Emerging therapeutic possibilities in prion diseases: patents 1993 - 1998

Bibliography

• PRUSINER SB: Novel proteinaceous infectious particles cause scrapie. Science (1982) 215:136–144.
   Google Scholar
• BRADLEY R: Animal prion diseases. In: Prion Diseases. Collinge J, Palmer MS (Eds.), OUP, Oxford (1997):89–129.
   Google Scholar
• PRUSINER SB: Prion diseases of humans and animals. J. Royal Coll. Physicians (1994) 28:1-30 (Suppl.).
   Google Scholar
• COLLINGE J, PALMER MS: Human prion diseases. In: Prion Diseases. Collinge J, Palmer MS (Eds.), OUP, Oxford (1997):18–56.
   Google Scholar
• HAUW J-J, SAZDOVITCH V, SEILHEAN D et al.: The no-sology and neuropathology of human conditions re-lated to unconventional infectious agents or prions. Eur. j Neurol (1996) 3:487–499.
   Google Scholar
• PARCHI P, GAMBETTI P: Prion diseases and dementia. In: Molecular Mechanisms of Dementia. Wasco W, Tanzi RE (Eds.), Humana Press, Totowa, NJ, (1997):293–306.
   Google Scholar
• HSIAO K: Human prion diseases. In: The Neuropathology of Dementia. Esiri MM, Morris JH (Eds.), CUP, Cambridge (1997):277–293.
   Google Scholar
• IRONSIDE JW, BELL JE: Pathology of prion diseases. In: Prion Diseases. Collinge J, Palmer MS (Eds.), OUP, Oxford (1997) 57–88.
   Google Scholar
• COLLINGE J, OWEN F, POULTER M et al: Prion dementia without characteristic pathology. Lancet (1990) 336:7–9.
   PubMed Web of Science ®Google Scholar
• GAMBETTI P, PETERSON R, MONARI L etal: Fatal familial insomnia and the widening spectrum of prion dis-eases. Brit. Med. Bull. (1993) 49:980–994.
   PubMedGoogle Scholar
• CLINTON J, FORSYTH C, ROYSTON MC, ROBERTS GW: Synaptic degeneration is the primary neuropathologi-cal feature in prion disease: a preliminary study. Neu-roReport (1993) 4:65–68.
   PubMed Web of Science ®Google Scholar
• LIBERSKI PP: Prions, 8-sheets and transmissible de-mentias: is there still something missing? Acta Neuro-pathol. (1995) 90:113-125.
   Google Scholar
• LABAT M-L: Possible retroviral origin of prion diseases. Med. Hypotheses (1997) 49:461–464.
   PubMedGoogle Scholar
• FARQUHAR CF, SOMERVILLE RA, BRUCE ME: Straining the prion hypothesis. Nature (1998) 391:345–346.
   PubMedGoogle Scholar
• PRUSINER SB: Prion diseases and the BSE crisis. Science (1997) 278:245–251.
   PubMed Web of Science ®Google Scholar
• OWEN F, POULTER M, LOFTHOUSE R et al.: Insertion inprion protein gene in familial Creutzfeldt-Jakob dis-ease. Lancet (1989) 1:51–52.
   PubMed Web of Science ®Google Scholar
• HSIAO K, BAKER HF, CROW TJ et al.: Linkage of a prionprotein missense variant to Gerstmann-Sträussler syn-drome. Nature (1989) 338:342–345.
   PubMed Web of Science ®Google Scholar
• HSIAO KK, SCOTT M, FOSTER D et al: Spontaneous neu-rodegeneration in transgenic mice with mutant prion protein. Science (1990) 250:1587–1590.
   PubMed Web of Science ®Google Scholar
• PAN K-M, BALDWIN M, NGUYEN J et al.: Conversion ofa-helices into 8-sheets features in the formation of the scrapie prion proteins. Proc. Natl. Acad. Sci. USA (1993) 90:10962–10966.
   PubMed Web of Science ®Google Scholar
• LANSBURY PT: Structural neurology: are seeds at theroot of neuronal degeneration? Neuron (1997) 19:1151–1154.
   PubMed Web of Science ®Google Scholar
• PRUSINER SB, SCOTT M, FOSTER D et al.: Transgeneticstudies implicate interactions between homologous PrP isoforms in scrapie prion replication. Cell (1990) 63:673–686.
   PubMed Web of Science ®Google Scholar
• BESSEN RA, KOCISKO DA, RAYMOND GJ et al.: Non-genetic propagation of strain-specific properties of scrapie prion protein. Nature (1995) 375:698–700.
   PubMed Web of Science ®Google Scholar
• TELLING GC, SCOTT M, MASTRIANNI J et al.: Prion propa-gation in mice expressing human and chimeric PrP transgenes implicates the interaction of cellular PrP with another protein. Cell (1995) 83:79–90.
   PubMed Web of Science ®Google Scholar
• BUELER H, FISCHER M, LANG Y et al.: Normal develop-ment and behaviour of mice lacking the neuronal cell-surface PrP protein. Nature (1992) 356:577–582.
   PubMed Web of Science ®Google Scholar
• BRANDNER S, ISENMANN S, RAEBER A etal.: Normal hostprion protein necessary for scrapie-induced neuro-toxicity. Nature (1996) 379:339–343.
   Google Scholar
• •In PrP null mice bearing a wild-type graft, pathological change does not develop in host tissue even where graft-derived PrPsc has migrated into host tissue, indicating the necessity for PrPc as well as PrPsc for pathological change to occur.
   Google Scholar
• COLLINGE J, PALMER MS, DRYDEN AJ: Genetic predispo-sition to iatrogenic Creutzfeldt-Jakob disease. Lancet (1991) 337:1441–1442.
   PubMed Web of Science ®Google Scholar
• BILLETTE DE VILLEMEUR T, DESLYS J-P, PRADEL A et al:Creutzfeldt-Jakob disease from contaminated growth hormone extracts in France. Neurology (1996) 47:690–695.
   PubMedGoogle Scholar
• PALMER MS, DRYDEN AJ, HUGHES JT, COLLINGE J: Ho- mozygous prion protein genotype predisposes to spo-radic Creutzfeldt-Jakob disease. Nature (1991) 352:340–342.
   PubMed Web of Science ®Google Scholar
• BAKER HF, POULTER M, CROW TJ et al: Amino acid poly-morphism in human prion protein and age at death in inherited prion disease. Lancet (1991) 337:1286.
   PubMedGoogle Scholar
• DESLYS J-P, JAEGLY A, HUILLARD D'AIGNAUX J et al: Genotype at codon 129 and susceptibility to Creutzfeldt-Jakob disease. Lancet (1998) 351:1251.
   Google Scholar
• GOLDFARB LG, PETERSEN RB, TABATON M et al: Fatal fa-milial insomnia and familial Creutzfeldt-Jakob dis-ease: disease phenotype determined by a DNA polymorphism. Science (1992) 258:806–808.
   PubMed Web of Science ®Google Scholar
• SAUNDERS AM, STRITTMATTER WJ, SCHMECHEL D et al: Association of apolipoprotein E allele 64 with late-onset familial and sporadic Alzheimer's disease. Neu-rology (1993) 43:1467–1472.
   Google Scholar
• AMOUYEL P, VIDAL O, LAUNAY JM et al.: The apolipo-protein E alleles as major susceptibility factors for Creutzfeldt-Jakob disease. Lancet (1994) 344:1315–1318.
   Google Scholar
• MANSON JC, CLARKE AR, HOOPER ML et al.: 129/01a mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal. Mot. Neurobiol (1994) 8:121–127.
   PubMed Web of Science ®Google Scholar
• COLLINGE J, WHITTINGTON MA, SIDLE KCL et al.: Prion protein is necessary for normal synaptic function. Na-ture (1994) 370:295–297.
   PubMed Web of Science ®Google Scholar
• LLEDO P-M, TREMBLAY P, DEARMOND SJ, PRUSINER SB, NICOLL RA: Mice deficient for prion protein exhibit normal neuronal excitability and synaptic transmis-sion in the hippocampus. Proc. Natl Acad. Sci. USA (1996) 93:2403–2407.
   PubMedGoogle Scholar
• FORLONI G, ANGERETTI N, CHIESA R et al: Neurotoxic-ity of a prion protein fragment. Nature (1993) 362:543–546.
   PubMed Web of Science ®Google Scholar
• FORLONI G, TAGLIAVINI F, BUGIANI O, SALMONA M: Amyloid in Alzheimer's disease and prion-related en-cephalopathies: studies with synthetic peptides. Prog. Neurobiol (1996) 49:287–315.
   PubMedGoogle Scholar
• BROWN DR, SCHMIDT B, KRETZCHMAR HA: Role of mi-croglia and host prion protein in neurotoxicity of a prion protein fragment. Nature (1996) 380:345–347.
   PubMed Web of Science ®Google Scholar
• LARNER AJ: Intracellular mechanisms of amyloid 9-pe-ptide A925-35 induced neurite outgrowth inhibition in vitro. Alzheimer's Reports (1998) 1:55–60.
   Google Scholar
• LARNER AJ, ROSSOR MN: Alzheimer's disease: towards therapeutic manipulation of the amyloid precursor protein and amyloid 9-peptides. Exp. Opin. Ther. Patents (1997) 7:1115–1127.
   Web of Science ®Google Scholar
• KORTH C, STIERLI B, STREIT P et al: Prion (PrPsc)-sp-ecific epitope defined by a monoclonal antibody. Na-ture (1997) 390:74–77.
   PubMed Web of Science ®Google Scholar
• •Description of a monoclonal antibody specifically recognis-ing the pathological conformer of PrP, opening up the possi-bility of diagnosis of prion diseases using immunological techniques.
   Google Scholar
• TARABOULOS A, RAEBER A, BORCHELT D et al: Bre-feldin A inhibits protease-resistant prion protein syn-thesis in scrapie-infected cultured cells. FASEB J (1991) 5:A1177 (Abstract 4678).
   Google Scholar
• TATZELT J, PRUSINER SB, WELCH WJ: Chemical chaper-ones interfere with the formation of scrapie prion pro-tein. EMBO J (1996) 15:6363–6373.
   PubMed Web of Science ®Google Scholar
• MERLINI G, ASCARI E, AMBOLDI N et al.: Interaction ofthe anthracycline 4'-iodo-4'-deoxydoxorubicin with amyloid fibrils: inhibition of amyloidogenesis. Proc. Natl. Acad. Sci. USA (1995) 92:2959–2963.
   PubMed Web of Science ®Google Scholar
• TAGLIAVINI F, MCARTHUR RA, CANCIANI B et al: Effec-tiveness of anthracycline against experimental prion disease in Syrian hamsters. Science (1997) 276:1119–1122.
   PubMed Web of Science ®Google Scholar
• ••In vivo study showing that Syrian hamsters inoculated withscrapie-infected brain homogenate coincubated with the anthracycline 4'-iodo-4'-deoxydoxorubicin (IDX) showed delayed disease onset and prolonged survival time.
   Google Scholar
• KISILEVSKY R, LEMIEUX LI FRASER PE et al.: Arresting amyloidosis in vivo using small-molecule anionic sul-phonates or sulphates: implications for Alzheimer's disease. Nature Med. (1995) 1:143–148.
   Google Scholar
• CAUGHEY B, RACE RE: Potent inhibition of scrapie-associated PrP accumulation by Congo Red. J. Neuro-chem. (1992) 59:768–771.
   PubMed Web of Science ®Google Scholar
• INGROSSO L, LADOGANA A, POCCHIARI M: Congo red prolongs the incubation period in scrapie-infected hamsters. J. Virol. (1995) 69:506–508.
   PubMed Web of Science ®Google Scholar
• CASPI S, HALIMI M, YANAI A et al.: The anti-prion activ-ity of Congo Red: putative mechanism. J. Biol. Chem. (1998) 273:3484–3489.
   PubMed Web of Science ®Google Scholar
• •In vitro study showing that CR renders PrPsc resistant to de-naturation with boiling SDS, a process of 'overstabilisation' which may block PrPsc-template-assisted conversion of PrPc to PrPsc.
   Google Scholar
• SOTO C, KINDY MS, BAUMANN M, FRANGIONE B: Inhibi-tion of Alzheimer's amyloidosis by peptides that pre-vent 9-sheet conformation. Biochem. Biophys. Res. Commun. (1996) 226:672–680.
   PubMed Web of Science ®Google Scholar
• OTTO M, BOEKHOFF I, RATZKA Petal.: First therapeutic experience with flupirtine in patients with Creutzfeldt-Jakob disease. J. Neurol. (1998) 245:486 [Ab-stract p549].
   Google Scholar
• LASMÉZAS CI, DESLYS J-P, ROBAIN 0 et al.: Transmission of the BSE agent to mice in the absence of detectable abnormal prion protein. Science (1997) 275:402–405.
   Google Scholar
• COLLINGE J, SIDLE KCL, MEADS J, IRONSIDE JW, HILL AF:Molecular analysis of prion protein strain variation and the aetiology of 'new variant' CID. Nature (1996) 383:685–690.
   PubMed Web of Science ®Google Scholar
• HILL AF, DESBRUSLAIS M, JOINERS et al.: The same prionstrain causes vCJD and BSE. Nature (1997) 389:448–450.
   PubMed Web of Science ®Google Scholar
• BRUCE ME, WILL RG, IRONSIDE JW et al: Transmissionsto mice indicate that 'new variant' CJD is caused by the BSE agent. Nature (1997) 389:498–501.
   PubMed Web of Science ®Google Scholar
• RAYMOND GJ, HOPE J, KOCISKO DA et al.: Molecular as-sessment of the potential transmissibilities of BSE and scrapie to humans. Nature (1997) 388:285–288.
   PubMed Web of Science ®Google Scholar
• COUSENS SN, VYNNYCKY E, ZEIDLER M, WILL RG, SMITH PG: Predicting the CJD epidemic in humans. Nature (1997) 385:197–198.
   PubMed Web of Science ®Google Scholar
• HILL AF, ZEIDLER M, IRONSIDE J, COLLINGE J: Diagnosis of new variant Creutzfeldt-Jakob disease by tonsil bi-opsy. Lancet (1997) 349:99–100.
   PubMed Web of Science ®Google Scholar
• PRUSINER SB: Cell biology and transgenic models of prion diseases. In: Prion Diseases. Collinge J, Palmer MS (Eds.), OUP, Oxford (1997):130–162.
   Google Scholar
• BUGIANI O, GIACCONE G, VERGA L et al: bPP partici-pates in PrP-amyloid plaques of Gerstmann-Sträussler-Scheinker disease, Indiana kindred. J. Neu-ropathol. Exp. Neurol. (1993) 52:64–70.
   PubMedGoogle Scholar
• TRANCHANT C, SERGEANT N, WATTEZ A et al.: Neurofib-rillary tangles in Gerstmann-Sträussler-Scheinker syn-drome with the Al 17V prion gene mutation. J. Neurol. Neurosurg. Psychiatry (1997) 63:240–246.
   PubMed Web of Science ®Google Scholar
• EL-HACHIMI KH, CERVENAKOVA L, BROWN P et al: Mixed features of Alzheimer's disease and Creutzfeldt-Jakob disease in a family with a presenilin-1 mutation on chromosome 14. Amyloid - Int. J. Clin. Invest. (1996) 3:223–233.
   Google Scholar
• DE STROOPER B, SAFTIG P, GAESSAERTS K et al.: Defi-ciency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein. Nature (1998) 391:387–390.
   PubMed Web of Science ®Google Scholar
• MEINER Z, GABIZON R, PRUSINER SB: Familial Creutzfeldt-Jakob disease: codon 200 prion disease in Libyan Jews. Medicine (1997) 76:227–237.
   PubMedGoogle Scholar
• POCCHIARI M, SCHMITTINGER S, MASULLO C: Ampho-tericin B delays the incubation period of scrapie in in-tracerebrally inoculated hamsters. J. Gen. Virol (1987) 68:219–223.
   PubMed Web of Science ®Google Scholar
• AGUZZI A, COLLINGE J: Post-exposure prophylaxis af-ter accidental prion inoculation. Lancet (1997) 350:1519–1520.
   PubMedGoogle Scholar
• MANUELIDIS L, FRITCH W, ZAITSEV I: Dapsone to delaysymptoms in Creutzfeldt-Jakob disease. Lancet (1998) 352:456.
   PubMed Web of Science ®Google Scholar