title: Hypothesis: amyloid beta-peptides truncated at the N-terminus contribute to the pathogenesis of Alzheimer's disease.
abstract: Fragments of amyloid beta-peptide truncated at the N-terminus are present in AD brain early in the course of Alzheimer's disease. It is proposed that these species contribute to the pathogenesis of AD, possibly through destabilization of elements of the neuronal cytoskeleton by small fibrillar deposits.
authors.affiliation: National Hospital for Neurology and Neurosurgery, London, United Kingdom.
authors.forename: A J
authors.initials: AJ
authors.lastname: Larner
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology*; D000595:Amino Acid Sequence; D016229:Amyloid beta-Peptides / Q000737:chemistry* / Q000502:physiology*; D006801:Humans; D008969:Molecular Sequence Data
chemical_list: D016229:Amyloid beta-Peptides