casp8↑, UPR↑,

3783-

FA,

Design, Synthesis, and Biological Evaluation of Ferulic Acid-Piperazine Derivatives Targeting Pathological Hallmarks of Alzheimer’s Disease

NA,

AD,

*ROS↓, *IronCh↑, *NLRP3↓, *Aβ↓, *AChE↓, *BChE↓, *antiOx↑, *BBB↑, *MMP↑, *memory↑, *SOD↑, *Catalase↑,

3780-

FA,

Ferulic Acid: A Natural Antioxidant with Application Towards Neuroprotection Against Alzheimer’s Disease

Review,

AD,

*antiOx↑, *SOD↑, *Catalase↑, *HO-1↑, *neuroP↑, *AChE↓, *MMP↑,

3721-

Gb,

Ginkgo biloba Extract in Alzheimer’s Disease: From Action Mechanisms to Medical Practice

Review,

AD,

*antiOx↑, *ROS↓, *SOD↑, *Catalase↑, *GSR↑, *MMP↑, *Inflam↓, *Aβ↓, *memory↑, *Dose↝, *BBB↑, *neuroP↑,

4238-

HNK,

Neuropharmacological potential of honokiol and its derivatives from Chinese herb Magnolia species: understandings from therapeutic viewpoint

Review,

AD,

NA,

Park,

*BDNF↑, *hepatoP↑, *ALAT↓, *AST↓, *TNF-α↓, *SIRT3↑, *Aβ↓, *Apoptosis↓, *ROS↓, *MMP↑, *Ca+2↓, *Casp3↓, *Ach↑, *PPARγ↑, *PGC-1α↑, *motorD↑, *TNF-α↓, *IL1β↓,

2869-

HNK,

Nature's neuroprotector: Honokiol and its promise for Alzheimer's and Parkinson's

Review,

AD,

Review,

Park,

*neuroP↑, *Inflam↓, *motorD↑, *Aβ↓, *p‑tau↓, *cognitive↑, *memory↑, *ERK↑, *p‑Akt↑, *PPARγ↑, *PGC-1α↑, *MMP↑, *mt-ROS↓, *SIRT3↑, *IL1β↓, *TNF-α↓, *GRP78/BiP↓, *CHOP↓, *NF-kB↓, *GSK‐3β↓, *β-catenin/ZEB1↑, *Ca+2↓, *AChE↓, *SOD↑, *Catalase↑, *GPx↑,

2887-

HNK,

Honokiol Restores Microglial Phagocytosis by Reversing Metabolic Reprogramming

in-vitro,

AD,

BV2

*Glycolysis↑, *ATP↑, *ROS↓, *MMP↑, *OXPHOS↑, *PPARα↑, *PGC-1α↑,

2904-

LT,

Luteolin from Purple Perilla mitigates ROS insult particularly in primary neurons

in-vitro,

Park,

SK-N-SH

in-vitro,

AD,

*ROS↓, *neuroP↑, *MMP↑, *Catalase↑, *GSH↑, selectivity↑, *eff↑, *Cyt‑c↓,

2916-

LT,

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

Review,

Var,

Review,

AD,

Review,

Park,

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

4147-

MF,

PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration

in-vitro,

AD,

PC12

PC12 cells exposed to hydrogen peroxide (H2O2)

*ROS↓, *Catalase↑, *MMP↑, *Casp3↓, *p‑ERK↓, *cAMP↑, *p‑CREB↑, *BDNF↑, *neuroP↑,

3336-

QC,

Neuroprotective Effects of Quercetin in Alzheimer’s Disease

Review,

AD,

*neuroP↑, *lipid-P↓, *antiOx↑, *Aβ↓, *Inflam↓, *BBB↝, *NF-kB↓, *iNOS↓, *memory↑, *cognitive↑, *AChE↓, *MMP↑, *ROS↓, *ATP↑, *AMPK↑, *NADPH↓, *p‑tau↓,

3099-

RES,

Resveratrol and cognitive decline: a clinician perspective

Review,

Nor,

NA,

AD,

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

3003-

RosA,

Comprehensive Insights into Biological Roles of Rosmarinic Acid: Implications in Diabetes, Cancer and Neurodegenerative Diseases

Review,

Var,

Review,

AD,

Review,

Park,

*Inflam↓, *antiOx↑, *neuroP↑, *IL6↓, *IL1β↓, *NF-kB↓, *PGE2↓, *COX2↓, *MMP↑, *memory↑, *ROS↓, *Aβ↓, *HMGB1↓, TumCG↓, MARK4↓, Zeb1↓, MDM2↓, BNIP3↑, ASC↑, NLRP3↓, PI3K↓, Akt↓, Casp1↓, E-cadherin↑, STAT3↓, TLR4↓, MMP↓, ICAM-1↓, AMPK↓, IL6↑, MMP2↓, Warburg↓, Bcl-xL↓, Bcl-2↓, TumCCA↑, EMT↓, TumMeta↓, mTOR↓, HSP27↓, Casp3↑, GlucoseCon↓, lactateProd↓, VEGF↓, p‑p65↓, GIT1↓, FOXM1↓, cycD1/CCND1↓, CDK4↓, MMP9↓, HDAC2↓,

3028-

RosA,

Network pharmacology mechanism of Rosmarinus officinalis L.(Rosemary) to improve cell viability and reduces apoptosis in treating Alzheimer’s disease

in-vitro,

AD,

HT22

in-vivo,

NA,

*Aβ↓, *Apoptosis↓, *antiOx↑, *neuroP↑, *eff↑, *IGF-1↑, *MMP9↑, *Src↓, *MAPK↓, *MMP↑,

3319-

SIL,

Silymarin and neurodegenerative diseases: Therapeutic potential and basic molecular mechanisms

Review,

AD,

Review,

Park,

Review,

Stroke,

*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *BBB?, *tau↓, *NF-kB↓, *IL1β↓, *TNF-α↓, *IL4↓, *MAPK↓, *memory↑, *cognitive↑, *Aβ↓, *ROS↓, *lipid-P↓, *GSH↑, *MDA↓, *SOD↑, *Catalase↑, *AChE↓, *BChE↓, *p‑ERK↓, *p‑JNK↓, *p‑p38↓, *GutMicro↑, *COX2↓, *iNOS↓, *TLR4↓, *neuroP↑, *Strength↑, *AMPK↑, *MMP↑, *necrosis↓, *NRF2↑, *HO-1↑,

3950-

Taur,

Taurine Supplementation as a Neuroprotective Strategy upon Brain Dysfunction in Metabolic Syndrome and Diabetes

Review,

Diabetic,

Review,

Stroke,

Review,

AD,

*Ca+2↝, *neuroP↑, *other↝, *pH↝, *ROS∅, eff↑, *MMP↑, *Apoptosis↓, *other↝, *ER Stress↓, *Bcl-xL↓, *BAX↑, *Cyt‑c↑, *cal2↓, *Casp3↓, *UPR↓, *other↝, *NF-kB↓, *NRF2↑, *GLUT1↑, *GLUT3↑, *memory↑,

3956-

Taur,

Mechanisms underlying taurine protection against glutamate-induced neurotoxicity

Review,

AD,

*MMP↑, *Ca+2↓, *cal2↓, *Bcl-2↑,

3954-

Taur,

Mode of action of taurine as a neuroprotector

in-vitro,

AD,

*MMP↑, *Ca+2↓,

2092-

TQ,

Dissecting the Potential Roles of Nigella sativa and Its Constituent Thymoquinone on the Prevention and on the Progression of Alzheimer's Disease

Review,

AD,

*iNOS↓, *ROS↓, *GSH↑, *neuroP↑, *MMPs↓, *MMP↑, *TXNIP↓, *Prx↑, *memory↑, *MDA↓, *SOD↑, *Catalase↑, *BioAv↑,

3404-

TQ,

The Neuroprotective Effects of Thymoquinone: A Review

Review,

Var,

Review,

AD,

Review,

Park,

Review,

Stroke,

*Inflam↓, AntiCan↑, *TNF-α↓, *IL6↓, *IL1β↓, *NF-kB↓, *iNOS↓, *NRF2↑, *neuroP↑, *MMP↑, *ROS↓, *MDA↓, *GSH↑, *Catalase↑, *SOD↑, *IL12↓, *MCP1↓, *IP-10/CXCL-10↓, *PGE2↓,

3432-

TQ,

Thymoquinone: Review of Its Potential in the Treatment of Neurological Diseases

Review,

AD,

Review,

Park,

*memory↑, *cognitive↑, *ROS↓, *Inflam↓, *antiOx↑, *TLR1↓, *AChE↓, *MMP↑, *neuroP↑, *lipid-P↓, *SOD↑, *GSH↑, *Ach↑,

3559-

TQ,

Molecular signaling pathway targeted therapeutic potential of thymoquinone in Alzheimer’s disease

Review,

AD,

Review,

Var,

*antiOx↑, *Inflam↓, *AChE↓, AntiCan↑, *cardioP↑, *RenoP↑, *neuroP↑, *hepatoP↑, TumCG↓, Apoptosis↑, PI3K↓, Akt↑, TumCCA↑, angioG↓, *NF-kB↓, *TLR2↓, *TLR4↓, *MyD88↓, *TRIF↓, *IRF3↓, *IL1β↓, *IL6↓, *IL12↓, *NRF2↑, *COX2↓, *VEGF↓, *MMP9↓, *cMyc↓, *cycD1/CCND1↓, *TumCP↓, *TumCI↓, *MDA↓, *TGF-β↓, *CRP↓, *Casp3↓, *GSH↑, *IL10↑, *iNOS↑, *lipid-P↓, *SOD↑, *H2O2↓, *ROS↓, *LDH↓, *Catalase↑, *GPx↑, *AChE↓, *cognitive↑, *MAPK↑, *JNK↑, *BAX↓, *memory↑, *Aβ↓, *MMP↑,

3564-

TQ,

The Potential Neuroprotective Effect of Thymoquinone on Scopolamine-Induced In Vivo Alzheimer's Disease-like Condition: Mechanistic Insights

in-vivo,

AD,

Thirty mice

*Inflam↓, *AntiCan↑, *antiOx↑, *neuroP↑, *cognitive↑, *Aβ↓, *PPARγ↑, *NF-kB↓, *p‑tau↓, *MMP↑, *memory↑, *NF-kB↓, *ROS↓,

4869-

Uro,

Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges

Review,

AD,

Review,

Park,

Review,

Stroke,

*MitoP↑, *Inflam↓, *antiOx↑, *Risk↓, *Aβ↓, *p‑tau↓, *p62↓, *PARK2↑, *MMP↑, *ROS↓, *Strength↑, *CRP↓, *IL1β↓, *IL6↓, *TNF-α↓, *AMPK↑, *NF-kB↓, *MAPK↓, *p62↑, *NRF2↑, *SOD↑, *Catalase↑, *HO-1↑, *Ferroptosis↓, *lipid-P↓, *Cartilage↑, *PI3K↓, *Akt↓, *mTOR↓, *Apoptosis↓, *neuroP↑, *Bcl-2↓, *BAX↑, *Casp3↑, *ATP↑, *eff↑, *motorD↑, *NLRP3↓, *radioP↑, *BBB↑,

4334-

VitB5,

Pantethine treatment is effective in recovering the disease phenotype induced by ketogenic diet in a pantothenate kinase-associated neurodegeneration mouse model

in-vivo,

AD,

concentration was established based on a dosage of 900 mg/day in an adult individua

mouse

*neuroP↑, *motorD↑, *MMP↑, *OCR↑,

2277-

VitK2,

Vitamin K2 suppresses rotenone-induced microglial activation in vitro

in-vitro,

Nor,

BV2

MK-4 (0.5–20 μmol/L

NA,

AD,

NA,

Park,

*p38↓, *ROS↓, *Casp1↓, *MMP↑, *NF-kB↓, *IL1β↓, *iNOS↓, *COX2↓, *TNF-α↓,

Showing Research Papers: 1 to 32 of 32

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 32

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 14, Catalase↑, 12, Ferroptosis↓, 1, GPx↑, 3, GSH↑, 10, GSR↑, 2, GSTs↑, 1, H2O2↓, 1, HO-1↑, 4, lipid-P↓, 7, MDA↓, 4, MPO↓, 2, NRF2↑, 6, OXPHOS↑, 1, PARK2↑, 1, Prx↑, 1, ROS?, 1, ROS↓, 26, ROS∅, 1, mt-ROS↓, 1, SIRT3↑, 2, SOD↑, 12, TOS↓, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Mitochondria & Bioenergetics ⓘ

ATP↑, 4, MMP↑, 31, OCR↑, 1, PGC-1α↑, 3,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, AMPK↑, 4, cAMP↑, 1, cMyc↓, 1, p‑CREB↑, 1, glucose↓, 1, GlucoseCon↑, 1, GlutMet↑, 1, Glycolysis↑, 1, LDH↓, 1, LDL↓, 1, NADPH↓, 1, PPARα↑, 1, PPARγ↑, 3, SIRT1↑, 1,

Cell Death ⓘ

Akt↓, 2, p‑Akt↑, 1, Apoptosis↓, 6, BAX↓, 2, BAX↑, 2, Bcl-2↓, 1, Bcl-2↑, 1, Bcl-xL↓, 1, Casp1↓, 1, Casp3↓, 6, Casp3↑, 1, Casp9↓, 1, Cyt‑c↓, 3, Cyt‑c↑, 1, Ferroptosis↓, 1, iNOS↓, 5, iNOS↑, 1, JNK↑, 1, p‑JNK↓, 1, MAPK↓, 4, MAPK↑, 1, necrosis↓, 1, p38↓, 1, p‑p38↓, 1,

Transcription & Epigenetics ⓘ

Ach↑, 3, other↑, 3, other↝, 5,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1, HSP70/HSPA5↑, 1, HSPs↑, 1, UPR↓, 1,

Autophagy & Lysosomes ⓘ

MitoP↑, 1, p62↓, 1, p62↑, 1,

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1, p‑ERK↓, 2, GSK‐3β↓, 1, GSK‐3β↑, 1, IGF-1↑, 1, mTOR↓, 1, PI3K↓, 2, Src↓, 1, STAT3↓, 1,

Migration ⓘ

Ca+2?, 1, Ca+2↓, 6, Ca+2↝, 1, cal2↓, 2, Cartilage↑, 1, MMP2↓, 1, MMP3↓, 1, MMP9↓, 4, MMP9↑, 1, MMPs↓, 1, TGF-β↓, 1, TumCI↓, 1, TumCP↓, 1, TXNIP↓, 1, β-catenin/ZEB1↑, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 2, VEGF↓, 1,

Barriers & Transport ⓘ

BBB?, 1, BBB↑, 5, BBB↝, 1, GLUT1↑, 1, GLUT3↑, 1,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 7, CRP↓, 3, CXCR4↓, 1, HMGB1↓, 1, IL10↑, 2, IL12↓, 2, IL17↓, 1, IL18↓, 1, IL1β↓, 10, IL4↓, 1, IL6↓, 6, Inflam↓, 13, IP-10/CXCL-10↓, 1, MCP1↓, 1, MyD88↓, 1, NF-kB↓, 14, PGE2↓, 5, TLR1↓, 1, TLR2↓, 1, TLR4↓, 2, TNF-α↓, 9, TRIF↓, 1,

Cellular Microenvironment ⓘ

pH↝, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 9, BChE↓, 2, BDNF↑, 3, tau↓, 1, p‑tau↓, 4,

Protein Aggregation ⓘ

Aβ↓, 14, NLRP3↓, 2, β-Amyloid↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 2, BioAv↝, 2, Dose⇅, 1, Dose↝, 2, eff↑, 4, eff↝, 1, Half-Life↓, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, CRP↓, 3, GutMicro↑, 2, IL6↓, 6, LDH↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, AntiTum↑, 1, cardioP↑, 2, cognitive↑, 9, hepatoP↑, 3, memory↑, 14, motorD↑, 4, neuroP↑, 26, radioP↑, 1, RenoP↑, 1, Risk↓, 1, Strength↑, 2, toxicity∅, 1,

Infection & Microbiome ⓘ

IRF3↓, 1,
Total Targets: 171

Scientific Paper Hit Count for: MMP, ΔΨm, mitochondrial membrane potential

5 Thymoquinone
3 Honokiol
3 Taurine
2 Ferulic acid
2 Luteolin
2 Rosmarinic acid
1 Alpha-Lipoic-Acid
1 Astaxanthin
1 Baicalein
1 Baicalin
1 Boron
1 Celastrol
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Ginkgo biloba
1 Magnetic Fields
1 Quercetin
1 Resveratrol
1 Silymarin (Milk Thistle) silibinin
1 Urolithin
1 Vitamin B5,Pantothenic Acid
1 Vitamin K2

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#:197  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

MMP Cancer Research Results

Brain Energy Systems Matrix (AD)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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