There is evidence that the α-synucleinopathies Parkinson’s disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Currently, there is no disease-modifying treatment for MSA. In other senses, it has been previously shown that next-generation active vaccination technology with short peptides, AFFITOPEs®, was effective in two transgenic models of synucleinopathies at reducing behavioral deficits, α-syn accumulation and inflammation. We demonstrate here for the first time a drug discovery platform for the generation of analogues of the heptapeptide H-Arg-Lys-Val-MePhe-Tyr-Thr-Trp- OH2, an novel multitargeted inhibitors of Aβ-peptide aggregation, to cross-react with α-synuclein interfering with its fibril formation through novel efficient algorithms for multipole energies and derivatives based on spherical harmonics and extensions to Aggregation simulated studies on Amyloid β-sheet helix-rich Val-Gly-Gly-Ala-Thr-Thr-Thr-Gly-Val-Thr peptide mimic modulators of α-Synuclein aggregation as a emerging template for drug discovery in α-synucleinopathy interfering amyloidogenesis particle mesh Ewald pathways.
Aggregation simulated studiesAmyloid β-sheet helix-richpeptide mimic modulators
α-Synuclein aggregationemerging templatedrug discoveryα-synucleinopathiesinterfering amyloidogenesis pathways