Posted on Nov 12, 2015 | 0 comments
- Z. Faghih, M. Fereidoonnezhad, S. M. H. Tabaei, Z. Rezaei, A. R. Zolghadr*
- Chemical Physics, 459 (2015) 31–39
The molecular basis of Alzheimer’s disease (AD) is a critical aspect for understanding the role of Aβ fibrils in neurotoxicity and for designing therapeutic strategies against AD. Molecular insight into the prevention of Aβ peptide aggregates in the presence of P7C3, a derivative of dibromocarbazole, molecule is presented for the first time. P7C3 protects newborn neurons from apoptotic cell death, but mechanistic details are lacking. The ability of P7C3 to prevent the onset or to slow the progression of the Alzheimer’s disease was studied by using molecular dynamics (MD) simulations. Two different mechanisms were considered: the disruption of Aβ aggregation by direct binding of P7C3 to Aβ and alterations in amyloid precursor protein processing through the inhibition of β-secretase. The results indicate that P7C3 molecule can efficiently bind to the β-secretase active site. The direct interactions of P7C3 with Aβ peptide are also important but in a lesser extent.