Hostname: page-component-586b7cd67f-vdxz6 Total loading time: 0 Render date: 2024-11-22T07:32:13.407Z Has data issue: false hasContentIssue false

Dimebon as a Potential Therapy for Alzheimer's Disease

Published online by Cambridge University Press:  07 November 2014

Extract

Excellent treatment for Alzheimer's disease remains an unmet medical need. Although current therapies improve patients' abilities compared to placebo and temporarily maintain performance above baseline on a number of outcome measures, additional therapies are needed to augment the benefits over baseline and to prolong these improvements.

Type
Expert Panel Supplement
Copyright
Copyright © Cambridge University Press 2009

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Doody, RS, Gavrilova, SI, Sano, M, et al, and the dimebon investigators. Effect of dimebon on cognition, activities of daily living, behaviour, and global function in patients with mild-to-moderate Alzheimer's disease: a randomised, double-blind, placebo-controlled study. Lancet. 2008;372(9634):207215.Google Scholar
2.Lermontova, NN, Lukoyanov, NV, SerkDva, TRLukoyanova, EA, Bachurin, SO. Dimebon improves learning in animals with experimental Alzheimer's disease. Bull Exp Biol Med.. 2000;129(6):544546.Google Scholar
3.Grigorev, W, Dranyi, OA, Bachurin, SO. Comparative study of action mechanisms of dimebon and memantine on AMPA- and NMDA-subtypes glutamate receptors in rat cerebral neurons. Bull Exp Biol Med. 2003:136(5):474477.Google Scholar
4.Bachurin, S, Bukatina, E, Lermontova, N, et al.Antihistamine agent Dimebon as a novel neuroprotector and a cognition enhancer. Ann N Y Acad Sci. 2001:939:425435.Google Scholar
5.Bachurin, SO, Shevtsova, EP, Kireeva, EG, Oxenkrug, GF, Sablin, SO. Mitochondria as a target for neurotoxins and neuroprotective agents. Ann N Y Acad Sci. 2003:993:334344.Google Scholar
6.Protter, AA. Dimebon induces neurite outgrowth and stabilization in the setting of cell stress. Paper presented at: 11th International Conference on Alzheimers Disease; July 26-31,2008; Chicago, Illinois.Google Scholar
1.Smith, MA, Perry, G, Richey, PL, et al.Oxidative damage in Alzheimer's. Nature. 1996:382:120121.CrossRefGoogle ScholarPubMed
2.Devi, L, Prabhu, BM, Galati, DF, Avadhani, NG, Anandatheerthavarada, HKAccumulation of amyloid precursor protein in the mitochondrial import channels of human Alzheimer's disease brain is associated with mitochondrial dysfunction. J Neurosci. 2006:26:90579068.CrossRefGoogle ScholarPubMed
3.Maurer, I, Zierz, S, Möller, HJ. A selective defect of cytochrome c oxidase is present in brain of Alzheimer disease patients. Neurobiol Aging. 2000:21:455462.CrossRefGoogle ScholarPubMed
4.Reddy, PH, McWeeney, S, Park, BS, et al.Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's disease. Hum Mol Genet. 2004:13:12251240Google Scholar
5.Reddy, PH, Beal, MF. Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. Trends Mol Med. 2008:14(2):4553.Google Scholar
6.Swerdlow, RH, Khan, SM. A “mitochondrial cascade hypothesis” for sporadic Alzheimer's disease. Med Hypotheses. 2004:63:820.Google Scholar
7.DiMauro, S, Schon, EA. Mitochondrial disorders in the nervous system. Annu RevNeurosci. 2008:31:91123.CrossRefGoogle ScholarPubMed
8.Gibson, GE, Sheu, KF, Blass, JPAbnormalities of mitochondrial enzymes in Alzheimer disease. J Neural Transm. 1998:105:855870.CrossRefGoogle ScholarPubMed
9.Hirai, K, Aliev, G, Nunomura, A, et al.Mitochondrial abnormalities in Alzheimer's disease. J Neurosci. 2001:21:30173023.Google Scholar
10.Nunomura, A, Perry, G, Aliev, G, et al.Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol. 2001:60:759767.Google Scholar
11.Reisberg, B, Doody, R, Stoffler, A, Schmitt, F, Ferris, S, Möbius, HJ, and the Memantine Study Group. Memantine in moderate-to-severe Alzheimer's disease. N Engl J Med. 2003:348(14):13331341.Google Scholar
12.Tariot, PN, Farlow, MR, Grossberg, GT, Graham, SM, McDonald, S, Gergel, I, and the Memantine Study Group. Memantine treatment in patients with moderate to severe Alzheimer disease already receiving donepezil: a randomized controlled trial. JAMA. 2004:291(3):317324.Google Scholar
13.Doody, RS, Gavrilova, SI, Sano, M, et, al, and the dimebon investigators. Effect of dimebon on cognition, activities of daily living, behaviour, and global function in patients with mild-to-moderate Alzheimer's disease: a randomised, double-blind, placebo-controlled study. Lancet. 2008:372(9634):207215.Google Scholar
14.Wu, J, Li, Q, Bezprozvanny, I.Evaluation of Dimebon in cellular model of Huntington's disease. Mol Neurodegener. 2008:3:15.Google Scholar
15.Lermontova, NN, Redkozubov, AE, Shevtsova, EF, Serkova, TP, Kireeva, EG, Bachurin, SO. Dimebon and tacrine inhibit neurotoxic action of beta-amyloid in culture and block L-type Ca(2+) channels. Bull ap Biol Med. 2001:132(5):10791083.Google Scholar
16.Protter, AA. Dimebon induces neurite outgrowth and stabilization in the setting of cell stress. Paper presented at: 11th International Conference on Alzheimers Disease: July 26-31,2008: Chicago, Illinois.Google Scholar
17.Courtney, C, Farrell, D, Gray, R, et al, and the A02000 Collaborative Group. Long-term donepezil treatment in 565 patients with Alzheimer's disease (AD2000): randomised double-blind trial. Lancet. 2004:363(9427):21052115.Google Scholar
18.Poling, A, Morgan-Paisley, K, Panos, JJ, et al.Oligomers of the amyloid-beta protein disrupt working memory: confirmation with two behavioral procedures. Behav Brain Res. 2008:193(2):230234.Google Scholar
19.Lesné, S, Kotilinek, L, Ashe, KH. Plaque-bearing mice with reduced levels of oligomeric amyloid-beta assemblies have intact memory function. Neuroscience. 2008:151(3):745749.Google Scholar
20.Salloway, S, Sperling, R, Gilman, S, et, al, for the Bapineuzumab 201 Clinical Trial Investigators. A phase 2 multiple ascending dose trial of bapineuzumab in mild to moderate Alzheimer's disease. Neurology. In press.Google Scholar
21.Ramsden, M, Kotilinek, L, Forster, C, et al.Age-dependent neurofibrillary tangle formation, neuron loss and memory impairment in a mouse model of human tauopathy (P301L). J Neurosci. 2005;25(46):1063710647.Google Scholar
22.Ashe, KH. A tale about tau. N EnglJMed. 2007:357(9):933935.Google Scholar
23.Reddy, PH. Mitochondrial medicine for aging and neurodegenerative diseases. Neuromolecular Med. 2008:10:291315.Google Scholar
24.Reddy, PH. Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer's disease. Exp Neurol. 2009:218:286292.Google Scholar
25.Reddy, PH, Mao, P, Manczak, M.Mitochondrial structural and functional dynamics in Huntington's disease. Brain Res Rev. 2009:61:3348.Google Scholar
26.Bachurin, S, Bukatina, E, Lermontova, N, et al.Antihistamine agent Dimebon as a novel neuroprotector and a cognition enhancer. Ann N YAcadSci. 2001:939:425435.Google Scholar
27.Bachurin, SO, Shevtsova, EP, Kireeva, EG, Oxenkrug, GF, Sablin, SO. Mitochondria as a target for neurotoxins and neuroprotective agents. Ann N YAcad Sci. 2003:993:334344.Google Scholar