title: The role of calsyntenin-3 in dystrophic neurite formation in Alzheimer's disease brain.
abstract: β-Amyloid (Aβ) oligomers may play an important role in the early pathogenesis of Alzheimer's disease: cognitive impairment caused by synaptic dysfunction. Dystrophic neurites surrounding Aβ plaques, another pathological feature of Alzheimer's disease, are plaque-associated neuritic alterations preceding the appearance of synaptic loss. In the present review, we focus on the mechanism of dystrophic neurite formation by Aß oligomers, and discuss the neurotoxic role of Aβ-induced calsyntenin-3 in mediating dystrophic neurite formation.
authors.affiliation: Research Team for Aging Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Uchida
authors.affiliation: Research Team for Aging Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Fujiya
authors.initials: F
authors.lastname: Gomi
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000502:physiology*; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology*; D016501:Neurites / Q000378:metabolism*
chemical_list: C472553:CLSTN3 protein, human; D002135:Calcium-Binding Proteins; D008565:Membrane Proteins
keywords: Alzheimer's disease; calsyntenin-3; dystrophic neurites; neurotoxicity; β-amyloid