Specific Memory Deficits; Rehabilitation of Memory Disorders

Albert, M. S. Cognitive and neurobiologic markers of early Alzheimer disease (1996). Proceedings of the National Academy of Sciences of the United States of America 93, 13,547–13,551. Borchelt, D. R., Ratovitski, T., Van Lare, J., Lee, M. K., Gonzales, V. B., Jenkins, N. A., Copeland, N. G., Price, D. L., and Sisodia, S. S. (1997). Accelerated amyloid deposition in the brains of transgenic mice co-expressing mutant presenilin 1 and amyloid precursor proteins. Neuron 19, 939–945. Borchelt, D. R., Thinakaran, G, Eckman, C. B., Lee, M. K., Davenport, F. Ratovitsky, F. Prada, C.-M., Kim, G. Seekins, S., Yager, D., Slunt, H. H., Wang, R., Seeger, M. Levey, A. I., Gandy, S. E., Copeland, N. G., Jenkins, N. A., Price, D. L., Younkin, S. G., and Sisodia, S. S. (1996). Familial Alzheimer’s disease-linked presenilin 1 variants elevate Aβ1–42/1–40 ratio in vitro and in vivo. Neuron 17, 1,005–1,1013. Cai, H., Wang, Y., McCarthy, D., Wen, H., Borchelt, D. R., Price, D. L., and Wong, P. C. (2001). BACE1 is the major β-secretase for generation of Aβ peptides by neurons. Nature Neuroscience 4, 233–234. Citron, M., Oltersdorf, T., Haass, C., McConlogue, L., Hung, A. H., Seubert, P., Vigo-Pelfrey, C., Lieberburg, I., and Selkoe, D. J. (1992). Mutation of the β-amyloid precursor protein in familial Alzheimer’s disease increases β-protein production. Nature 360, 672–674. De Strooper, B., Saftig, P., Craessaerts, K., Vanderstichele, H., Guhde, G., Annaert, W., Von Figura, K., and Van Leuven, F. (1998). Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein. Nature 391, 387–390. Price, D. l., Tanzi, R. E., Borchelt, D. R., and Sisodia, S. S. (1998). Alzheimer’s disease, genetic studies and transgenic models. Annual Review of Genetics 32, 461–493.