disease-type neuropathological changes with Alzheimer ' s disease and Alzheimer ' s Lack of association of neprilysin polymorphism
暂无分享,去创建一个
[1] P. Mcgeer,et al. Reduced neprilysin in high plaque areas of Alzheimer brain: a possible relationship to deficient degradation of β-amyloid peptide , 2001, Neuroscience Letters.
[2] T. Saido,et al. Biochemical identification of the neutral endopeptidase family member responsible for the catabolism of amyloid beta peptide in the brain. , 2000, Journal of biochemistry.
[3] T. Saido,et al. Identification of the major Aβ1–42-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition , 2000, Nature Medicine.
[4] E. Otomo,et al. Presenilin 1 intronic polymorphism is not associated with Alzheimer type neuropathological changes or sporadic Alzheimer’s disease , 1998, Journal of neurology, neurosurgery, and psychiatry.
[5] J. P. Schwartz,et al. Involvement of cytokines in normal CNS development and neurological diseases: Recent progress and perspectives , 1998, Journal of neuroscience research.
[6] T. Nagatsu,et al. Neurotrophins and cytokines in Parkinson's disease. , 1999, Advances in neurology.