Regular ArticleNeuropathological Characterization of Mutant Amyloid Precursor Protein Yeast Artificial Chromosome Transgenic Mice
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2018, Neuroscience LettersCitation Excerpt :High levels of oxidative damage in AD patients have been confirmed [91]. The following neuropathological sequence of events in AD has been hypothesized: regional deposition of beta amyloid, extensive neuritic abnormalities, hyper-phosphorylated tau protein, increased inflammation and deposition of beta amyloid with apolipoprotein E and J [51]. Neuropathological markers similar to those found in AD have been reported in chromosome 3 dementias, familial British dementia and familial Danish dementia, [86].
Sex-related dimorphism in dentate gyrus atrophy and behavioral phenotypes in an inducible tTa:APPsi transgenic model of Alzheimer's disease
2016, Neurobiology of DiseaseCitation Excerpt :A number of transgenic mouse models have been created that overexpress amyloid precursor protein (APP) and successfully reproduce Aβ deposition and age-associated cognitive deficits (Ashe and Zahs, 2010; Eriksen and Janus, 2007; Savonenko and Borchelt, 2008; Webster et al., 2014). Interestingly, in APP transgenic mice with different strain backgrounds, promoters, and AD-linked mutations, female mice tend to show more severe plaque pathology than males (Callahan et al., 2001; Hirata-Fukae et al., 2008; Hutter-Paier et al., 2004; Kulnane and Lamb, 2001; LaClair et al., 2013; Lee et al., 2002; Perez et al., 2011; Wang et al., 2003). There have been relatively few studies addressing sex differences in cognitive deficits; these have pointed to the development of more severe or earlier declines in female APP transgenic mice than in males (Berger-Sweeney et al., 1995; Clinton et al., 2007; King and Arendash, 2002; King et al., 1999; Pistell et al., 2008).
Short-term treatment with tolfenamic acid improves cognitive functions in alzheimer's disease mice
2013, Neurobiology of AgingCitation Excerpt :Therefore, after the characterization of learning and memory impairment in female hemizygous R1.40 transgenic mice, 5 and 50 mg/kg/d tolfenamic acid was administered to female R1.40 mice aging between 14 and 21 months via oral gavage for 34 days and learning and memory functions were assessed in the Morris water maze (MWM) and the Y-maze. On day 35, mice were euthanized and AD-associated proteins including SP1, APP, and soluble and insoluble Aβ1–40 and Aβ1–42 were assessed in the frontal cortex, which displays extensive AD pathology in this animal model (Kulnane and Lamb, 2001; Lehman et al., 2003). The transgenic mouse model R1.40 was used for this study.
Ibuprofen attenuates oxidative damage through NOX2 inhibition in Alzheimer's disease
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2011, Progress in Molecular Biology and Translational ScienceCX3CR1 deficiency alters microglial activation and reduces beta-amyloid deposition in two Alzheimer's disease mouse models
2010, American Journal of PathologyCitation Excerpt :Thus, the apparent discrepancy in the results of the two studies may be reflective of the cellular location of the Aβ aggregates and is supported by our findings that the steady-state levels of Aβ in predepositing CX3CR1-deficient APPPS1 and R1.40 animals remained unchanged (data not shown). Furthermore, we did not observe any obvious alterations in neurodegeneration in the APPPS1;Cx3cr1−/− and R1.40;Cx3cr1−/− animals, consistent with previous studies demonstrating no overt neurodegeneration in either the APPPS1 or R1.40 animals.21,36 Notably, similar types of studies also did not detect robust neuronal loss in aged 3xTg animals,62 and it remains to be determined how the neuronal loss observed by Fuhrmann et al via two photon microscopy relates to the amyloid toxicity observed in the 3xTg, APPPS1 and R1.40 mouse models.