Black Seed OilvsMagnesium L-Threonate

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.

The L-threonate carrier forms stable complexes with magnesium and transports it across the blood-brain barrier via specific transporters more effectively than inorganic magnesium salts or other chelated forms. Once in the brain, magnesium acts as a voltage-dependent blocker of the NMDA receptor channel at the physiological magnesium binding site within the ion pore, preventing excessive calcium influx and glutamate-mediated excitotoxicity. Magnesium also serves as a cofactor for over 300 enzymes including those involved in neurotransmitter synthesis (tyrosine hydroxylase, glutamic acid decarboxylase), ATP production (creatine kinase, pyruvate kinase), and DNA/RNA polymerase. Elevated brain magnesium enhances synaptic density and plasticity in the hippocampus and prefrontal cortex, likely through CREB-mediated gene expression and increased density of postsynaptic AMPA receptors.