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Effects of intrahippocampal CT105, a carboxyl terminal fragment of β‐amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats
Author(s) -
Matsumoto Yuji,
Watanabe Shigenori,
Suh YooHun,
Yamamoto Tsuneyuki
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.00944.x
Subject(s) - working memory , tumor necrosis factor alpha , hippocampus , memory impairment , cytokine , amyloid precursor protein , medicine , endocrinology , chemistry , neuroscience , disease , psychology , alzheimer's disease , cognition
In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β‐amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three‐panel runway set‐up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co‐administered tumor necrosis factor‐alpha (TNF‐α) and interleukin‐1β (IL‐1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF‐α (100 ng/side) produced a synergistic deficit of working memory, whereas IL‐1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105‐induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF‐α, which may occur in the brains of patients with Alzheimer's disease.