Review on the APP/PS1KI mouse model:: intraneuronal Aβ accumulation triggers axonopathy, neuron loss and working memory impairment
Review on the APP/PS1KI mouse model:: intraneuronal Aβ accumulation triggers axonopathy, neuron loss and working memory impairment
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DOI：
10.1111/j.1601-183x.2007.00372.x
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发表时间：
2008-02-01
影响因子：
2.5
通讯作者：
Wirths, O.
中科院分区：
文献类型：
--
作者：
Bayer, T. A.;Wirths, O.
Accumulating evidence points to an important role of intraneuronal A beta as a trigger of the pathological cascade of events leading to neurodegeneration and eventually to Alzheimer's disease (AD) with its typical clinical symptoms, like memory impairment and change in personality. As a new concept, intraneuronal accumulation of A beta instead of extracellular A beta deposition has been introduced to be the disease-triggering event in AD. The present review compiles current knowledge on the amyloid precursor protein (APP)/PS1KI mouse model with early and massive intraneuronal A beta 42 accumulation: (1) The APP/PS1KI mouse model exhibits early robust brain and spinal cord axonal degeneration and hippocampal CA1 neuron loss. (2) At the same time-point, a dramatic, age-dependent reduced ability to perform working memory and motor tasks is observed. (3) The APP/PS1KI mice are smaller and show development of a thoracolumbar kyphosis, together with an incremental loss of body weight. (4) Onset of the observed behavioral alterations correlates well with robust axonal degeneration in brain and spinal cord and with abundant hippocampal CA1 neuron loss.
