Antibody therapy for Alzheimer’s disease

References

• Bartus RI, Dean RL III, Beer B, Lippa AS. The cholinergic hypothesis of geriatric memory dysfunction. Science 217(4558), 408–414 (1982).
   PubMed Web of Science ®Google Scholar
• Whitehouse PJ, Price DL, Struble RG, Clark AVV, Coyle JT, Delon MR. Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain. Science 215(4537), 1237–1239 (1982).
   PubMed Web of Science ®Google Scholar
• Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 297(5580), 353–356 (2002).
   PubMed Web of Science ®Google Scholar
• Savage MJ, Trusko SP, Howland DS et al. Turnover of amyloid beta-protein in mouse brain and acute reduction of its level by phorbol ester. J. NeumscL 18 (5), 1743–1752 (1998).
   PubMedGoogle Scholar
• Solomon B, Koppel R, Hanan E, Katzav T Monoclonal antibodies inhibit in vitro fibrillar aggregation of the Alzheimer beta-amyloid peptide. Proc. Natl Acad. Li. USA 93(1), 452–455 (1996).
   Google Scholar
• Solomon B, Koppel R, Frankel D, Hanan- Aharon E. Disaggregation of Alzheimer beta-amyloid by site-directed mAb. Proc. N7t1 Arad Sci. USA 94(8), 4109–4112 (1997).
   Google Scholar
• Solomon B. 1mmunotherapeutic strategies for prevention and treatment of Alzheimer's disease. DNA Cell Biol. 20(11), 697–703 (2001).
   Google Scholar
• Frenkel D, Balass M, Solomon B. N- terminal EFRH sequence of Alzheimer's beta-amyloid peptide represents the epitope of its anti-aggregating antibodies. J. Neuroimmunol 88(1–2), 85–90 (1998).
   Google Scholar
• Games D, Adams D, Alessandrini R etal. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature 373, 523–527 (1995).
   Google Scholar
• Hsiao K, Chapman P, Nilsen S etal. Correlative memory deficits, Abeta elevation and amyloid plaques in transgenic mice. Science 274, 99–102 (1996).
   Google Scholar
• Schenk D, Barbour R, Dunn W etal. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 400, 173–177 (1999).
   Google Scholar
• Bard F, Cannon C, Barbour R etal. Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer's disease. Nat. Med. 6(8), 916–919 (2000).
   Google Scholar
• Holcomb LA, Gordon MN, McGowan E etal. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. A& Med 4,97–100 (1998).
   Google Scholar
• Duff K. Transgenic models for Alzheimer's disease. Neumpathol AppL Neumbiol 24, 101–103 (1998).
   PubMed Web of Science ®Google Scholar
• Gordon MN, King DL, Diamond DM etal. Correlation between cognitive deficits and AB deposits in transgenic APP+PS1 mice. Neumbiol Aging 22, 377–385 (2001).
   Google Scholar
• Arendash GVV, King DL, Gordon MN etal. Progressive age-associated behavioral impairments in transgenic mice carrying both mutant APP and PS1 transgenes. Brain Res. 891,45-53 (2001).
   Google Scholar
• Justice A, Motter R. Behavioral characterization of PDAPP transgenic Alzheimer mice. Neurosci. Abst. 23(2), 1637 (1997).
   Google Scholar
• Dodart JC, Meziane H, Mathis C, Bales KR, Paul SM, Ungerer A. Memory and learning impairment precede amyloid deposition in the V717F PDAPP transgenic mouse. NeuroscL Abst. 23(2), 1637 (1997).
   Google Scholar
• Dodart JC, Mathis C, Saura J, Bales KR, Paul SM, Ungerer A. Neuroanatomical abnormalities in behaviorally characterized APP 0/7179 transgenic mice. Neurobiol Dis. 7(2), 71–85 (2001).
   Google Scholar
• Gonzalez-Lima F, Berndt JD, Valla JE, Games D, Reiman EM. Reduced corpus callosum, fornix and hippocampus in PDAPP transgenic mouse model of Alzheimer's disease. NeuroReport 12 (11), 2375–2379 (2001).
   PubMedGoogle Scholar
• Morgan D, Diamond DM, Gottschall PE et al A beta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease. Nature 408(6815), 982–985 (2000).
   PubMed Web of Science ®Google Scholar
• Janus C, Pearson J, McLaurin J etal. A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease. Nature 408(6815), 979–982 (2000).
   PubMed Web of Science ®Google Scholar
• Wilcock DM, Gordon MN, Ugen KE etal. Number of Abeta inoculations in APP+PS1 transgenic mice influences antibody titers, microglial activation and congophilic plaque levels. DNA Cell Biol. 20(11), 731–736 (2001).
   Google Scholar
• Gordon MN, Holcomb LA, Jantzen PT etal. Time course of the development of Alzheimer-like pathology in the doubly transgenic PS1+APP mouse. Exp. Neurol 173,183–195 (2002).
   Google Scholar
• DeMattos RB, Bales KR, Cummins DJ, Dodart JC, Paul SM, Holtzman DM. Peripheral anti-A beta antibody alters CNS and plasma A beta clearance and decreases brain A beta burden in a mouse model of Alzheimer's disease. Proc. Natl Acad Sci USA 98(15), 8850–8855 (2001).
   PubMed Web of Science ®Google Scholar
• DeMattos RB, Brendza RP, Heuser JE etal. Purification and characterization of astrocyte-secreted apolipoprotein E and J-containing lipoproteins from wild type and human apoE transgenic mice. Neurochem Lit. 39(5-6), 415–425 (2001).
   PubMedGoogle Scholar
• Chen G, Chen KS, Knox J etal. A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease. Abture 408(6815), 975–979 (2000).
   Google Scholar
• Westerman MA, Cooper-Blacketer D, Mariash A etal. The relationship between Abeta and memory in the Tg2576 mouse model of Alzheimer's disease. J. Neurosci. 22(5), 1858-1867(2002).
   Google Scholar
• Dodart JC, Bales KR, Gannon KS etal. Immunization reverses memory deficits without reducing brain Abeta burden in Alzheimer's disease model. Nat. Neurosci. 5(5), 452–457 (2002).
   Google Scholar
• Kotilinek LA, Bacskai B, Westerman M etal. Reversible memory loss in a mouse transgenic model of Alzheimer's disease. J. Neumsci. 22(15), 6331–6335 (2002).
   Google Scholar
• Walsh DM, Klyubin I, Fadeeva JV etal. Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in viva Nature 416(6880), 535–539 (2002).
   Google Scholar
• Lambert MP, Viola KL, Chromy BA etal. Vaccination with soluble Abeta oligomers generates toxicity- neutralizing antibodies. Neurochem 79(3), 595–605 (2001).
   PubMed Web of Science ®Google Scholar
• Bacskai BJ, Kajdasz ST, Christie PH etal. Imaging of amyloid-13 deposits in living mice permits direct observation of clearance of plaques with immunotherapy. Nat. Med. 7, 369–372 (2001).
   Google Scholar
• Bacskai BJ, Kajdasz ST McLellan ME etal. Non-Fc-mediated mechanisms are involved in clearance of amyloid-beta in vivo by immunotherapy. j Neurosci. 22(18), 7873–7878 (2002).
   PubMed Web of Science ®Google Scholar
• Wilcock D, DiCarlo G, Henderson D etal. Intracranially administered antiAB antibodies reduce beta-amyloid deposition by mechanisms both independent of and associated with microglial activation. J. Neumsci. an Press) (2003).
   Google Scholar
• Dickey CA, Morgan DG, Kudchodkar S etal. Duration and specificity of humoral immune responses in mice vaccinated with the Alzheimer's disease-associated beta-amyloid 1–42 peptide. DNA Cell Biol. 20(11), 723–729 (2001).
   Google Scholar
• McLaurin J, Cecal R, Kierstead ME et al. Therapeutically effective antibodies against amyloid-beta peptide target amyloid-beta residues 4–10 and inhibit cytotoxicity and fibrillogenesis. Nat. Med. 8(11), 1263–1269 (2002).
   Google Scholar
• DeMattos RB, Bales KR, Cummins DJ, Paul SM, Holtzman DM. Brain to plasma amyloid-beta efflux: a measure of brain amyloid burden in a mouse model of Alzheimer's disease. Science 295(5563), 2264–2267 (2002).
   PubMed Web of Science ®Google Scholar
• Frenkel D, Katz 0, Solomon B. Immunization against Alzheimer's beta — amyloid plaques via EFRH phage administration. Proc. Natl Acad. Li. USA 97 (21), 11455–11459 (2000).
   Google Scholar
• Sigurdsson EM, Scholtzova H, Mehta PD, Frangione B, Wisniewski T Immunization with a nontoxic/nonfibrillar amyloid-beta homologous peptide reduces Alzheimer's disease-associated pathology in transgenic mice. ATM I Pathol 159(2), 439–447(2001).
   PubMedGoogle Scholar
• Nicolau C, Greferath R, Balaban TS, Lazarte JE, Hopkins RJ. A liposome-based therapeutic vaccine against beta -amyloid plaques on the pancreas of transgenic NORBA mice. Proc. Nat/Acad. Li. USA 99(4), 2332–2337 (2002).
   Google Scholar
• Das P, Murphy MP, Younkin LH, Younkin SG, Golde TE. Reduced effectiveness of Abetal -42 immunization in APP transgenic mice with significant amyloid deposition. Neurobiol Aging22(5), 721-727(2002).
   Google Scholar
• Monsonego A, Maron R, Zota V, Selkoe DJ, Weiner HL. Immune hyporesponsiveness to amyloid beta-peptide in amyloid precursor protein transgenic mice: implications for the pathogenesis and treatment of Alzheimer's disease. Proc. Natl Acad Li. USA 98(18), 10273–10278 (2001).
   Google Scholar
• Schenk D. Amyloid-beta immunotherapy for Alzheimer's disease; the end of the beginning. Nat. Rev. Ai.unasci. 3,824–828 (2002).
   Google Scholar
• Hock C, Konietzko U, Papassotiropoulos A etal Generation of antibodies specific for beta-amyloid by vaccination of patients with Alzheimer's disease. Nat. Med. 8(11), 1270–1275 (2002).
   PubMed Web of Science ®Google Scholar
• Hyman BT, Smith C, Buldyrev I et al. Autoantibodies to amyloid-beta and Alzheimer's disease. Ann. Neurol 49(6), 808–810 (2001).
   PubMedGoogle Scholar
• Pfeifer M, Boncristiano S, Bondolfi L etal. Cerebral hemorrhage after passive antiAbeta immunotherapy. Science 298(5597), 1379 (2002).
   PubMedGoogle Scholar
• Grubeck-Lcebenstein B, Blasko I, Marx FK, Trieb I. Immunization with beta-amyloid: could T-cell activation have a harmful effect? Bend Nato:6cl 23(3), 114 (2000).
   Google Scholar
• Matsuoka Y, Lemere CA, Duff K Abeta sequester therapy in AD mouse model. Neurosci. Abstr #227.5 (2002).
   Google Scholar
• Weiner HL, Lemere CA, Maron R etal Nasal administration of amyloid-beta peptide decreases cerebral amyloid burden in a mouse model of Alzheimer's disease. Ann. Neurol 48(4), 567–579 (2000).
   PubMed Web of Science ®Google Scholar