BETA-AMYLOID PROTEIN PROMOTES NEURITIC BRANCHING IN HIPPOCAMPAL CULTURES

In the neuritic plaques of Alzheimer's disease, abnormal neuritic processes cluster around a core of β-amyloid protein. Previous data have shown that β1-28, a peptide homologous to the first 28 amino acid residues of β-amyloid protein, enhanced survival without affecting neuritic extension or branching in cultures of hippocampal neurons. In this paper we show that β1-42, a synthetic peptide which corresponds to the full 42 amino acid sequence of β-amyloid protein, increased cell survival and also promoted the elongation of axon-like processes, raised the number of dendrite-like processes, and increased their arborization. © 1990.