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.