| Rank | Pathway / Axis | Cells | TSF | Primary Effect | Notes / Interpretation |
| 1 |
AChE ↓ → ACh ↑ (cholinergic synapse) |
ACh ↑ (via AChE inhibition) |
P/R |
Improved synaptic cholinergic transmission |
Extract inhibits acetylcholinesterase → reduced ACh breakdown → increased synaptic ACh. Symptomatic mechanism analogous to donepezil-class drugs. |
| 2 | Neuroinflammation (NF-κB / cytokines) |
↓ | R/G |
Reduced inflammatory stress |
Extracts show anti-inflammatory signaling in cell/biochemical models; relevance to AD progression is supportive. |
| 3 | ROS / lipid peroxidation |
↓ | P/R |
Oxidative burden reduction |
Phenolics/diterpenes contribute to antioxidant effects; typically requires sustained intake for tissue adaptation. |
| 4 | NRF2 antioxidant-response program |
↔ / ↑ (context-dependent) | R/G |
Stress-defense regulation |
Consider as a supportive axis; not always directly measured in human cognition trials. |
| 5 | Ca²⁺ excitotoxicity interplay |
↔ | P/R |
Not primary |
More relevant to essential-oil neurotoxicity discussions than leaf-extract cognition trials; include only with explicit Ca²⁺ endpoints. |
| 6 | Aβ / tau-associated pathology |
↔ (limited human evidence) | G |
Not established clinically |
Any anti-amyloid/tau claims are largely preclinical; avoid over-weighting without biomarker-confirmed replication. |
| 7 | Clinical Translation Constraint |
↓ (constraint) | — |
Safety + product variability |
Essential oil/thujone can be pro-convulsant; regulators specify limits for thujone exposure in herbal products. Extract standardization and duration (weeks–months) matter. |