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Peptides for Alzheimer's Prevention Protocol Evidence Guide: Comparison Table
Cerebrolysin Neurotrophic factor mixture (BDNF, GDNF, CNTF). Promotes synaptic plasticity via TrkB receptor activation 11 human RCTs in mild-to-moderate dementia (1,804 patients total) 10–30 mL IV, 5 days/week for 4 weeks Evidence limited to symptomatic patien
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- Cerebrolysin
- Neurotrophic factor mixture (BDNF, GDNF, CNTF). Promotes synaptic plasticity via TrkB receptor activation
- 11 human RCTs in mild-to-moderate dementia (1,804 patients total)
- 10–30 mL IV, 5 days/week for 4 weeks
- Evidence limited to symptomatic patients; prevention trials do not exist
- Strongest human evidence, but mechanism may enhance existing synapses rather than prevent loss
- Dihexa
- HGF/c-Met pathway agonist. Potentiates synaptogenesis at 10-million-fold greater potency than BDNF
- Rodent models only (scopolamine-induced amnesia, aged rats)
- 0.5–2 mg/kg subcutaneous in rodents
- Zero human safety or efficacy data
- Most potent synaptogenic effect in preclinical models, but completely untested in humans
- P21
- CREB transcription factor activator. Restores long-term potentiation and hippocampal neurogenesis
- Rodent TBI and age-related memory decline models
- 1–5 mg/kg subcutaneous in rodents
- CREB activation alone does not address amyloid or tau pathology
- Selective hippocampal action reduces off-target risk, but single-pathway intervention may be insufficient
- Thymalin
- Thymic peptide. Modulates immune function and reduces microglial hyperactivation
- Observational studies in immunosenescence; limited neuroinflammation data
- 10–30 mg intramuscular 2–3×/week
- Indirect neuroprotection via immune regulation; no direct synaptic mechanism
- May reduce chronic neuroinflammation contributing to Alzheimer's but lacks targeted CNS action