Cell and Tissue Research 2026 Review: Brain Peptides in Alzheimer's Disease, Pathogenic Amyloid-Beta Oligomers and Tau-Derived Fragments Versus Neuroprotective NPY, VIP, PACAP; Aggregation Inhibitors and Receptor-Selective Neuropeptide Analogues Define the 2026 Therapeutic Frontier
A 2026 review published in Cell and Tissue Research (Springer Nature) synthesized the current understanding of brain peptides in Alzheimer's disease pathophysiology and therapeutic development. The review's central organizing distinction is between pathogenic peptide species (amyloid-β oligomers, tau-derived fragments) that drive neuronal dysfunction and endogenous neuropeptides that exert neuroprotective effects: neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase-activating peptide (PACAP) are the three best-characterized protective classes. Adjacent April 2026 IJMS review covers the same neuropeptide neuroprotection thesis with broader Parkinson's-disease applicability. Advances in peptide chemistry are enabling two distinct therapeutic strategies: aggregation inhibitors that prevent amyloid-β oligomerization, and receptor-selective neuropeptide analogues that recapitulate endogenous NPY/VIP/PACAP signaling with improved blood-brain-barrier penetration. The peptide-neurodegeneration thread runs parallel to the BioArctic-Lilly $800 million BrainTransporter pact (June 23, peptide-delivery focus), Insilico-SK Biopharm $2.5B AI-neuroimmune deal (June 22 BIO 2026 opening), and the NVG-291 PTPσ inhibitor that NervGen is preparing for Phase 3 in chronic SCI mid-2026.