Kamikihi-to (KKT) Rescues Axonal and Synaptic Degeneration Associated with Memory Impairment in a Mouse Model of Alzheimer's Disease, 5XFAD

REFERENCES

• Abdul, H. M., Sama, M. A., Furman, J. L., Mathis, D. M., Beckett, T. L., Weidner, A. M., (2009). Cognitive decline in Alzheimer's disease is associated with selective changes in calcineurin/NFAT signaling. Journal of Neuroscience, 29, 12957–12969.
   Google Scholar
• Barker, G. R., Bird, F., Alexander, V., & Warburton, E. C. (2007). Recognition memory for objects, place, and temporal order: a disconnection analysis of the role of the medial prefrontal cortex and perirhinal cortex. Journal Neuroscience, 27, 2948–2957.
   PubMed Web of Science ®Google Scholar
• Brendza, R. P., Bacskai, B. J., Cirrito, J. R., Simmons, K. A., Skoch, J. M., Klunk, W. E., (2005). Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice. Journal of Clinical Investigation, 115, 428–433.
   PubMed Web of Science ®Google Scholar
• Cai, Y., Xiong, K., Zhang, X. M., Cai, H., Luo, X. G., Feng, J. C., (2010). β-Secretase-1 elevation in aged monkey and Alzheimer's disease human cerebral cortex occurs around the vasculature in partnership with multisystem axon terminal pathogenesis and β-amyloid accumulation. European Journal of Neuroscience, 32, 1223–238.
   Google Scholar
• DeCoteau, W. E., & Kesner, R. P. (1998). Effects of hippocampal and parietal cortex lesions on the processing of multiple-object scenes. Behavioral Neuroscience, 112, 68–82.
   Google Scholar
• Dickson, T. C., King, C. E., McCormack, G. H., & Vickers, J. C. (1999). Neurochemical diversity of dystrophic neurites in the early and late stages of Alzheimer's disease. Experimental Neurology, 156, 100–110.
   Google Scholar
• Dickson, T. C., & Vickers, J. C. (2001). The morphological phenotype of β-amyloid plaques and associated neuritic changes in Alzheimer's disease. Neuroscience, 105, 99–107.
   PubMed Web of Science ®Google Scholar
• Eriksen, J. L., & Janus, C. G. (2007). Plaques, tangles, and memory loss in mouse models of neurodegeneration. Behavior Genetics, 37, 79–100.
   Google Scholar
• Ghosh, A. K., Gemma, S., & Tang, J. (2005). β-Secretase as a therapeutic target for Alzheimer's disease. Neurotherapeutics, 5, 399–408.
   Google Scholar
• Grace, E. A., & Busciglio, J. (2003). Aberrant activation of focal adhesion proteins mediates fibrillar amyloid β-induced neuronal dystrophy. Journal of Neuroscience, 23, 493–502.
   Google Scholar
• Henley, D. B., May, P. C., Dean, R. A., & Siemers, E. R. (2009). Development of semagacestat (LY450139), a functional gamma-secretase inhibitor, for the treatment of Alzheimer's disease. Expert Opinion on Pharmacotherapy, 10, 1657–1664.
   PubMed Web of Science ®Google Scholar
• Imbimbo, B. P. (2008). Therapeutic potential of gamma-secretase inhibitors and modulators. Current Topics in Medicinal Chemistry, 8, 54–61.
   PubMed Web of Science ®Google Scholar
• Jacobsen, J. S., Reinhart, P., & Pangalos, M. N. (2005). Current concepts in therapeutic strategies targeting cognitive decline and disease modification in Alzheimer's disease. NeuroRx, 2, 612–626.
   Google Scholar
• Joyashiki, E., Matsuya, Y., & Tohda, C. (2011). Sominone improves memory impairments and increases axonal density in Alzheimer's disease model mice, 5XFAD. International Journal of Neuroscience, 121, 181–190.
   PubMed Web of Science ®Google Scholar
• Kuboyama, T., Tohda, C., & Komatsu, K. (2005). Neuritic regeneration and synaptic reconstruction induced by withanolide A. British Journal of Pharmacology, 144, 961–971.
   PubMed Web of Science ®Google Scholar
• Mucke, L. (2009). Neuroscience: Alzheimer's disease. Nature, 461, 895–897.
   PubMed Web of Science ®Google Scholar
• Naito, R., & Tohda, C. (2006). Characterization of anti-neurodegenerative effects of Polygala tenuifolia in Aβ(25–35)-treated cortical neurons. Biological & Pharmaceutical Bulletin, 29, 1892–1896.
   Google Scholar
• Oakley, H., Cole, S. L., Logan, S., Maus, E., Shao, P., Craft, J., (2006). Intraneuronal β-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: Potential factors in amyloid plaque formation. Journal of Neuroscience, 26, 10129–10140.
   PubMed Web of Science ®Google Scholar
• Ohno, M. (2009). Failures to reconsolidate memory in a mouse model of Alzheimer's disease. Neurobiology of Learning and Memory, 92, 455–459.
   Google Scholar
• Ohno, M., Chang, L., Tseng, W., Oakley, H., Citron, M., Klein, W. L., (2006). Temporal memory deficits in Alzheimer's mouse models: Rescue by genetic deletion of BACE1. European Journal of Neuroscience, 23, 251–260.
   PubMed Web of Science ®Google Scholar
• Ohno, M., Cole, S. L., Yasvoina, M., Zhao, J., Citron, M., Berry, R., (2007). BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice. Neurobiology of Disease, 26, 134–145.
   PubMed Web of Science ®Google Scholar
• Pike, C. J., Walencewicz-Wasserman, A. J., Kosmoski, J., Cribbs, D. H., Glabe, C. G., & Cotman, C. W. (1995). Structure-activity analyses of β-amyloid peptides: Contribution of the β25–35 region to aggregation and neurotoxicity. Journal of Neurochemistry, 64, 253–265.
   PubMed Web of Science ®Google Scholar
• Salloway, S., Sperling, R., Gilman, S., Fox, N. C., Blennow, K., Raskind, M., (2009). A phase 2 multiple ascending dose trial of bapineuzumab in mild to moderate Alzheimer disease. Neurology, 73, 2061–2070.
   PubMed Web of Science ®Google Scholar
• Soto, P., Griffin, M. A., & Shea, J. E. (2007). New insights into the mechanism of Alzheimer amyloid-beta fibrillogenesis inhibition by N-methylated peptides. Biophysical Journal, 93, 3015–3025.
   Google Scholar
• Taniguchi, S., Suzuki, N., Masuda, M., Hisanaga, S., Iwatsubo, T., Goedert, M., (2005). Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins. Journal of Biological Chemistry, 280, 7614–7623.
   PubMed Web of Science ®Google Scholar
• Tohda, C., Hashimoto, I., Kuboyama, T., & Komatsu, K. (2006). Metabolite 1 of protopanaxadiol-type saponins, an axonal regenerative factor, stimulates teneurin-2 linked by PI3-kinase cascade. Neuropsychopharmacology, 31, 1158–1164.
   Google Scholar
• Tohda, C., Matsumoto, N., Zou, K., Meselhy, M. R., & Komatsu, K. (2002). Axonal and dendritic extension by protopanaxadiol-type saponins from ginseng drugs in SK-N-SH cells. Japanese Journal of Pharmacology, 90, 254–262.
   PubMedGoogle Scholar
• Tohda, C., Matsumoto, N., Zou, K., Meselhy, M. R., & Komatsu, K. (2004). Aβ(25–35)-induced memory impairment, axonal atrophy, and synaptic loss are ameliorated by M1, A metabolite of protopanaxadiol-type saponins. Neuropsychopharmacology, 29, 860–868.
   PubMedGoogle Scholar
• Tohda, C., Naito, R., & Joyashiki, E. (2008). Kamikihi-to, a herbal traditional medicine, improves Aβ(25–35)-induced memory impairment and losses of neurites and synapses. BMC Complementary and Alternative Medicine, 8, 49.
   Google Scholar
• Tohda, C., Tamura, T., & Komatsu, K. (2003). Repair of amyloid β(25–35)-induced memory impairment and synaptic loss by a Kampo formula, Zokumei-to. Brain Research, 990, 141–147.
   PubMed Web of Science ®Google Scholar
• Tohda, C., Tamura, T., Matsuyama, S., & Komatsu, K. (2006). Promotion of axonal maturation and prevention of memory loss in mice by extracts of Astragalus mongholicus. British Journal of Pharmacology, 149, 532–541.
   PubMed Web of Science ®Google Scholar
• Tsai, J., Grutzendler, J., Duff, K., & Gan, W. B. (2004). Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches. Nature Neuroscience, 7, 1181–1183.
   PubMed Web of Science ®Google Scholar
• Urano, T., & Tohda, C. (2010). Icariin improves memory impairment in Alzheimer's disease model mice (5xFAD) and attenuates amyloid β-induced neurite atrophy. Phytotherapy Research, 24, 1658–1663.
   PubMed Web of Science ®Google Scholar
• Wu, H. Y., Hudry, E., Hashimoto, T., Kuchibhotla, K., Rozkalne, A., Fan, Z., (2010). Amyloid β induces the morphological neurodegenerative triad of spine loss, dendritic simplification, and neuritic dystrophies through calcineurin activation. Journal of Neuroscience, 30, 2636–2649.
   PubMed Web of Science ®Google Scholar
• Zhang, X. M., Cai, Y., Xiong, K., Cai, H., Luo, X. G., Feng, J. C., (2009). β-secretase-1 elevation in transgenic mouse models of Alzheimer's disease is associated with synaptic/axonal pathology and amyloidogenesis: Implications for neuritic plaque development. European Journal of Neuroscience, 30, 2271–2283.
   PubMed Web of Science ®Google Scholar