beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease.

@article{Masliah2001betaamyloidPE,
  title={beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease.},
  author={Eliezer Masliah and Edward M. Rockenstein and Isaac Veinbergs and Yutaka Sagara and Margaret E Mallory and Makoto Hashimoto and Lennart Mucke},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2001},
  volume={98 21},
  pages={12245-50}
}
Alzheimer's disease and Parkinson's disease are associated with the cerebral accumulation of beta-amyloid and alpha-synuclein, respectively. Some patients have clinical and pathological features of both diseases, raising the possibility of overlapping pathogenetic pathways. We generated transgenic (tg) mice with neuronal expression of human beta-amyloid peptides, alpha-synuclein, or both. The functional and morphological alterations in doubly tg mice resembled the Lewy-body variant of Alzheimer… CONTINUE READING
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