Reduction of Soluble Aβ and Tau, but Not Soluble Aβ Alone, Ameliorates Cognitive Decline in Transgenic Mice with Plaques and Tangles*
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F. LaFerla | M. Kitazawa | A. Caccamo | S. Oddo | V. Vasilevko | D. Cribbs
[1] M. Gallagher,et al. A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.
[2] W. Klein,et al. Temporal Profile of Amyloid-β (Aβ) Oligomerization in an in Vivo Model of Alzheimer Disease , 2006, Journal of Biological Chemistry.
[3] B. Hyman,et al. Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function , 2005, Science.
[4] Nick C Fox,et al. Clinical effects of Aβ immunization (AN1792) in patients with AD in an interrupted trial , 2005, Neurology.
[5] J. D. McGaugh,et al. Intraneuronal Aβ Causes the Onset of Early Alzheimer’s Disease-Related Cognitive Deficits in Transgenic Mice , 2005, Neuron.
[6] F. LaFerla,et al. Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[7] E. Masliah,et al. Aβ vaccination effects on plaque pathology in the absence of encephalitis in Alzheimer disease , 2005, Neurology.
[8] J. Trojanowski,et al. The cytoskeleton in neurodegenerative diseases , 2004, The Journal of pathology.
[9] R. Nitsch. Immunotherapy of Alzheimer Disease , 2004, Alzheimer disease and associated disorders.
[10] Dominic M. Walsh,et al. Deciphering the Molecular Basis of Memory Failure in Alzheimer's Disease , 2004, Neuron.
[11] David H. Cribbs,et al. Aβ Immunotherapy Leads to Clearance of Early, but Not Late, Hyperphosphorylated Tau Aggregates via the Proteasome , 2004, Neuron.
[12] D. Dickson,et al. Dimeric Amyloid β Protein Rapidly Accumulates in Lipid Rafts followed by Apolipoprotein E and Phosphorylated Tau Accumulation in the Tg2576 Mouse Model of Alzheimer's Disease , 2004, The Journal of Neuroscience.
[13] I. Ferrer,et al. Neuropathology and Pathogenesis of Encephalitis following Amyloid β Immunization in Alzheimer's Disease , 2004, Brain pathology.
[14] E. Mandelkow,et al. Clogging of axons by tau, inhibition of axonal traffic and starvation of synapses , 2003, Neurobiology of Aging.
[15] E. Mandelkow,et al. CSF-tau, CSF-Aß1-42, ApoE-genotype and clinical parameters in the diagnosis of Alzheimer’s disease: combination of CSF-tau and MMSE yields highest sensitivity and specificity , 2003, Journal of Neural Transmission.
[16] M. Mattson,et al. Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles Intracellular Aβ and Synaptic Dysfunction , 2003, Neuron.
[17] K. Henke,et al. Antibodies against β-Amyloid Slow Cognitive Decline in Alzheimer's Disease , 2003, Neuron.
[18] C. Cotman,et al. Adjuvant-dependent modulation of Th1 and Th2 responses to immunization with beta-amyloid. , 2003, International immunology.
[19] C. Holmes,et al. Neuropathology of human Alzheimer disease after immunization with amyloid-β peptide: a case report , 2003, Nature Medicine.
[20] James L McGaugh,et al. Amygdala Modulation of Memory Consolidation: Interaction with Other Brain Systems , 2002, Neurobiology of Learning and Memory.
[21] D. Schenk. Amyloid-β immunotherapy for Alzheimer's disease: the end of the beginning , 2002, Nature Reviews Neuroscience.
[22] Xin Wu,et al. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model , 2002, Nature Neuroscience.
[23] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[24] George A. Carlson,et al. The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease , 2002, The Journal of Neuroscience.
[25] E. Check. Nerve inflammation halts trial for Alzheimer's drug , 2002, Nature.
[26] Robert Lalonde,et al. The neurobiological basis of spontaneous alternation , 2002, Neuroscience & Biobehavioral Reviews.
[27] J. Bureš,et al. Specific spatial learning deficits become severe with age in β-amyloid precursor protein transgenic mice that harbor diffuse β-amyloid deposits but do not form plaques , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[28] S. Younkin,et al. Reduced effectiveness of Aβ1-42 immunization in APP transgenic mice with significant amyloid deposition , 2001, Neurobiology of Aging.
[29] David J. Cummins,et al. Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[30] Joshua M. Shulman,et al. Tauopathy in Drosophila: Neurodegeneration Without Neurofibrillary Tangles , 2001, Science.
[31] D. Selkoe. Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.
[32] J. Hardy,et al. Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease , 2000, Nature.
[33] Ralph A. Nixon,et al. Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease , 2000, Nature.
[34] R. Motter,et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease , 2000, Nature Medicine.
[35] C. Masters,et al. Soluble pool of Aβ amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease , 1999, Annals of neurology.
[36] L. Lue,et al. Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease , 1999 .
[37] R. Motter,et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse , 1999, Nature.
[38] R. Nicoll,et al. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[39] E. Mandelkow,et al. On the structure of microtubules, tau, and paired helical filaments , 1995, Neurobiology of Aging.
[40] Bradley T. Hyman,et al. Distribution of Alzheimer‐type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's disease , 1992, Neurology.
[41] K. Kosik,et al. Neuritic pathology and dementia in alzheimer's disease , 1991, Annals of neurology.
[42] F. LaFerla,et al. A dynamic relationship between intracellular and extracellular pools of Abeta. , 2006, The American journal of pathology.
[43] D. Selkoe,et al. Natural oligomers of the amyloid-β protein specifically disrupt cognitive function , 2005, Nature Neuroscience.
[44] J. Trojanowski,et al. Tau and axonopathy in neurodegenerative disorders , 2002, NeuroMolecular Medicine.