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| transgenic mouse models expressing human Alzheimer's A beta peptide exhibit brain regions severely affected in Alzheimer's disease resulting in extensive neuronal degeneration (LaFerla 1995) | |
double mutant (tau/APP) mice exhibited neurofibrillary tangle pathology substantially enhanced in the limbic system and olfactory cortex (Lewis 2001) |
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co-expression of both mutant transgenes presenilin 1 and APP results in acceleration of amyloid accumulation and associative learning deficits (Dineley 2002) |
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expression of human Abeta42 peptide in the Drosophila brain led to the formation of diffused amyloid deposits, age-dependent learning defects, and extensive neurodegeneration and Abeta40 caused only age-dependent learning defects (Iijima 2004) |
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FVB/N mice overexpressing human APP695 develop a central nervous system disorder and die prematurely, precluding development of Abeta peptide amyloid plaques whereas 129S6 mice are resistant to the lethal effects of APP overexpression (Krezowski 2004) |
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gene expression analysis revealed that the genes related to mitochondrial energy metabolism and apoptosis were up-regulated in 2-month-old Tg2576 mouse AD model and that the same genes were up-regulated at 5 and 18 months of age suggesting that mitochondrial energy metabolism is impaired by the expression of mutant APP and/or Abeta, and that the up-regulation of mitochondrial genes is a compensatory response (Reddy 2004) |
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estrogen-deficient APP23 mice exhibited greatly reduced brain estrogen, early-onset and increased beta amyloid peptide (Abeta) deposition and increased Abeta production (Yue 2005) |
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memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-beta assembly suggesting that Abeta*56 impairs memory independently of plaques or neuronal loss, and may contribute to cognitive deficits associated with Alzheimer's disease (Lesné 2006) |
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Lack of NO synthase 2 in the amyloid precursor protein Swedish mutant mouse increased insoluble beta-amyloid peptide levels, neuronal degeneration, caspase-3 activation, and tau cleavage (Colton 2006) |
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Alzheimer disease mice deficient in Ccr2 accumulated Abeta earlier and died prematurely. Ccr2 deficiency accelerates early disease progression and markedly impairs microglial accumulation (El Khoury 2007) |