| Rank |
Pathway / Axis |
Neural / Glial Systems |
TSF |
Primary Effect |
Notes / Interpretation |
| 1 |
Cholinergic axis (AChE) |
↓ (model-dependent) |
R→G |
Memory/cognition support |
Frequently presented as a nootropic mechanism; evidence base varies by extract and assay type. :contentReference[oaicite:22]{index=22} |
| 2 |
ROS / antioxidant defense |
↓ (often primary) |
P→R→G |
Oxidative stress reduction |
Reports include decreased lipid peroxidation markers and increased antioxidant defense metrics in cognitive impairment paradigms. :contentReference[oaicite:23]{index=23} |
| 3 |
Neuroinflammation (broad cytokine/glial tone) |
↓ (model-dependent) |
R→G |
Neuroprotection / slower degeneration pressure |
Often included in dementia-herb reviews as part of multi-target neuroprotection; direct causal evidence depends on study design. :contentReference[oaicite:24]{index=24} |
| 4 |
Proteinopathy stress (tau-associated toxicity) |
↓ (protective; model-dependent) |
R→G |
Protection from tau-driven neuronal injury |
Aqueous extract reported to mitigate hMAPτ-induced neurotoxicity (cell-based). :contentReference[oaicite:25]{index=25} |
| 5 |
Ca²⁺ signaling (excitotoxicity / ER-mito coupling) |
↔/↓ (secondary; context-dependent) |
R |
Stress-amplification modulation |
Mechanistically relevant when excitotoxic/mitochondrial stress endpoints are present; often not directly quantified in Shankhpushpi experiments. |
| 6 |
NRF2 antioxidant response |
↑ (adaptive/protective; context-dependent) |
R→G |
Transcriptional antioxidant program |
Frequently inferred from antioxidant enzyme changes and redox outcomes rather than directly measured NRF2 pathway activation in many studies. :contentReference[oaicite:26]{index=26} |
| 7 |
Clinical Translation Constraint |
↔ |
— |
Standardization + PK/BBB uncertainty |
Multiple botanicals sold as “Shankhpushpi,” variable extraction/chemistry, and limited human PK/CNS delivery data constrain translation to AD claims. :contentReference[oaicite:27]{index=27} |