Passive Immunization against Pyroglutamate-3 Amyloid-β Reduces Plaque Burden in Alzheimer-Like Transgenic Mice: A Pilot Study
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B. Liu | C. Lemere | S. Schilling | H. Demuth | M. Kleinschmidt | J. Frost
[1] T. Bayer,et al. Identification of low molecular weight pyroglutamate A{beta} oligomers in Alzheimer disease: a novel tool for therapy and diagnosis. , 2010, The Journal of biological chemistry.
[2] T. Bayer,et al. Identification of Low Molecular Weight Pyroglutamate Aβ Oligomers in Alzheimer Disease , 2010, The Journal of Biological Chemistry.
[3] T. Bayer,et al. Pyroglutamate Abeta pathology in APP/PS1KI mice, sporadic and familial Alzheimer’s disease cases , 2009, Journal of Neural Transmission.
[4] T. Bayer,et al. Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model , 2009, Acta Neuropathologica.
[5] Hans-Ulrich Demuth,et al. Glutaminyl cyclase inhibition attenuates pyroglutamate Aβ and Alzheimer's disease–like pathology , 2008, Nature Medicine.
[6] T. Saido,et al. Amyloidogenic processing of amyloid precursor protein: evidence of a pivotal role of glutaminyl cyclase in generation of pyroglutamate-modified amyloid-beta. , 2008, Biochemistry.
[7] G. Damonte,et al. Association of a presenilin 1 S170F mutation with a novel Alzheimer disease molecular phenotype. , 2007, Archives of neurology.
[8] B. Bohrmann,et al. High sensitivity analysis of amyloid-beta peptide composition in amyloid deposits from human and PS2APP mouse brain , 2006, Neuroscience.
[9] Brian J. Bacskai,et al. Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease , 2006, Neurobiology of Disease.
[10] Hans-Ulrich Demuth,et al. On the seeding and oligomerization of pGlu-amyloid peptides (in vitro). , 2006, Biochemistry.
[11] A. Gliozzi,et al. β-Amyloid Is Different in Normal Aging and in Alzheimer Disease* , 2005, Journal of Biological Chemistry.
[12] B. Ghetti,et al. Amino-terminally truncated Abeta peptide species are the main component of cotton wool plaques. , 2005, Biochemistry.
[13] T. Hoffmann,et al. Glutaminyl cyclases unfold glutamyl cyclase activity under mild acid conditions , 2004, FEBS letters.
[14] Joanna L. Jankowsky,et al. Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase , 2004 .
[15] C. Lemere,et al. Intranasal immunotherapy for the treatment of Alzheimer’s disease: Escherichia coli LT and LT(R192G) as mucosal adjuvants , 2002, Neurobiology of Aging.
[16] D. Selkoe. Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.
[17] C. Barrow,et al. The Aβ 3-Pyroglutamyl and 11-Pyroglutamyl Peptides Found in Senile Plaque Have Greater β-Sheet Forming and Aggregation Propensities in Vitro than Full-Length Aβ† , 1999 .
[18] Kenneth S. Kosik,et al. The E280A presenilin 1 Alzheimer mutation produces increased Aβ42 deposition and severe cerebellar pathology , 1996, Nature Medicine.
[19] T. Iwatsubo,et al. Amino- and carboxyl-terminal heterogeneity of β-amyloid peptides deposited in human brain , 1996, Neuroscience Letters.
[20] D. Selkoe,et al. Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation , 1996, Neurobiology of Disease.
[21] D. Mann,et al. Dominant and differential deposition of distinct β-amyloid peptide species, Aβ N3(pE), in senile plaques , 1995, Neuron.
[22] D. Borchelt,et al. Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. , 2004, Human molecular genetics.