The cerebral proteopathies

Neurobiology of Aging

Volumn 21, Issue 4, 2000, Pages 559-561

  Walker, Lary C ^a   Levine III, Harry ^a  

^a PFIZER INC   (United States)

Author keywords

Aging; Alzheimer's disease; Amyloid; Dementia; Diabetes; Neurodegenerative disorders; Prion; Proteopathy

Indexed keywords

AMYLOID; AMYLOID BETA PROTEIN; PRION PROTEIN;

AGING; ALZHEIMER DISEASE; DEGENERATIVE DISEASE; DEMENTIA; GENE MUTATION; HUMAN; NON INSULIN DEPENDENT DIABETES MELLITUS; NOTE; PATHOGENESIS; POINT MUTATION; PRIORITY JOURNAL; PROTEIN FOLDING;

BRAIN CHEMISTRY; HUMANS; NEURODEGENERATIVE DISEASES; PROTEIN FOLDING;

EID: 0034622229     PISSN: 01974580     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0197-4580(00)00160-3     Document Type: Note

References (24)

1. Aguzzi, Weissmann C. Prion research: the next frontiers. Nature (London) 1997;389:795-8.
2. Carrell R.W., Lomas D.A. Conformational disease. Lancet. 350:1997;134-138.
3. Clark A, Morris JF, Scott LA, et al. Intracellular formation of amyloid fibrils in β-cells of human insulinoma and pre-diabetic monkey islets. In: Natvis JB, editor. Amyloid and amyloidosis. Amsterdam: Kluwer, 1991. p. 453-6.
4. Davis R.L., Shrimpton A.E., Holohan P.D., et al. Familial dementia caused by polymerization of mutant neuroserpin. Nature (London). 401:1999;376-379.
5. Gajdusek D.C. Spontaneous generation of infectious nucleating amyloids in the transmissible and nontransmissible cerebral amyloidoses. Mol Neurobiol. 8:1994;1-13.
6. Glenner GG. Amyloid deposits and amyloidoses: the β-fibrilloses (Parts 1 and 2). New Engl J Med 1980;302:1283-92, 1333-43.
7. Janson J., Ashley R.H., Harrison D., McIntyre S., Butler P.C. The mechanism of islet amyloid polypeptide toxicity is membrane disruption by intermediate-sized toxic amyloid particles. Diabetes. 48:1999;491-498.
8. Jellinger KA. Movement disorders with tau protein cytoskeletal pathology. In: Stern GM, editor. Parkinson's disease: advances in neurology(Vol.80). Philadelphia: Lippincott, Williams and Wilkins, 1999. p. 303-11.
9. Kisilevsky R., Fraser P.E. Aβ amyloidogenesis. Unique, or variation on a systemic theme? Crit Rev Biochem Mol Biol. 32:1997;361-404.
10. Koo E.H., Lansbury P.T., Kelly J.W. Amyloid diseases. Abnormal protein aggregation in neurodegeneration. Proc Natl Acad Sci USA. 96:1999;9989-9990.
11. Lansbury P.T. Structural neurology. Are seeds at the root of neuronal degeneration? Neuron. 19:1997;1151-1154.
12. Lambert M.P., Barlow A.K., Chromy B.A., et al. Diffusible, nonfibrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA. 95:1998;6448-6453.
13. Lue L.-F., Kuo Y.-M., Roher A.E., et al. Soluble amyloid β peptide concentration as a predictor of synaptic change in Alzheimer's disease. Am J Pathol. 155:1994;853-862.
14. Price D.L., Sisodia S.S., Borchelt D.R. Genetic neurodegenerative diseases the human illness and transgenic models . Science. 282:1998;1079-1083.
15. Prusiner SB, Safar J, Cohen FE, DeArmond SJ. The prion diseases. In: Terry RD, Katzman R, Bick KL, Sisodia SS, editors. Alzheimer disease. Philadelphia: Lippincott, Williams and Wilkins, 1999. p. 161-79.
16. Schwartz P. Über den Ursprung der Bezeichnung "Amyloidose." Ein Vorschlag zu ihrer Ersetzung. Zentralbl Allg Pathol. 115:1972;453-462.
17. Selkoe DJ. Biology of β-amyloid precursor protein and the mechanism of Alzheimer disease. In: Terry RD, Katzman R, Bick KL, Sisodia SS, editors. Alzheimer disease. Philadelphia: Lippincott, Williams and Wilkins, 1999. p. 293-310.
18. Terry R.D. The pathogenesis of Alzheimer disease an alternative to the amyloid hypothesis . J Neuropathol Exp Neurol. 55:1996;1023-1025.
19. Tolnay M., Probst A. Tau protein pathology in Alzheimer's disease and related disorders. Neuropathol Appl Neurobiol. 25:1999;171-187.
20. Trojanowski J.Q., Lee VM-Y. Aggregation of neurofilament and α-synuclein proteins in Lewy bodies. Arch Neurol. 55:1998;151-152.
21. Vidal R., Frangione B., Rostagno A., et al. A stop-codon mutation in the BRI gene associated with familial British dementia. Nature (London). 399:1999;776-781.
22. Wakabayashi K., Hayashi S., Kakita A., et al. Accumulation of α-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy. Acta Neuropathol (Berlin). 96:1998;445-452.
23. Walker L.C., Durham R.A. Cerebrovascular amyloidosis. Experimental analysis in vitro and in vivo. Histol Histopathol. 14:1999;827-837.
24. Westermark P. Classification of amyloid fibril proteins and their precursors an ongoing discussion . Amyloid. 4:1997;216-218.