M Naoi

Summary

Affiliation: Gifu International Institute of Biotechnology
Country: Japan

Publications

  1. ncbi request reprint Monoamine oxidase inhibitors as neuroprotective agents in age-dependent neurodegenerative disorders
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, 1 1 Nakafudogaoka, Kakamigahara, Gifu 504 0838, Japan
    Curr Pharm Des 16:2799-817. 2010
  2. ncbi request reprint Neuroprotection by propargylamines in Parkinson's disease: intracellular mechanism underlying the anti-apoptotic function and search for clinical markers
    M Naoi
    Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm Suppl . 2007
  3. ncbi request reprint Involvement of type A monoamine oxidase in neurodegeneration: regulation of mitochondrial signaling leading to cell death or neuroprotection
    M Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm Suppl . 2006
  4. doi request reprint Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm (Vienna) 116:1371-81. 2009
  5. doi request reprint Glutathione redox status in mitochondria and cytoplasm differentially and sequentially activates apoptosis cascade in dopamine-melanin-treated SH-SY5Y cells
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, 1 1 Nakafudogaoka, Kakamigahara, Gifu 504 0838, Japan
    Neurosci Lett 465:118-22. 2009
  6. doi request reprint Functional mechanism of neuroprotection by inhibitors of type B monoamine oxidase in Parkinson's disease
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Kakamigahara, Gifu 504 0838, Japan
    Expert Rev Neurother 9:1233-50. 2009
  7. doi request reprint Neuromelanin selectively induces apoptosis in dopaminergic SH-SY5Y cells by deglutathionylation in mitochondria: involvement of the protein and melanin component
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neurochem 105:2489-500. 2008
  8. ncbi request reprint Oxidative stress in mitochondria: decision to survival and death of neurons in neurodegenerative disorders
    Makoto Naoi
    Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    Mol Neurobiol 31:81-93. 2005
  9. ncbi request reprint Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: occurrence, metabolism and function in human brains
    Makoto Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park, Matake, Gifu 505 0116, Japan
    Neurotoxicology 25:193-204. 2004
  10. ncbi request reprint Dopamine-derived endogenous N-methyl-(R)-salsolinol: its role in Parkinson's disease
    Makoto Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park, Mitake, 505 0116 Gifu, Japan
    Neurotoxicol Teratol 24:579-91. 2002

Collaborators

Detail Information

Publications35

  1. ncbi request reprint Monoamine oxidase inhibitors as neuroprotective agents in age-dependent neurodegenerative disorders
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, 1 1 Nakafudogaoka, Kakamigahara, Gifu 504 0838, Japan
    Curr Pharm Des 16:2799-817. 2010
    ....
  2. ncbi request reprint Neuroprotection by propargylamines in Parkinson's disease: intracellular mechanism underlying the anti-apoptotic function and search for clinical markers
    M Naoi
    Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm Suppl . 2007
    ..Products of cell survival-related gene induced by propargylamines may be applied as markers of neuroprotection in clinical samples...
  3. ncbi request reprint Involvement of type A monoamine oxidase in neurodegeneration: regulation of mitochondrial signaling leading to cell death or neuroprotection
    M Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm Suppl . 2006
    ..Future studies will clarify more detailed mechanism behind regulation of mitochondrial death signaling by MAO-A, and bring out new strategies to cure or ameliorate the decline of neurons in neurodegenerative disorders...
  4. doi request reprint Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm (Vienna) 116:1371-81. 2009
    ..This review discusses the new role of mitochondria in regulation of neuronal cell death of neurodegenerative disorders...
  5. doi request reprint Glutathione redox status in mitochondria and cytoplasm differentially and sequentially activates apoptosis cascade in dopamine-melanin-treated SH-SY5Y cells
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, 1 1 Nakafudogaoka, Kakamigahara, Gifu 504 0838, Japan
    Neurosci Lett 465:118-22. 2009
    ..The regulation of apoptotic processing by SH redox state is discussed in relation to degeneration of nigra-striatal DA neurons in aging and PD, where oxidative stress is increased with impaired antioxidant capacity...
  6. doi request reprint Functional mechanism of neuroprotection by inhibitors of type B monoamine oxidase in Parkinson's disease
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Kakamigahara, Gifu 504 0838, Japan
    Expert Rev Neurother 9:1233-50. 2009
    ..This review presents recent advances in our understanding of the neuroprotection offered by MAOB-Is and possible evaluation of neuroprotective efficacy in clinical samples is discussed...
  7. doi request reprint Neuromelanin selectively induces apoptosis in dopaminergic SH-SY5Y cells by deglutathionylation in mitochondria: involvement of the protein and melanin component
    Makoto Naoi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neurochem 105:2489-500. 2008
    ..The novel function of NM is discussed in relation to the pathogenesis of PD...
  8. ncbi request reprint Oxidative stress in mitochondria: decision to survival and death of neurons in neurodegenerative disorders
    Makoto Naoi
    Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    Mol Neurobiol 31:81-93. 2005
    ..The mechanism was proved to be the result of the modification of the 20S beta-subunit with acrolein and to the binding of other acrolein-modified proteins to the 20S beta-subunit...
  9. ncbi request reprint Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: occurrence, metabolism and function in human brains
    Makoto Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park, Matake, Gifu 505 0116, Japan
    Neurotoxicology 25:193-204. 2004
    ..These results are discussed in relation to role of dopamine-derived endogenous salsolinol derivatives as the regulators of neurotransmission, dopaminergic neurotoxins and neuro-hormonal transmitters in the human brain...
  10. ncbi request reprint Dopamine-derived endogenous N-methyl-(R)-salsolinol: its role in Parkinson's disease
    Makoto Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park, Mitake, 505 0116 Gifu, Japan
    Neurotoxicol Teratol 24:579-91. 2002
    ..In this article, we review the recent advance in proving our hypothesis that the dopamine-derived neurotoxin causes the selective depletion of dopamine neurons in PD...
  11. ncbi request reprint Mitochondria determine the survival and death in apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, and neuroprotection by propargylamines
    M Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Mitake, Gifu, Japan
    J Neural Transm (Vienna) 109:607-21. 2002
    ..These results indicate that mitochondria are the site to determine the cell death induced by neurotoxins and also the neuroprotection by anti-apoptotic propargylamines...
  12. ncbi request reprint Overexpression of amyloid precursor protein induces susceptibility to oxidative stress in human neuroblastoma SH-SY5Y cells
    K Matsumoto
    Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm (Vienna) 113:125-35. 2006
    ..These results indicate that increased expression of wild type APP renders neuronal cells more vulnerable to oxidative stress leading to cell death...
  13. ncbi request reprint N-Propargylamine protects SH-SY5Y cells from apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, through stabilization of mitochondrial membrane and induction of anti-apoptotic Bcl-2
    H Yi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neural Transm 113:21-32. 2006
    ..The anti-apoptotic function of N-propargylamine is discussed in terms of neuroprotection by propargylamines in neurodegenerative diseases, including Parkinson's disease...
  14. ncbi request reprint Cell death of dopamine neurons in aging and Parkinson's disease
    M Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Mitake, Gifu, Japan
    Mech Ageing Dev 111:175-88. 1999
    ..These results indicate that in aging and PD oxidative stress induces degeneration of dopamine neurons, and the antioxidant therapy may delay the decline of dopamine neurons in the brain...
  15. ncbi request reprint Apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, is mediated by activation of caspase 3
    Y Akao
    Gifu International Institute of Biotechnology, Mitake, Japan
    Neurosci Lett 267:153-6. 1999
    ..These results demonstrate that caspase 3 mediates apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, which may cause apoptotic cell death of dopamine neurons in Parkinson's disease...
  16. ncbi request reprint Anti-apoptotic function of L-(-)deprenyl (Selegiline) and related compounds
    M Naoi
    Institute of Applied Biochemistry, Mitake, Gifu, Japan
    Neurobiology (Bp) 8:69-80. 2000
    ..These results suggest that (-)deprenyl and related compounds may be applicable as neuroprotective agents in neurodegenerative diseases...
  17. ncbi request reprint Future of neuroprotection in Parkinson's disease
    M Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Gifu, Japan
    Parkinsonism Relat Disord 8:139-45. 2001
    ..These results suggest that propargylamines may rescue or protect dopamine neurons in Parkinson's disease...
  18. ncbi request reprint Apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopamine neurons
    M Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park, Mitake, Gifu, Japan
    Toxicology 153:123-41. 2000
    ..These results are discussed in relation to the role of apoptosis in neurodegenerative diseases and the involvement of the endogenous toxin in the pathogenesis of Parkinson's disease...
  19. ncbi request reprint Type A monoamine oxidase is the target of an endogenous dopaminergic neurotoxin, N-methyl(R)salsolinol, leading to apoptosis in SH-SY5Y cells
    Hong Yi
    Department of Neurosciences, Gifu International Institute of Biotechnology, Kakamigahara, Gifu, Japan
    J Neurochem 96:541-9. 2006
    ..These results demonstrate a novel function of MAO-A in the binding of neurotoxins and the induction of apoptosis, which may account for neuronal cell death in neurodegenerative disorders, including Parkinson's disease...
  20. ncbi request reprint Involvement of endogenous N-methyl(R)salsolinol in Parkinson's disease: induction of apoptosis and protection by (-)deprenyl
    M Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Mitake, Gifu, Japan
    J Neural Transm Suppl . 2000
    ..In Parkinson's disease apoptosis may be induced in dopamine neurons by this endogenous neurotoxin, and (-)deprenyl may protect them from apoptotic death process...
  21. ncbi request reprint A highly bioactive lignophenol derivative from bamboo lignin exhibits a potent activity to suppress apoptosis induced by oxidative stress in human neuroblastoma SH-SY5Y cells
    Yukihiro Akao
    Gifu International Institute of Biotechnology, Kakamigahara, Gifu 504 0838, Japan
    Bioorg Med Chem 12:4791-801. 2004
    ..These data suggest that lig-8 is a promising neuroprotector, which affects the signaling pathway of neuronal cell death and that it would be of benefit to delay the progress of neurodegenerative diseases...
  22. ncbi request reprint Gene therapy for mitochondrial disease by delivering restriction endonuclease SmaI into mitochondria
    Masashi Tanaka
    Department of Gene Therapy, Gifu International Institute of Biotechnology, Mitake, Japan
    J Biomed Sci 9:534-41. 2002
    ..Delivery of restriction enzymes into mitochondria is a novel strategy for gene therapy of a special form of mitochondrial diseases...
  23. ncbi request reprint A potent apoptosis-inducing activity of a sesquiterpene lactone, arucanolide, in HL60 cells: a crucial role of apoptosis-inducing factor
    Yoshihito Nakagawa
    Gifu International Institute of Biotechnology, Japan
    J Pharmacol Sci 97:242-52. 2005
    ..Taken together, the findings presented here indicate that arucanolide induced marked apoptosis in HL60 cells mainly by dissipating mitochondrial membrane potential, which would trigger AIF-induced apoptosis...
  24. ncbi request reprint Anti-apoptotic function of propargylamine inhibitors of type-B monoamine oxidase
    M Naoi
    Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park, Mitake, Kani gun, Gifu 505 0116, Japan
    Inflammopharmacology 11:175-81. 2003
    ..These results suggest that rasagiline and other propargylamines may regulate the apoptotic machinery in mitochondria and rescue or protect deteriorated neurons in neurodegenerative disorders...
  25. ncbi request reprint Mitochondrial permeability transition mediates apoptosis induced by N-methyl(R)salsolinol, an endogenous neurotoxin, and is inhibited by Bcl-2 and rasagiline, N-propargyl-1(R)-aminoindan
    Yukihiro Akao
    Gifu International Institute of Biotechnology and Department of Brain Sciences, Mitake, Gifu, Japan
    J Neurochem 82:913-23. 2002
    ..Altogether, mitochondrial PT plays a key role both in NM(R)Sal-induced cell death and the neuroprotective effect of rasagiline...
  26. doi request reprint Metabolites of sesamin, a major lignan in sesame seeds, induce neuronal differentiation in PC12 cells through activation of ERK1/2 signaling pathway
    Nanako Hamada
    Department of Longevity and Aging Research, Gifu International Institute of Biotechnology, 1 1 Naka fudogaoka, Kakamigahara, Gifu 504 0838, Japan
    J Neural Transm (Vienna) 116:841-52. 2009
    ..It is therefore concluded that SC-1 may promote neuronal differentiation by tapping into the ERK1/2-MAPK (mitogen-activated protein kinase) signaling pathway downstream from the TrkA receptor in PC12 cells...
  27. ncbi request reprint An anti-Parkinson's disease drug, N-propargyl-1(R)-aminoindan (rasagiline), enhances expression of anti-apoptotic bcl-2 in human dopaminergic SH-SY5Y cells
    Yukihiro Akao
    Gifu International Institute of Biotechnology, Mitake, Kani gun, Gifu, Japan
    Neurosci Lett 326:105-8. 2002
    ..Enhanced expression of bcl-2 family indicates the ability of rasagiline to adjust the apoptotic threshold and protect degenerating neurons in PD...
  28. ncbi request reprint Glyceraldehyde-3-phospate dehydrogenase is translocated into nuclei through Golgi apparatus during apoptosis induced by 6-hydroxydopamine in human dopaminergic SH-SY5Y cells
    Wakako Maruyama
    Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute for Longevity Sciences, Obu, Aichi 474 8522, Japan
    Neurosci Lett 321:29-32. 2002
    ..These results suggest that the Golgi apparatus may be involved in the compartmentalization of GAPDH from cytosol to nuclei...
  29. ncbi request reprint An inhibitor of mitochondrial complex I, rotenone, inactivates proteasome by oxidative modification and induces aggregation of oxidized proteins in SH-SY5Y cells
    Masayo Shamoto-Nagai
    Department of Basic Gerontology, National Institute for Longevity Sciences, Obu, Aichi, Japan
    J Neurosci Res 74:589-97. 2003
    ..This mechanism might account for the accumulation of modified protein and, at least partially, for cell death of the dopamine neurons in Parkinson's disease...
  30. ncbi request reprint Cell death in Parkinson's disease
    Wakako Maruyama
    Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, Institute for Longevity Sciences, Obu, Aichi, 474 8522, Japan
    J Neurol 249:II6-10. 2002
    ..N-Methyl( R)salsolinol induced apoptosis in human dopaminergic neuroblastoma cells. It was suggested that in the mitochondria there is a molecule which interacts with N-methyl( R)salsolinol and initiates an apoptotic signal...
  31. ncbi request reprint Neuroprotective function of R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane, [R-(-)-BPAP], against apoptosis induced by N-methyl(R)salsolinol, an endogenous dopaminergic neurotoxin, in human dopaminergic neuroblastoma SH-SY5Y cells
    Wakako Maruyama
    Department of Basic Gerontology, National Institute for Longevity Sciences, Obu, Aichi 474 8522, Japan
    Life Sci 75:107-17. 2004
    ..These results are discussed with the possible application of BPAP derivatives as neuroprotective agents in Parkinson's disease and other neurodegenerative disorders...
  32. ncbi request reprint Anti-apoptotic action of anti-Alzheimer drug, TV3326 [(N-propargyl)-(3R)-aminoindan-5-yl]-ethyl methyl carbamate, a novel cholinesterase-monoamine oxidase inhibitor
    Wakako Maruyama
    Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute for Longevity Sciences, Obu, Aichi, Japan
    Neurosci Lett 341:233-6. 2003
    ..This resulted in stabilization of the mitochondrial membrane potential, the collapse of which initiates the apoptotic cascade...
  33. ncbi request reprint N-Propargyl-1 (R)-aminoindan, rasagiline, increases glial cell line-derived neurotrophic factor (GDNF) in neuroblastoma SH-SY5Y cells through activation of NF-kappaB transcription factor
    Wakako Maruyama
    Department of Basic Gerontology, National Institute for Longevity Sciences, Gengo 36 3, Morioka chio, Obu Aichi 474 8522, Japan
    Neurochem Int 44:393-400. 2004
    ....
  34. ncbi request reprint Neuroprotection by propargylamines in Parkinson's disease: suppression of apoptosis and induction of prosurvival genes
    Wakako Maruyama
    Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute for Longevity Sciences, Obu, Aichi 474 8522, Japan
    Neurotoxicol Teratol 24:675-82. 2002
    ..Rasagiline and related propargylamines may rescue degenerating dopamine neurons through inhibiting death signal transduction initiated by mitochondria PT...
  35. ncbi request reprint Allicin inhibits cell growth and induces apoptosis through the mitochondrial pathway in HL60 and U937 cells
    Talia Miron
    Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel
    J Nutr Biochem 19:524-35. 2008
    ..The emerging mechanistic basis for the antiproliferative function of allicin, therefore, involves the activation of the mitochondrial apoptotic pathway by GSH depletion and by changes in the intracellular redox status...