The APP/PS1ki mouse model for Alzheimer's disease (AD) exhibits robust brain and spinal cord axonal degeneration and hippocampal CA1 neuron loss starting at 6 months of age. It expresses human mutant APP751 with the Swedish and London mutations together with two FAD-linked knocked-in mutations (PS1 M233T and PS1 L235P) in the murine PS1 gene. The present report covers a phenotypical analysis of this model using either behavioral tests for working memory and motor performance, as well as an analysis of weight development and body shape. At the age of 6 months, a dramatic, age-dependent change in all of these properties and characteristics was observed, accompanied by a significantly reduced ability to perform working memory and motor tasks. The APP/PS1ki mice were smaller and showed development of a thoracolumbar kyphosis, together with an incremental loss of body weight. While 2-month-old APP/PS1ki mice were inconspicuous in all of these tasks and properties, there is a massive age-related impairment in all tested behavioral paradigms. We have previously reported robust axonal degeneration in brain and spinal cord, as well as abundant hippocampal CA1 neuron loss starting at 6 months of age in the APP/PS1ki mouse model, which coincides with the onset of motor and memory deficits described in the present report.
The APP / PS1ki mouse model for Alzheimer 's disease ( AD ) exhibits robust brain and spinal cord axonal degeneration and hippocampal CA1 neuron loss starting at 6 months of age . It expresses human mutant APP751 with the Swedish and London mutations together with two FAD - linked knocked - in mutations ( PS1 M233 T and PS1 L235P ) in the murine PS1 gene . The present report covers a phenotypical analysis of this model using either behavioral tests for working memory and motor performance , as well as an analysis of weight development and body shape . At the age of 6 months , a dramatic , age - dependent change in all of these properties and characteristics was observed , accompanied by a significantly reduced ability to perform working memory and motor tasks . The APP / PS1ki mice were smaller and showed development of a thoracolumbar kyphosis , together with an incremental loss of body weight . While 2-month - old APP / PS1ki mice were inconspicuous in all of these tasks and properties , there is a massive age - related impairment in all tested behavioral paradigms . We have previously reported robust axonal degeneration in brain and spinal cord , as well as abundant hippocampal CA1 neuron loss starting at 6 months of age in the APP / PS1ki mouse model , which coincides with the onset of motor and memory deficits described in the present report .
Which disease the London mutation involved in?
Which disease the London mutation involved in ?
Alzheimer's Disease AD
Alzheimer's Disease AD