1[1]Bird TD. Genetic factors in Alzheimer's disease. N Engl J Med,2005, 352:862-864.
2[2]Nussbaum RL, Ellis CE. Alzheimer's disease and Parkinson's disease. N Engl J Med, 2003, 348:1356-1364.
3[3]Torreilles F, Touchon J. Pathogenic theories and intrathecal analysis of the sporadic form of Alzheimer's disease. Prog Neurobiol, 2002,66:191-203.
4[4]De Strooper B. Aph-l, Pen-2, and Nicastrin with Presenilin generate an active gamma-Secretase complex. Neuron, 2003, 38:9-12.
5[5]Nyabi O, Bentahir M, Horre K, et al. Presenilins mutated at Asp-257 or Asp-385 restore Pen-2 expression and Nicastrin glycosylation but remain catalytically inactive in the absence of wild type Presenilin. J Biol Chem, 2003, 278:43430-43436.
6[6]Qyang Y, Chambers SM, Wang P, et al. Myeloproliferative disease in mice with reduced presenilin gene dosage: effect of gamma-secretase blockage. Biochemistry, 2004, 43:5352-5359.
7[7]Marjaux E, Hartmann D, De Strooper B. Presenilins in memory,Alzheimer's disease, and therapy. Neuron, 2004, 42:189-192.
9[9]Barghorn S, Zheng-Fischhofer Q, Ackmann M, et al. Structure, microtubule interactions, and paired helical filament aggregation by tau mutants of frontotemporal dementias. Biochemistry, 2000, 39:11714-11721.
10[10]Bertram L, Hiltunen M, Parkinson M, et al. Family-based association between Alzheimer's disease and variants in UBQLN1. N Engl J Med, 2005, 352:884-894.
