[4] De Leon M J, George A E, Stylopoulos L A, et al. Early marker for Alzheimer’s disease: the atrophic hippocampus [J]. Lancet, 1989, II(8664): 672-673.
[5] Jobst K A, Smith A D, Barker C S, et al. Association of atrophy of medial temporal lobe with reduced blood flow in patients with a clinical and pathological diagnosis of Alzheimer’s disease [J]. J Neurol Neurosury Psychiatry, 1992, 55: 190-196.
[7] Masters C L, Simms G, Weinman N A, et al. Amyloid plaque core protein in Alzheimer disease and Down syndrome [J]. Proc Natl Acad Sci USA, 1985, 82(12): 4245-4248.
[8] McCarron M O, Nicoll J A, Love S, et al. Surgical intervention, biopsy and APOE genotype in cerebral amyloid angiopathy 2 related haemorrhage [J]. Br J Neurosurg, 1999, 13: 462-465.
[9] Maat-Schieman M, Roos R, Van Duinen S. Hereditary cerebral hemorrhage with amyloidosis-Dutch type[J]. Neuropathology, 2005, 25(4): 288-297.
[10] Attems J. Sporadic cerebral amyloid angiopathy: pathology,clinical implications, and possible pathomechanisms [J]. Acta Neuropathol(Berl), 2005, 110(4): 345-359.
[11] Rosand J, Muzikansky A, Kumar A, et al. Spatial clustering of hemorrhages in probable cerebral amyloid angiopathy [J]. Ann Neurol, 2005, 58(3): 459-462.
[12] Izumihara A, Suzuki M, Ishihara T. Recurrence and extension of lobar hemorrhage related to cerebral amyloid ngilpathy:multivariate analysis of clinical risk factors[J]. Surg Neurol, 2005, 64(2): 160-164.
[13] Iwata N, Tsubuki S, Takaki Y, et al. Metabolic regulation of brain Aβ by neprilysin[J]. Scienc, 2001, 292: 1550-1552.
[14] Mouri A, Zou L B, Iwata N, et al. Inhibition of neprilysin by thiorphan (i.c.v) causes an accumulation of amyloid and impairment of learning and memory[J]. Behav Br Res, 2006, 168: 83-91.
[15] Iwata N, Takaki Y, Fukami S, et al. Region-specific reduction of A β degrading endopeptidase, neprilysin, in mouse hippocampus upon aging[J]. J Neurosci Res, 2002,70: 493-500.
[16] Nobuhisa I, Tsubuki S. Identification of the major Aβ 1-42-degrading catabolic pathway in brain parenchyma: Su-ppression leads to biochemical and pathological deposition [J]. Natrue Med, 2000, 6: 143-150.
[17] Nobuhisa I, Mizukami H, Sirotani K, et al. Presynaptic localization of neprilysin contributes to efficient clearance of amyloid –β peptide in mouse brain [J]. J Neurosci, 2004, 24(4): 991-998.
[21] Huang J, Guan H, Booze R M, et al. Estrogen regulates neprilysin activity in rat brain [J]. Neurosci Lett, 2004, 367(1): 85-87.
[22] Shirotani K, Tsubuki S, Iwata N, et al. Neprilysin degrades both amyloid beta peptides 1-40 and 1-42 most rapidlyand drriciently among thiorphan-and phosphoramidon-sensitive endopeptidases[J]. J Biol Chem, 2001, 276(24): 21895-21901.
[23] Marr R A, Rockenstein E, Mukherjee A, et al. Neprilysin gene transfer reduces human amyloid pathology in transgenic mice[J]. J Neurosci, 2003, 23(6): 1992-1996.
[24] Tian J, Shi J, Bailey K, et al. Relationships between arteriosclerosis, cerebral amyloid angiopathy and myelin loss from cerebral cortical white matter in Alzheimer’s disease [J]. Neuropathol Appl Neurobiol, 2004, 30(1): 46-56.
[25] Hauss-Wegrzyniak B, Wenk G L. Beta-amyloid deposition in the brains of rats chronically infused with thiorphan or lipopolysaccharide: the role of ascorbic acid in the vehicle [J]. Neurosci Lett, 2002, 322(2): 75-78.