Topic: Aβ1-16

Recent studies have highlighted the dual role of amyloid beta peptide (Aβ) in both Alzheimer’s disease (AD) and normal brain function. Particularly, Αβ1-40 and Αβ1-42 are key in regulating homeostatic synaptic plasticity in the dentate gyrus. This study aimed to identify specific amyloid fragments (N- and C- terminus fragments of Αβ) involved in synaptic plasticity modulation. Using entorhino-hippocampal tissue cultures, combined with whole-cell patch clamp recordings, light- and electron microscopy and molecular biology techniques, we found that the N-terminal fragment Aβ1-16 is essential for