Spelling suggestions: "subject:"alzheimer's's disease -- animal models""
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Development and validation of memory and attentional tasks for mouse models of Alzheimer's diseaseKim, Chi Hun January 2016 (has links)
No description available.
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Tau and App in Alzheimer's disease modelsDassie, Elisa January 2011 (has links)
No description available.
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Pathways of amyloid-β neurotoxicity in a Drosophila model of Alzheimer's diseasePage, Richard Mark Donald January 2007 (has links)
No description available.
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Investigating inflammation in a Drosophila model of Alzheimer's diseaseMichel, Claire Hélène Marie January 2010 (has links)
No description available.
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Pax6/c-Myb regulates neuronal apoptosis in a mouse model of Alzheimer's diseaseZhang, Yalun, 张亚伦 January 2011 (has links)
Alzheimer’s disease (AD) is the most frequent neurodegenerative disorder which
is characterized by impaired mental functions such as memory, language,
perception, behavior and personality, as well as cognitive skills. The molecular
mechanisms underlying this disease is still largely unknown, but numerous
evidence emerge to support a cell cycle hypothesis which implicates the
deregulation of cell cycle proteins as key mediators of neuronal dysfunction and
loss in AD brains. One of these signals in Aβ-induced neuronal death model is
Cdk/Rb/E2F pathway, where Aβ insult evokes activation of Cdk4/6, which
subsequently phosphorylates pRb protein, resulting in activation of E2F
transcription factors. However, the mechanism(s) by which Cdk/Rb/E2F mediates
neuronal death remains elusive. Therefore, the goal of this project is to
characterize the downstream events of cell cycle pathway, which include the
involvement of transcription factors c-Myb, Pax6 and Patz1 in Aβ-induced
neuronal death signaling. In this study, we showed that Pax6 is a direct target gene
for Both E2F1 and c-Myb. Both Pax6 and c-Myb are up-regulated by Aβ insults in
cultured cortical neurons. And with E2F1 silencing by siRNA, Aβ-induced Pax6
and c-Myb expression is blocked, suggesting E2F1 is responsible for their
elevation. Importantly, siRNA-mediated downregulation of either c-Myb or Pax6
protects neurons from death evoked by Aβ peptide, suggesting they are proapoptotic
proteins, delivering death signals sent from upstream E2F1. Next,
though ChIP assay, we identified two target genes for Pax6. One is Patz1, another
transcription factor that is Aβ-induced pro-apoptotic protein. The other one is
GSK3β, which is a pathogenic kinase involved in Tau protein
hyperphosphorylation and NFT formation. In conclusion, this dissertation shows
that cell cycle regulators Cdk/Rb/E2F modulate neuronal death signals by
activating downstream transcription factors c-Myb and Pax6, further upregulating
GSK3β. We provided evidence suggesting that Aβ induced neurotoxicity leads to
Tau hyperphosphorylation through a mechanism involving cell cycle activation
and subsequent activation of c-Myb/Pax6/GSK3β. In brief, in the present study,
we delineate a transcriptional cascade downstream of cell cycle pathway leads to
neuronal apoptosis as well as Tau/NFT pathology. The characterization of this
novel pathway lends support for development of new therapeutic agents and for
better experimental models for AD. Lastly, the cascade between cell cycle
activation and tauopathy in Aβ-induced neuronal death needs to be further
researched in the future. / HKU 3 Minute Thesis Award, Champion (2011) / published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy
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Iron mediated amyloid beta toxicity and oxidative stress in a Drosophila melanogaster model of Alzheimer's diseaseLiu, Beinan January 2010 (has links)
No description available.
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Mutational analysis of the aggregation and toxicity of the amyloid beta peptide in a Drosophila model of Alzheimer's DiseaseLuheshi, Leila Mohamed January 2007 (has links)
No description available.
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The effects of a human b-amyloid gene on learning and memory in transgenic mice / / Effects of a human beta-amyloid gene on learning in transgenic miceTirado Santiago, Giovanni January 1994 (has links)
Brain deposition of the $ beta$-amyloid protein is an early marker of Alzheimer's disease (AD). AD is a neurodegenerative disorder characterized by learning and memory impairments. Here, mice (B6C3, 8 and 20 months old) transgenic for a human $ beta$-amyloid fragment were compared to normal litter mates in spatial and non-spatial learning tasks in the Morris water maze, according to standard procedures. Four measures of learning and performance were analyzed statistically: latency, total distance swam, mean distance to a platform, and number of trials correct in reaching a platform. Transgenic mice were impaired relative to their litter mates in spatial learning and performed better in the non-spatial task than in the spatial task in the first three measures. An age effect for transgenics was observed in the total distance measure. The results suggest that expression of the human $ beta$-amyloid protein may produce a selective learning deficit in mice.
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The effects of a human b-amyloid gene on learning and memory in transgenic mice /Tirado Santiago, Giovanni January 1994 (has links)
No description available.
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Biconditional discrimination learning in rats with 192 IgG-saporin lesions of the nucleus basalis magnocellularisKitto, Michael Ryan 01 January 2006 (has links)
The experiment tested the hypothesis that 192 IgG-saporin lesions of the nucleus basalis magnocellularis (NBM) in rats would impair performance in a biconditional visual discrimination task, which requires configural association learning. Experiment used 22 male Long-Evan rats (Harlan Sprague-Dawley). Behavioral testing was conducted in two identical T-mazes. Rats were randomly assigned to either a bilateral 192 IgG-saporin lesion group (n = 10) or to a control group (n = 12). Results support the hypothesis that NBM is critically involved in configural but not simple association learning and suggest that NBM may be involved more generally in cognitive flexibility.
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