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P1–020: Genetic analysis of Alzheimer's beta–amyloid toxicity in Drosophila
Author(s) -
Konsolaki Mary,
Gangi Tina,
Cao Weihaun
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.2006.05.395
Subject(s) - neurodegeneration , amyloid (mycology) , amyloid beta , phenotype , biology , drosophila melanogaster , amyloid precursor protein , transgene , mutant , microbiology and biotechnology , genetics , gene , alzheimer's disease , biochemistry , pathology , medicine , disease , peptide , botany
system, cortex and hippocampus were observed in young APOE KO mice as compared to WT. There were minimal differences between APOE KO and APOE 3 and 4 mice. In middle aged mice, increased LCGU was detected in hippocampal and cortical regions in APOE KO mice compared to WT. The pattern of LCGU was similar between APOE KO, APOE 3 and 4 mice. Conclusions: This study indicates that apoE-deficiency causes marked alterations in energy metabolism that are not ‘rescued’ by human APOE. However, in young mice deficits in prospective learning can be restored with human APOE.