| Rank |
Pathway / Axis |
AD Direction |
Mechanism Snapshot |
TSF |
Evidence |
Notes / Clinical Relevance |
| 1 |
AChE Inhibition |
ACh ↑ |
Potent reversible acetylcholinesterase inhibitor → increases synaptic acetylcholine |
P, R |
Human trials (moderate) |
Primary mechanism; similar functional class to donepezil. Improves memory and cognition scores in mild–moderate AD. |
| 2 |
NMDA Receptor Modulation |
Excitotoxicity ↓ |
Partial antagonistic modulation of NMDA receptor signaling |
R |
Preclinical + supportive |
Reduces glutamate-mediated excitotoxicity; complementary to cholinergic effects. |
| 3 |
Mitochondrial Protection |
Mito dysfunction ↓ |
Preserves mitochondrial membrane potential; reduces cytochrome c release |
R, G |
Preclinical |
Supports neuronal survival under oxidative stress conditions. |
| 4 |
ROS Modulation |
ROS ↓ (neuronal models) |
Reduces oxidative stress markers; improves antioxidant enzyme activity |
R, G |
Preclinical |
Neuroprotective antioxidant effect; contrasts with pro-oxidant effect in some cancer cells. |
| 5 |
Aβ Toxicity Modulation |
Aβ neurotoxicity ↓ |
Reduces Aβ-induced neuronal apoptosis |
G |
Preclinical |
Protects against Aβ-mediated mitochondrial and synaptic injury. |
| 6 |
Tau Pathology |
p-tau ↓ (model data) |
Indirect reduction of hyperphosphorylated tau via neuroprotective signaling |
G |
Limited preclinical |
Not a primary anti-tau agent but supportive. |
| 7 |
BDNF Support |
BDNF ↑ (indirect) |
Enhances synaptic plasticity signaling |
G |
Preclinical |
Supports cognitive resilience. |
| 8 |
Neuroinflammation |
IL-1β ↓, TNF-α ↓ (model data) |
Reduces pro-inflammatory cytokines in brain models |
G |
Preclinical |
Anti-inflammatory contribution secondary to cholinergic signaling. |