Specific spatial learning deficits become severe with age in beta -amyloid precursor protein transgenic mice that harbor diffuse beta -amyloid deposits but do not form plaques.

@article{Koistinaho2001SpecificSL,
  title={Specific spatial learning deficits become severe with age in beta -amyloid precursor protein transgenic mice that harbor diffuse beta -amyloid deposits but do not form plaques.},
  author={Milla Koistinaho and Michael H. Ort and Jos{\'e} Manuel Cimadevilla and R. Vondrous and B. Cordell and Jari Koistinaho and Jan Bures̆ and Linda S. Higgins},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2001},
  volume={98 25},
  pages={
          14675-80
        }
}
Memory impairment progressing to dementia is the main clinical symptom of Alzheimer's disease (AD). AD is characterized histologically by the presence of beta-amyloid (Abeta) plaques and neurofibrillary tangles in specific brain regions. Although Abeta derived from the Abeta precursor protein (beta-APP) is believed to play a central etiological role in AD, it is not clear whether soluble and/or fibrillar forms are responsible for the memory deficit. We have generated and previously described… CONTINUE READING

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