BromantanevsPanax Ginseng

Bromantane upregulates tyrosine hydroxylase (TH)—the rate-limiting enzyme in catecholamine synthesis—and aromatic L-amino acid decarboxylase (AADC), the enzymes responsible for converting L-tyrosine to L-DOPA and then to dopamine. This increases neuronal dopamine production capacity rather than depleting vesicular stores like traditional stimulants. The mechanism may involve modulation of transcription factors or enzyme phosphorylation. Bromantane also has anxiolytic properties through enhancement of GABAergic transmission, possibly via GABA-A receptor modulation or increased GABA synthesis. The combination of upregulated dopamine synthesis in mesolimbic and nigrostriatal pathways with GABAergic dampening of anxiety circuits produces sustained motivation, focus, and reduced mental fatigue without the jitteriness or crash typical of dopamine-releasing agents.

Ginsenosides (Rb1, Rg1, Rg3, Re, and others) have diverse pharmacological actions. They modulate the hypothalamic-pituitary-adrenal (HPA) axis, reducing cortisol release under stress through glucocorticoid receptor modulation. Ginsenosides inhibit acetylcholinesterase (AChE), increasing acetylcholine levels in the hippocampus and enhancing muscarinic and nicotinic receptor function. They enhance nitric oxide production via endothelial nitric oxide synthase (eNOS) for cerebral vasodilation. Rb1 and Rg1 promote BDNF and NGF expression through activation of CREB and TrkB/TrkA signaling, supporting neuroplasticity. Rg1 specifically enhances hippocampal neurogenesis via the PI3K/Akt pathway and Wnt/β-catenin signaling, and improves spatial learning in animal models. Ginsenosides may also modulate GABA-A receptors and have antioxidant properties.