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作业主旨是让学生 能够进入基本文献领域。 通过这些文献，每个学生将提出他的 发现。
学生陈述
要求学生依据下列文献阅读结果，在课堂上就某专题进行陈述。陈述主要源于基本文献阅读和课堂讨论。一些专题包括：正常衰老过程中记忆和其它认知能力的衰退；帕金森氏症和阿尔兹海默氏征等推行性疾病。
题目
学生就下列文章提出一个简短的大纲
Bard, F., C. Cannon, R. Barbour, R. L. Burke, D. Games, H. Grajeda, T. Guido, K. Hu, J. Huang, et al. "Peripherally administered antibodies against amyloid ?-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease（题目：老鼠阿尔兹海默氏征模型小鼠外周给予淀粉样肽抗体，药物进入中枢神经系统减少模型小鼠病理学特征）." Nat Med 6(8) (2000): 916-9.
Blanchard, B. J., A. E. Hiniker, C. C. Lu, Y. Margolin, A. S. Yu, and V. M. Ingram. "Elimination of Amyloid ? Neurotoxicity.（题目：淀粉样肽神经毒性的消减）" J Alzheimers Dis. 2(2) (2000): 137-149.
Blanchard, B. J., G. Konopka, M. Russell, and V. M. Ingram. "Mechanism and prevention of neurotoxicity caused by ?-amyloid peptides: relation to Alzheimer's disease（题目：关于阿尔兹海默氏征：淀粉样R肽引起神经毒性的机制与预防）." Brain Res. 776(1-2) (1997): 40-50.
Citron, M., T. Oltersdorf, C. Haass, L. McConlogue, A. Y. Hung, P. Seubert, C. Vigo-Pelfrey, I. Lieberburg, and D. J. Selkoe. "Mutation of the ?-amyloid precursor protein in familial Alzheimer's disease increases ?-protein production." Nature 360(6405) (1992): 672-4.（题目：β淀粉样前体蛋白突变体使家族性阿尔兹海默氏征患者β淀粉样蛋白增生）
Hartley, D. M., D. M. Walsh, C. P. Ye, T. Diehl, S. Vasquez, P. M. Vassilev, D. B. Teplow, and D. J. Selkoe. "Protofibrillar intermediates of amyloid ? -protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons（题目：β淀粉样蛋白前纤维原的中间体可引起电生理学的急剧改变和皮层神经元的渐进性神经毒性。）." J Neurosci 19(20) (1999): 8876-84.
Morgan, D., et al. "A ? peptide vaccination prevents memory loss in an animal model of Alzheimer's disease（题目：在阿尔兹海默氏征疾病的动物模型上淀粉样肽的疫苗可以防止记忆的丧失）." Nature 408(6815) (2000): 982-5.
Schenk, D., et al. "Immunization with amyloid-? attenuates Alzheimerdisease- like pathology in the PDAPP mouse（题目：PDAPP模型老鼠被淀粉样肽免疫后，阿尔兹海默氏征样的病理学表征有所减轻）." Nature 400(6740) (1999): 173-7.
Selkoe. "Part 3: Inhibition of ?-Secretase.（题目：第三部分：γ分泌酶的抑制）" 556-564.
Selkoe. "Part 4: Immunological Approach to Therapy.（题目：第四部分：阿尔兹海默氏征的免疫学治疗方法）" 564-571.
Selkoe. "Part 5: Other Approaches to Therapy.（题目：第五部分：治疗阿尔兹海默氏征的其它方法）" 571-576.
Sherrington, R., E. I. Rogaev, Y. Liang, E. A. Rogaeva, G. Levesque, M. Ikeda, H. Chi, C. Lin, G. Li, K. Holman, et al. "Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease（题目：早发家族性阿尔兹海默氏征错义突变基因的克隆）." Nature 375(6534) (1995 ): 754-60.
Walsh, D. M., I. Klyubin, J. V. Fadeeva, W. K. Cullen, R. Anwyl, M. S. Wolfe, M. J. Rowan, and D. J. Selkoe. "Naturally secreted oligomers of amyloid ? protein potently inhibit hippocampal long-term potentiation in vivo（题目：体内正常分泌的淀粉样蛋白的寡聚体，在体内强有力地抑制了海马的长时程增强）." Nature 416(6880) (2002): 535-9.
Yan, R., P. Han, H. Miao, P. Greengard, and H. Xu. "The transmembrane domain of the Alzheimer's ?-secretase (BACE1) determines its late Golgi localization and access to ?-amyloid precursor protein (APP) substrate（题目：阿尔兹海默氏病人的β分泌酶的穿膜结构域决定了其晚期在高尔基体的定位，以及与其底物—β淀粉样前体蛋白APP的接近）." J Biol Chem. 276(39) (2001) : 36788-96.
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