Bibliography
- MOUNT C, DOWNTON C: Alzheimer’s disease: progress or profit? Nat. Med. (2006) 12:780-784.
- SELKOE DJ: The molecular pathology of Alzheimer’s disease. Neuron (1991) 6:487-498.
- GLENNER GG, WONG CW: Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem. Biophys. Res. Comm. (1984) 120(3):885-890.
- SELKOE DJ: Alzheimer’s disease: a central role for amyloid. J. Neuropathol. Exp. Neurol. (1994) 53:438-447.
- HARDY J, SELKOE DJ: The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science (2002) 297:353-356.
- HARDY J, DUFF K, HARDY KG, PEREZ-TUR J, HUTTON M: Genetic dissection of Alzheimer’s disease and related dementias: amyloid and its relationship to τ. Nat. Neurosci. (1998) 1:355-358.
- CHARTIER-HARLIN MC, CRAWFORD F, HOULDEN H et al.: Early-onset Alzheimer’s disease caused by mutations at codon 717 of the β-amyloid precursor protein gene. Nature (1991) 353:844-846.
- NÄSLUND J, HAROUTUNIAN V, MOHS R et al.: Correlation between elevated levels of amyloid β-peptide in the brain and cognitive decline. JAMA (2000) 283:1571-1577.
- TERRY RD, PECK A, DETERESA R, SCHECHTER R, HOROUPIAN DS: Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Ann. Neurol. (1981) 10:184-192.
- SELKOE D: Alzheimer’s disease is a synaptic failure. Science (2002) 298:789-791.
- LESNÉ S, TENG KOH M, KOTILINEK L et al.: A specific amyloid-β protein assembly in the brain impairs memory. Nature (2006) 440:352-357.
- DRACHMAN DA: Preventing and treating Alzheimer’s disease: strategies and prospects. Expert Rev. Neurother. (2003) 3:565-569.
- MAGGIO JE, MANTYH PW: Brain amyloid – a physicochemical perspective. Brain Pathol. (1996) 6:147-162.
- CARLSON JD, YARMUSH ML: Antibody assisted protein refolding. Biotechnology (1992) 10:86-91.
- SOLOMON B, SCHWARTZ F: Chaperone-like effect of monoclonal antibodies on refolding of heat-denatured carboxypeptidase A. J. Mol. Recogn. (1995) 8:72-76.
- SOLOMON B, KOPPEL R, HANAN E, KATZAV T: Monoclonal antibodies inhibit in vitro fibrillar aggregation of the Alzheimer β-amyloid peptide. Proc. Natl. Acad. Sci. USA (1996) 93:452-455.
- SOLOMON B, KOPPEL R, FRENKEL D, HANAN-AHARON E: Disaggregation of Alzheimer β-amyloid by site-directed mAb. Proc. Natl. Acad. Sci. USA (1997) 94:4109-4112.
- HANNAN E, SOLOMON B: Protective effect of monoclonal antibodies against Alzheimer’s β-amyloid aggregation. Amyloid (1996) 3:130-133.
- FRENKEL D, BALASS M, SOLOMON B: N-terminal EFRH sequence of Alzheimer’s β-amyloid peptide represents the epitope of its anti-aggregating antibodies. J. Neuroimmunol. (1998) 88:85-90.
- FRENKEL D, BALASS M, KATCHALSKI-KATZIR E, SOLOMON B: High affinity binding of monoclonal antibodies to the sequential epitope EFRH of β-amyloid peptide is essential for modulation of fibrillar aggregation. J. Neuroimmunol. (1999) 95:136-142.
- GAMES D, ADAMS D, ALESSANDRINI R et al.: Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein. Nature (1995) 373:523-527.
- HSIAO K, CHAPMAN P, NILSEN S et al.: Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice. Science (1996) 274:99-102.
- DUFF K, ECKMAN C, ZEHR C et al.: Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1. Nature (1996) 383:710-713.
- HIGGINS GA, JACOBSEN H: Transgenic mouse models of Alzheimer’s disease: phenotype and application. Behav. Pharmacol. (2003) 14:419-438.
- ODDO S, CACCAMO A, SHEPHERD JD et al.: Triple-transgenic model of Alzheimer’s disease with plaques and tangles: intracellular Aβ and synaptic dysfunction. Neuron (2003) 39(3):409-421.
- WEINER HL, FRENKEL D: Immunology and immunotherapy of Alzheimer’s disease. Nat. Rev. Immunol. (2006) 6:404-416.
- SCHENK D, BARBOUR R, DUNN W et al.: Immunization with amyloid-β attenuates Alzheimer’s disease-like pathology in the PDAPP mouse. Nature (1999) 400:173-177.
- JANUS C, PEARSON J, MCLAURIN J et al.: Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer’s disease. Nature (2000) 408:979-982.
- MORGAN D, DIAMOND DM, GOTTSCHALL PE et al.: Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer’s disease. Nature (2000) 408:982-985.
- DODART JC, BALES KR, GANNON KS et al.: Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer’s disease model. Nat. Neurosci. (2002) 5:452-457.
- SIGURDSSON EM, SCHOLTZOVA H, MEHTA PD, FRANGIONE B, WISNIEWSKI T: Immunization with a nontoxic/nonfibrillar amyloid-β homologous peptide reduces Alzheimer’s disease-associated pathology in transgenic mice. Am. J. Pathol. (2001) 159:439-447.
- FRENKEL D, DEWACHTER I, VAN LEUVEN F, SOLOMON B: Reduction of β-amyloid plaques in brain of transgenic mouse model of Alzheimer’s disease by EFRH-phage immunization. Vaccine (2003) 21:1060-1065.
- LAVIE V, BECKER M, COHEN-KUPIEC R et al.: EFRH – phage immunization of Alzheimer’s disease animal model improves behavioral performance in Morris Water Maze trials. J. Molec. Neurosci. (2004) 24(1):105-113.
- WEINER HL, LEMERE CA, MARON R et al.: Nasal administration of amyloid-β peptide decreases cerebral amyloid burden in a mouse model of Alzheimer’s disease. Ann. Neurol. (2000) 48:567-579.
- BARD F, CANNON C, BARBOUR R et al.: Peripherally administered antibodies against amyloid-β peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer’s disease. Nat. Med. (2000) 6:916-919.
- WILCOCK DM, ROJIANI A, ROSENTHAL A et al.: Passive immunotherapy against Aβ in aged APP-transgenic mice reverses cognitive deficits and depletes parenchymal amyloid deposits in spite of increased vascular amyloid and microhemorrhage. J. Neuroinflammation (2004) 1:24.
- DEMATTOS RB, BALES KR, CUMMINS DJ, DODART JC, PAUL SM, HOLTZMAN DM: Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer’s disease. Proc. Natl. Acad. Sci. USA (2001) 98:8850-8855.
- LEVITES, Y, SMITHSON LA, PRICE RW et al.: Insights into the mechanisms of action of anti-Aβ antibodies in Alzheimer’s disease mouse models. FASEB J. (2006) 20:2576-2578.
- ODDO S, BILLINGS L, KESSLAK JP, CRIBBS DH, LAFERIA FM: Aβ immunotherapy leads to clearance of early, but not late, hyperphosphorylated τ aggregates via the proteasome. Neuron (2004) 43(3):321-322.
- GILMAN S, KOLLER M, BLACK RS et al. Clinical effects of Aβ immunization (AN1792) in patients with AD in an interrupted trial. Neurology (2005) 64:1553-1562.
- BAYER AJ, BULLOCK R, JONES RW et al.: Evaluation of the safety and immunogenicity of synthetic Aβ42 (AN1792) in patients with AD. Neurology (2005) 64:94-101.
- SCHENK DB, SEUBERT P, GRUNDMAN M, BLACK R: Aβ immunotherapy: lessons learned for potential treatment of Alzheimer’s disease. Neurodegen. Dis. (2005) 2:255-260.
- NICOLL JA, WILKINSON D, HOLMES C, STEART P, MARKHAM H, WELLER RO: Neuropathology of human Alzheimer’s disease after immunization with amyloid-β peptide: a case report. Nat. Med. (2003) 9(4):448-452.
- FERRER I, BOADA-ROVIRA M, SANCHEZ-GUERRA ML, REY MJ, COSTA-JUSSA F: Neuropathology and pathogenesis of encephalitis following amyloid-β immunization in Alzheimer’s disease. Brain Pathol. (2004) 14:11-20.
- MASLIAH E, HANSEN L, ADAME A et al.: Aβ vaccination effects on plaque pathology in the absence of encephalitis in Alzheimer’s disease. Neurology (2005) 64:129-131.
- ORGOGOZO JM, GILMAN S, DARTIGUES JF et al.: Subacute meningoencephalitis in a subset of patients with AD after Aβ42 immunization. Neurology (2003) 61:46-54.
- CRIBBS DH, GHOCHIKYAN A, TRAN M et al.: Adjuvant-dependent modulation of TH1 and TH2 responses to immunization with β-amyloid. Int. Immunol. (2003) 15:505-514.
- MONSONEGO A, ZOTA V, KARNI A et al.: Increased T cell reactivity to amyloid-β protein in older humans and patients with Alzheimer’s disease. J. Clin. Invest. (2003) 112:415-422.
- NICOLL JA, BARTON E, BOCHE D et al.: Aβ species removal after Aβ42 immunization. J. Neuropathol. Exp. Neurol. (2006) 65:1040-1048.
- O’TOOLE M, JANSZEN DB, SLONIM DK et al.: Risk factors associated with β-amyloid1-42 immunotherapy in preimmunization gene expression patterns of blood cells. Arch. Neurol. (2005) 62:1531-1536.
- HOCK C, KONIETZKO U, STREFFER JR et al.: Antibodies against β-amyloid slow cognitive decline in Alzheimer’s disease. Neuron (2003) 38:547-554.
- FOX NC, BLACK RS, GILMAN S et al.: Effects of Aβ immunization (AN1792) on MRI measures of cerebral volume in Alzheimer’s disease. Neurology (2005) 64:1563-1572.
- PATTON RL, KALBACK WM, ESH CL et al.: Amyloid-β peptide remnants in AN-1792-immunized Alzheimer’s disease patients: a biochemical analysis. Am. J. Pathol. (2006) 169:1048-1063.
- BLACK RS: A single ascending dose study of bapineuzumab, a humanized monoclonal antibody to Aβ, in AD. 9th Annual Geneva Springfield Symposium on Advances in Alzheimer’s Therapy. Geneva, Switzerland (19 – 22 April 2006).
- DALAKAS MC: Mechanisms of action of IVIg and therapeutic considerations in the treatment of acute and chronic demyelinating neuropathies. Neurology (2002) 59:S13-S19.
- DODEL R, HAMPEL H, DEPBOYLU C et al.: Human antibodies against amyloid β peptide: a potential treatment for Alzheimer’s disease. Ann. Neurol. (2002) 52(2):253-256.
- DODEL RC, DU Y, DEPBOYLU C et al.: Intravenous immunoglobulins containing antibodies against β-amyloid for the treatment of Alzheimer’s disease. J. Neurol. Neurosurg. Psychiatry (2004) 75(10):1472-1474.
- ISTRIN G, BOSIS E, SOLOMON B: Intravenous immunoglobulin enhances the clearance of fibrillar amyloid-β peptide. J. Neurosci. Res. (2006) 84(2):434-443.
- SELKOE DJ: Alzheimer’s disease: genes, proteins, and therapy. Physiol. Rev. (2001) 81:741-766.
- AKIYAMA H, ARAI T, TANNO E et al.: Cell mediators of inflammation in the Alzheimer’s disease brain. Alzheimer Dis. Assoc. Disord. (2000) 14:S47-S53.
- BRUCE-KELLER AJ, ESTUS T: Concern over the amyloid vaccine: amyloid heterogeneity and Fc receptor signaling. Neurobiol. Aging (2002) 23:667-670.
- DAS P, GOLDE TE: Open peer commentary regarding Aβ immunization and CNS inflammation by Pasinetti et al. Neurobiol. Aging (2002) 23:671-674.
- TAKAI T: Roles of Fc receptors in autoimmunity. Nat. Rev. (2002) 2:580-592.
- SAMUELSSON A, TOWERS TL, RAVETCH JV: Anti-inflammatory activity of IVIG mediated through the inhibitory Fc receptor. Science (2001) 291:484-486.
- FRENKEL D, SOLOMON B, BENHAR I: Modulation of Alzheimer’s β-amyloid neurotoxicity by site-directed single-chain antibody. J. Neuroimmunol. (2000) 106:23-31.
- TAMMER AH, COIA G, CAPPAI R et al.: Generation of a recombinant Fab antibody reactive with the Alzheimer’s disease-related Aβ peptide. Clin. Exp. Immunol. (2002) 129:453-463.
- LIU R, YUAN B, EMADI S et al.: Single chain variable fragments against β-amyloid (Aβ) can inhibit Aβ aggregation and prevent Aβ-induced neurotoxicity. Biochemistry (2004) 43(22):6959-6967.
- FRENKEL D, SOLOMON B: Filamentous phage as vector-mediated antibody delivery to the brain. Proc. Natl. Acad. Sci. USA (2002) 99:5675-5679.
- THOMAS CE, SCHIEDNER G, KOCHANEK S, CASTRO MG, LOWENSTEIN PR: Peripheral infection with adenovirus causes unexpected long-term brain inflammation in animals injected intracranially with first-generation, but not with high-capacity, adenovirus vectors: toward realistic long-term neurological gene therapy for chronic diseases. Proc. Natl. Acad. Sci. USA (2000) 97:7482-7487.
Websites
- http://www.alzforum.org/drg/drc/ default.aspPhase IIA, multicenter, randomized, double-blind, placebo-controlled, multiple ascending-dose, safety, tolerability, pharmacokinetic, pharmacodynamic and immunogenicity trial of AAB-001 in patients with mild-to-moderate Alzheimer’s disease.
- http://www.alzforum.org/drg/drc/ detail.asp?id=101The first human study of the clinical program of Eli Lilly using LY-206430. This humanized version of the m266 mAb binds to Aβ16-23, the peptide’s midsection.
- http://www.clinicaltrials.gov/ct/show/ NCT00299988The overall goal of this double-blind Phase II study is to evaluate the safety, efficacy and biologic mechanisms of action of IVIG in the treatment of mild-to-moderate-stage Alzheimer’s disease.
- http://www.alzforum.org/drg/drc/ detail.asp?id=102ACC-001: Elan research indicates that antibodies specific for Aβ peptide can cross the blood–brain barrier and act directly in the CNS to induce plaque clearance. These findings suggest that this novel method may clear plaques in human patients.
- http://www.alzforum.org/new/ detail.asp?id=1437Novartis Institutes for BioMedical Research in Basel disclosed preclinical data for a new active vaccine, named CAD-106, that the company is testing in humans in Sweden.