Black Seed OilvsBromantane

Thymoquinone is the primary bioactive, providing neuroprotection through multiple mechanisms: it scavenges reactive oxygen species (superoxide, hydroxyl radical, peroxynitrite) and upregulates Nrf2/ARE pathway, increasing glutathione (via GCLC, GSS), superoxide dismutase (SOD1/SOD2), and catalase. It inhibits NF-kB by preventing IkB-alpha degradation and blocking p65 nuclear translocation, reducing neuroinflammation and pro-inflammatory cytokine release. Thymoquinone inhibits acetylcholinesterase (AChE) at the peripheral anionic site, increasing synaptic acetylcholine. It modulates GABA-A receptors (positive allosteric modulation at benzodiazepine site), providing anxiolytic effects. Thymoquinone protects neurons from amyloid-beta toxicity by reducing oxidative stress and inhibiting beta-secretase (BACE1). It reduces tau hyperphosphorylation by inhibiting GSK-3beta and CDK5.

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.