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P1–082: Using a Drosophila model of Alzheimer's disease to direct the search for genetic modifiers of Aβ 1–42 neurotoxicity
Author(s) -
Page Richard,
Crowther Damian C.,
Chandraratna Dhia,
Ryder Ed,
Bautista-Llacer Rosa,
Lomas David A.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.457
Subject(s) - drosophila melanogaster , neurodegeneration , biology , phenotype , gene , gene knockdown , genetics , neurotoxicity , microbiology and biotechnology , disease , chemistry , medicine , pathology , toxicity , organic chemistry
mance significantly differed from that of nontransgenic control already at 15 min delay. The Morris water maze test was performed at 18 months of age. Both transgenic and wild-type mice showed similarly long escape latencies in the hidden and visible platform test. Conclusions: Our data indicate that spontaneous alternation impairment may be independent from plaque generation, however it can be in connection with the presence of soluble amyloid or can reflect a transgene-associated effect. The disruption in the place recognition developed in old transgenic mice can be a sensitive marker of cognitive decline in this mouse model of Alzheimer s disease.