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Peptides for Lyme Disease Support Research: Compound Comparison
Researchers investigating peptides for Lyme disease support are exploring multiple compounds with distinct mechanisms targeting immune dysregulation, neuroinflammation, and mitochondrial dysfunction—three core pathways implicated in post-treatment Lyme disease
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- Researchers investigating peptides for Lyme disease support are exploring multiple compounds with distinct mechanisms targeting immune dysregulation, neuroinflammation, and mitochondrial dysfunction—three core pathways implicated in post-treatment Lyme disease syndrome.
- Thymosin Alpha 1
- TLR modulation, dendritic cell regulation
- Immune recalibration (Th1/Th2 balance, NK cell function)
- 1.6–3.2mg subcutaneous 2×/week
- Gold standard for immune dysregulation research—extensive clinical data in chronic infections
- Thymalin
- Thymic hormone upregulation, Treg differentiation
- Autoimmune modulation, cytokine normalization
- 10–30mg intramuscular or subcutaneous, 5–10 day cycles
- Strong candidate for autoantibody-driven PTLDS cases—bioregulatory rather than suppressive
- Cerebrolysin
- BDNF-like activity, neurotrophin signaling
- Neuroprotection, neurogenesis, microglial modulation
- 10–30mL intravenous over 10–20 sessions
- Best-evidenced for cognitive dysfunction—proven in stroke and TBI models
- Semax
- Melanocortin receptor agonism, BDNF upregulation
- Synaptic plasticity, attention/memory circuits
- 300–600mcg intranasal or subcutaneous daily
- Fastest onset for brain fog and executive function—effects within days
- BPC-157
- Angiogenesis, growth hormone receptor signaling
- Tissue repair, gut-brain axis stabilization
- 250–500mcg subcutaneous daily
- Addresses gut permeability and systemic inflammation—underappreciated in PTLDS research
- SS-31 (Elamipretide)
- Cardiolipin stabilization, ETC protection
- Mitochondrial membrane integrity, ATP production
- 5–40mg subcutaneous daily
- Most direct mitochondrial rescue mechanism—clinical validation in primary mitochondrial diseases