Selective neurotoxicity of COOH-terminal fragments of the β-amyloid precursor protein
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APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)
2012, Neuroscience and Biobehavioral ReviewsCitation Excerpt :In addition, two separate mouse lines expressing APP751WT regulated by the rat neuron-specific Nse promoter are available (Mucke et al., 1994; Quon et al., 1991), together with APP WT regulated by the PDGFβ promoter (line I5) (Mucke et al., 2000). In view of the neurotoxic properties of C-terminal fragments in cell cultures (Fukuchi et al., 1993; Kim and Suh, 1996) and their accumulation in Alzheimer brain (McPhie et al., 1997), liable to influence disease onset and progression (Turner et al., 2003), it is of interest to examine their neurobehavioural impact. APP/C104 mice with the human 104-amino acid C-terminal fragment transgene driven by the human NEFL promoter have Aβ plaques surrounded by reactive microglia and astrocytes as well as reduced neuronal counts in the CA1 hippocampal subregion (Nalbantoglu et al., 1997).
Neuronal neprilysin overexpression is associated with attenuation of Aβ-related spatial memory deficit
2006, Neurobiology of DiseaseTransgenic mice expressing the human C99 terminal fragment of βAPP: Effects on cytochrome oxidase activity in skeletal muscle and brain
2004, Journal of Chemical NeuroanatomyAlzheimer's disease: A dysfunction of the amyloid precursor protein
2000, Brain ResearchCitation Excerpt :Interestingly, we had proposed previously that C100 is involved in the etiology of Alzheimer disease [73]. It is neurotoxic in vitro [116,24,97,101,57] and is amyloidogenic [17–19,64,111,27,105]. In addition, expression of C100 in vivo can cause neuropathology that is similar in some ways to that in AD, including neurodegeneration and cognitive dysfunction [3,25,48,71,72,80,91,104], as well as increases in acetylcholinesterase [92] and abnormalities in synaptic transmission [28].