Abstract:
:In the neuritic plaques of Alzheimer's disease, abnormal neuritic processes cluster around a core of beta-amyloid protein. Previous data have shown that beta 1-28, a peptide homologous to the first 28 amino acid residues of beta-amyloid protein, enhanced survival without affecting neuritic extension or branching in cultures of hippocampal neurons. In this paper we show that beta 1-42, a synthetic peptide which corresponds to the full 42 amino acid sequence of beta-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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Whitson JS,Glabe CG,Shintani E,Abcar A,Cotman CWdoi
10.1016/0304-3940(90)90867-9subject
Has Abstractpub_date
1990-03-14 00:00:00pages
319-24issue
3eissn
0304-3940issn
1872-7972pii
0304-3940(90)90867-9journal_volume
110pub_type
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