There are two main pathological features of Alzheimer disease (AD) which are still at a loss: amyloid plaques formed by misfolded amyloid β-protein,Aβ deposition in the brain and nerve fiber tangles caused by over phosphorylation of Tau protein. In the process of continuous research on amyloid β-protein,Aβ, a lot of peptide fragments have emerged, among which Amyloid β-Protein (5-42) is one of them.
The Amyloid β-Protein (5-42), composed of 38 amino acids, shortens the first four amino acids at the N-terminal: Asp-Ala-Glu-Phe. Therefore, the mechanism of β - amyloid protein (a β) can be further understood through comparative experiments.