| Rank |
Pathway / Axis |
Cancer / Tumor Context |
Normal Tissue Context |
TSF |
Primary Effect |
Notes / Interpretation |
| 1 |
Antioxidant systems (Nrf2/ARE; SOD, GSH) |
Stress adaptation modulation (context-dependent) |
Nrf2 ↑; antioxidant enzymes ↑; oxidative injury ↓ |
R, G |
Redox buffering |
Flavonol glycosides commonly activate antioxidant defenses; direction in tumors is model-dependent. |
| 2 |
NF-κB inflammatory transcription |
NF-κB ↓; cytokines/COX-2 ↓ (reported) |
Inflammation tone ↓ |
R, G |
Anti-inflammatory signaling |
Preclinical studies report NF-κB modulation; strength varies by constituent and dose. |
| 3 |
PAF receptor antagonism (ginkgolides) |
Pro-tumor inflammatory signaling ↓ (context) |
Platelet activation ↓; microcirculation effects |
P, R |
Lipid mediator antagonism |
Ginkgolides are PAF antagonists; clinically relevant for antiplatelet/vascular effects. |
| 4 |
PI3K → AKT (± mTOR) survival axis |
PI3K/AKT modulation (reported; model-dependent) |
↔ |
R, G |
Growth/survival modulation |
Observed in some tumor models; best described as reported/context-dependent. |
| 5 |
MAPK re-wiring (ERK / JNK / p38) |
MAPK modulation (context-dependent) |
↔ |
P, R, G |
Stress/mitogenic signaling adjustment |
Directions vary by extract composition and cell type. |
| 6 |
Cell-cycle control (Cyclins/CDKs) |
Cell-cycle arrest ↑ (reported) |
↔ |
G |
Cytostasis |
Reported in vitro; typically downstream of signaling changes. |
| 7 |
Intrinsic apoptosis (mitochondrial/caspase linked) |
Apoptosis ↑ (reported) |
↔ |
G |
Cell death execution |
Seen in selected cancer cell lines; not a universal cytotoxin signature. |
| 8 |
Angiogenesis signaling (VEGF & related) |
Angiogenic outputs ↓ (reported) |
↔ |
G |
Anti-angiogenic phenotype |
Phenotype-level outcomes in some models; strength varies. |
| 9 |
Drug metabolism / transport (CYPs, P-gp) |
Potential interaction with chemo agents (context) |
CYP/P-gp modulation (product- and dose-dependent) |
R, G |
Interaction constraint |
Reports of CYP (e.g., CYP2C19/3A4) and P-gp modulation are mixed; interaction risk depends on extract and dose. |
| 10 |
Safety constraint (antiplatelet / bleeding risk) |
— |
Platelet aggregation ↓; bleeding risk ↑ (context) |
— |
Clinical risk management |
PAF antagonism and antiplatelet effects warrant caution with anticoagulants/antiplatelets and perioperatively. |
| Rank |
Pathway / Axis |
AD / Neural Context |
TSF |
Primary Effect |
Notes / Interpretation |
| 1 |
Oxidative stress reduction (Nrf2/ARE; SOD, GSH) |
Oxidative injury ↓; lipid peroxidation ↓ |
R, G |
Neuroprotection via redox buffering |
Flavonol glycosides enhance endogenous antioxidant defenses and reduce oxidative stress, a core driver in AD pathology. |
| 2 |
Mitochondrial protection |
ATP production stabilization; mitochondrial membrane integrity ↑ |
P, R |
Energy support |
EGb 761 has been reported to protect mitochondrial function and reduce ROS generation in neuronal models. |
| 3 |
Neuroinflammation (NF-κB; microglial activation) |
Microglial activation ↓; pro-inflammatory cytokines ↓ |
R, G |
Anti-inflammatory neuroprotection |
Reduction of neuroinflammatory signaling may contribute to slowed neurodegenerative processes. |
| 4 |
Platelet-activating factor (PAF) antagonism |
Improved cerebral microcirculation; reduced inflammatory mediator activity |
P |
Vascular support |
Ginkgolides act as PAF antagonists; improved cerebral blood flow may support cognition in vascular/mixed dementia. |
| 5 |
β-amyloid aggregation modulation |
Aβ aggregation ↓ (reported in vitro) |
G |
Protein aggregation modulation |
Preclinical studies suggest interference with Aβ toxicity and aggregation; clinical relevance remains uncertain. |
| 6 |
Synaptic plasticity / neurotransmission |
Cholinergic tone modulation (reported); synaptic resilience ↑ |
G |
Cognitive support |
Some evidence suggests improved synaptic function and neurotransmission in aging models. |
| 7 |
Apoptosis suppression (neuronal survival) |
Pro-apoptotic signaling ↓ (reported) |
G |
Neuronal preservation |
Reduction of caspase activation and mitochondrial apoptotic signaling has been reported in neuronal injury models. |
| 8 |
Clinical cognitive outcomes |
Modest cognitive benefit in mild-to-moderate dementia (mixed results) |
— |
Symptom-level effect |
Some randomized trials suggest small improvements in cognition or activities of daily living; others show limited effect. Benefit appears modest. |
| 9 |
Safety constraint (antiplatelet effect) |
Bleeding risk ↑ in susceptible patients |
— |
Clinical risk management |
PAF antagonism and platelet aggregation inhibition require caution with anticoagulants and perioperative settings. |