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Opening of non-NMDA receptors causes the majority of the excitatory postsynaptic potentials (EPSPs) in the nervous system

Bioregulator theory and mechanism Khavinson's bioregulator concept: Each organ produces specific regulatory peptides These peptides maintain tissue homeostasis With aging, peptide production declines Supplementing organ-specific peptides restores function Gene regulation is key mechanism How Cartalax works (theory): Enters cartilage cells (chondrocytes) Binds to specific DNA sequences Upregulates cartilage-protective genes Downregulates degradative genes Optimizes cartilage matrix production Gene expression changes: Upregulated (increased): Collagen Type II: Main cartilage structural protein Proteoglycans: Water-holding molecules Aggrecan: Cartilage compressive strength TGF-: Growth factors for cartilage Chondrocyte proliferation genes Downregulated (decreased): Matrix Metalloproteinases (MMPs): Cartilage-degrading enzymes Inflammatory cytokines: IL-1, TNF- Apoptosis genes: Prevents cartilage cell death Oxidative stress markers Mechanism comparison: Why bioregulation different: Works at DNA/gene level (root cause) Tissue-specific (only cartilage affected) Long-lasting effects (genes stay regulated) Cyclic dosing sufficient (vs continuous) Preventive and restorative Compare to other mechanisms and joint peptides

Allopregnanolone levels are reduced in temporal cortex in patients with Alzheimers disease compared to cognitively intact control subjects

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