Tetrapeptide Ac-HAEE-NH₂ Protects α4β2 nAChR from Inhibition by Aβ.

ABSTRACT: The cholinergic deficit in Alzheimer's disease (AD) may arise from selective loss of cholinergic neurons caused by the binding of Aβ peptide to nicotinic acetylcholine receptors (nAChRs). Thus, compounds preventing such an interaction are needed to address the cholinergic dysfunction. Recent findings suggest that the ¹¹EVHH¹⁴ site in Aβ peptide mediates its interaction with α4β2 nAChR. This site contains several charged amino acid residues, hence we hypothesized that the formation of Aβ-α4β2 nAChR complex is based on the interaction of ¹¹EVHH¹⁴ with its charge-complementary counterpart in α4β2 nAChR. Indeed, we discovered a ³⁵HAEE³⁸ site in α4β2 nAChR, which is charge-complementary to ¹¹EVHH¹⁴, and mole

SUBMITTER: Barykin EP 

PROVIDER: S-EPMC7504039 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature