The major component of senile plaques observed in the brain of Alzheimer patients is the β-Amyloid peptide (Aβ), more particularly, the β-Amyloid 1-42 peptide (Aβ 1- 42). It is well known that the Apoliprotein E (ApoE) polymorphism plays a role in the susceptibility to Alzheimer, with the ε4 allele carriers being the most susceptible and the ε2,3 allele carriers, the least. It is hypothesized that the protective effect of the ε2,3 genotypes is due to the interaction of the ApoE with the C-terminal portion of the Aβ (Aβ 29- 42), preventing its aggregation. The scientists of the University of Liège and the University of Gembloux have designed new peptides which are complementary to the C-terminal portion of the Aβ peptide.

Patent pending (PCT)

Licensing opportunities available