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The role of calsyntenin‐3 in dystrophic neurite formation in A lzheimer's disease brain
Author(s) -
Uchida Yoko,
Gomi Fujiya
Publication year - 2016
Publication title -
geriatrics and gerontology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 57
eISSN - 1447-0594
pISSN - 1444-1586
DOI - 10.1111/ggi.12737
Subject(s) - neurite , senile plaques , pathogenesis , neuroscience , medicine , pathological , disease , alzheimer's disease , mechanism (biology) , amyloid (mycology) , degenerative disease , pathology , psychology , biology , biochemistry , philosophy , epistemology , in vitro
β‐Amyloid ( A β) oligomers may play an important role in the early pathogenesis of Alzheimer's disease: cognitive impairment caused by synaptic dysfunction. Dystrophic neurites surrounding A β plaques, another pathological feature of A lzheimer'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 A ß oligomers, and discuss the neurotoxic role of A β‐induced calsyntenin‐3 in mediating dystrophic neurite formation. Geriatr Gerontol Int 2016; 16 (Suppl. 1): 43–50.