Lack of β-Amyloidosis in transgenic mice expressing low levels of familial Alzheimer's disease missense mutations

Neurobiology of Aging

Volumn 17, Issue 2, 1996, Pages 205-214

  Malherbe, P ^a   Richards, J G ^a   Martin, J R ^a   Bluethmann, H ^b   Maggio, J ^c   Huber, G ^a  

^a F HOFFMANN LA ROCHE LTD   (Switzerland)

^b F HOFFMANN LA ROCHE LTD   (Switzerland)

^c HARVARD MEDICAL SCHOOL   (United States)

Author keywords

A Binding; Behavior; Familial Alzheimer's disease; Histology; Hybridization; Immunohistochemistry; Missense mutation; Transgenic mice; APP

Indexed keywords

AMYLOID PRECURSOR PROTEIN;

ALZHEIMER DISEASE; AMYLOIDOSIS; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; GENE EXPRESSION; GENE MUTATION; GENETIC AND FAMILIAL DISORDERS; HISTOLOGY; IMMUNOHISTOCHEMISTRY; MOUSE; NONHUMAN; PRIORITY JOURNAL; TRANSGENIC MOUSE;

EID: 0029954289     PISSN: 01974580     EISSN: None     Source Type: Journal    
DOI: 10.1016/0197-4580(95)02070-5     Document Type: Article

References (21)

1. Chartier-Harlin, M.-C.; Crawford, F.; Houldon, H.; Warren, A.; Hughes, D.; Fidani, L.; Goate, A.; Rossor, M.; Roques, P.; Hardy, J.; Mullan, M. Early onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene. Nature 353:844-846: 1991.
2. Citron, M.; Oltersdorf, T.; Haass, C.; McConlogue, L.; Hung, A.; Seubert, P.; Vigo-Pelfrey, C.; Lieberburg, I.; Selkoe, D. Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production. Nature 360:672-674; 1992.
3. Cumin, R.; Bandle, E. F.; Gamzu, E.; Haefely, W. E. Effects of the novel compound aniracetam (Ro 13-5057) upon impaired learning and memory in rats. Psychopharmacology (Berlin) 78:104-111; 1982.
4. Forss-Petter, S.; Danielson, P. E.; Catsicas, S.; Battenberg, E.; Price, J.; Nierenberg, M.; Sutcliffe, J. G. Transgenic mice expressing β-galactosidase in mature neurons under neuron-specific enolase promoter control. Neuron 5:187-197; 1990.
5. Games, D.: Adams, D.; Alessandrini, R.; et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein. Nature 373:523-527; 1995.
6. Goate, A.; Chartier-Harlin, M. C.; Mullan, M.; Brown, J.; Crawford, F.; Fidani, L.; Giuffra, L.; Haynes, A.; Irving, N.; James, L.; Mant, R.; Newton. P.; Roole, K.; Roques, P.; Talbot, C.; Pericak-Vance, M.; Roses, A.; Williamson. R.; Rossor, M.: Owen, M.; Hardy, J. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature 349:704-706; 1991.
7. Higgins, L. S.; Holtzman, D. M.; Rabin, J.: Mobley, W. C.; Cordell, B. Transgenic mouse brain histopathology resembles early Alzheimer's disease. Ann. Neurol. 35:598-607; 1994.
8. Hogan, B.; Costanini, F.; Lacy. E. Manipulating the mouse embryo. A laboratory manual. Cold Spring Harbor, NY: Cold Spring Harbor Labs; 1986:322 pp.
9. Huber, G.; Matus, A. Difference in the cellular distribution of two microtubule-associated proteins. MAP1 and MAP2 in rat brain. J. Neurosci. 4:151-160: 1984.
10. LaFerla, F. M.; Tinkle, B. T.; Bieberich, C. J.: Haudenschild, C. C.; Jay, G. The Alzheimer's peptide induces neurodegeneration and apoptotic cell death in transgenic mice. Nat. Genet. 9:21-28: 1995.
11. Lamb, B. T. Making models for Alzheimer's Disease. Nat. Genet. 9:4-6; 1995.
12. Loeffler, J.; Huber, G. β-Amyloid precursor protein isoforms in various rat brain regions and during brain development. J. Neurochem. 59:1316-1324; 1992.
13. Maggio, J.; Stimson, E. R.; Ghilardi, J. R.; Allen, C. J.; Fahl, C. E.; Whitcomb, D. C.; Vigna, S. R.; Vinters, H. V.; Labenski, M. E.; Mantyh, P. W. Reversible in vitro growth of Alzheimer's disease β-amyloid plaques by deposition of labeled amyloid peptide. Proc. Natl. Acad. Sci. USA 89:5462-5466; 1992.
14. Martin, J. R.; Fuchs, A.: Bender, R.; Harting, J. Altered light/dark activity difference with aging in two rat strains. J. Gerontol. 41:2-7; 1986.
15. Martin, J. R.; Schoch. P.; Jenck, F.; Moreau, J.-L.: Haefely, W. E. Pharmacological characterization of benzodiazepine receptor ligands with intrinsic efficacies ranging from high to zero. Psychopharmacology (Berlin) 111:415-422; 1993.
16. Morris, R. G. M. Development of a water-maze procedure for studying spatial learning in the rat. J. Neurosci. Methods 11:47-60; 1984.
17. Mullan, M.; Crawford, F.; Axelman, K.; Houldne, H.; Lilius, L.; Winblad, B.; Lannfelt, L. A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N-terminus of β-amyloid. Nat. Genet. 1:345-347; 1992.
18. Murrell, J.; Farlow, M.; Ghetti, B.; Benson, M. A mutation in the amyloid precursor protein associated with hereditary Alzheimer's disease. Science 254:97-99; 1991.
19. A receptor subunits in the rat CNS J. Comp. Neurol. 326:193-216; 1992.
20. Saura, J.; Luque, J. M.; Cesura, A. M.; DaPrada, M.; Chan-Palay, V.; Huber, G.; Loeffler, J.; Richards, J. G. Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography. Neuroscience 62:15-30; 1994.
21. Suzuki, N.; Cheung. T. T.; Cai, K.-D.; Odaka. A.; Otvos, L., Jr.; Eckman, C.; Golde, T. E.; Younkin, S. G. An increased percentage of long amyloid β protein secreted by familial amyloid β protein precursor (βAPP717) mutants. Science 264:1336-1340; 1994.