A Takashima

Summary

Affiliation: RIKEN Brain Science Institute
Country: Japan

Publications

  1. ncbi request reprint Tau aggregation is a therapeutic target for Alzheimer's disease
    A Takashima
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 351 0198, Japan
    Curr Alzheimer Res 7:665-9. 2010
  2. ncbi request reprint [Drug development for tauopathy and Alzheimer's disease]
    Akihiko Takashima
    Brain Science Institute, RIKEN, Wako, Japan
    Nihon Shinkei Seishin Yakurigaku Zasshi 30:177-80. 2010
  3. ncbi request reprint GSK-3 is essential in the pathogenesis of Alzheimer's disease
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN, Brain Science Institute, 2 1 Hirosawa, Wako si, Saitama 351 0198, Japan
    J Alzheimers Dis 9:309-17. 2006
  4. doi request reprint Amyloid-beta, tau, and dementia
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako, Saitama, Japan
    J Alzheimers Dis 17:729-36. 2009
  5. ncbi request reprint Activation of tau protein kinase I/glycogen synthase kinase-3beta by amyloid beta peptide (25-35) enhances phosphorylation of tau in hippocampal neurons
    A Takashima
    Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan
    Neurosci Res 31:317-23. 1998
  6. ncbi request reprint Involvement of cyclin dependent kinase5 activator p25 on tau phosphorylation in mouse brain
    A Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, 2 1 Hirosawa, Wako Shi, 351 0198, Saitama, Japan
    Neurosci Lett 306:37-40. 2001
  7. ncbi request reprint Direct association of presenilin-1 with beta-catenin
    M Murayama
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, Saitama, Japan
    FEBS Lett 433:73-7. 1998
  8. ncbi request reprint Familial Alzheimer's disease-associated mutations block translocation of full-length presenilin 1 to the nuclear envelope
    T Honda
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 351 0198, Saitama, Japan
    Neurosci Res 37:101-11. 2000
  9. ncbi request reprint Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100
    X Sun
    Lab for Alzheimer s Disease, The Brain Science Institute of RIKEN, 2 1 Hirosawa, Wako, 351 0198 Saitama, Japan
    Neurosci Lett 321:61-4. 2002
  10. pmc Presenilin 1 associates with glycogen synthase kinase-3beta and its substrate tau
    A Takashima
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 350 01, Japan
    Proc Natl Acad Sci U S A 95:9637-41. 1998

Collaborators

Detail Information

Publications52

  1. ncbi request reprint Tau aggregation is a therapeutic target for Alzheimer's disease
    A Takashima
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 351 0198, Japan
    Curr Alzheimer Res 7:665-9. 2010
    ..Therefore, inhibition of tau aggregation and tau phosphorylation is expected to prevent synapse loss and neuron loss, and may slow or halt the progressive dementia in AD...
  2. ncbi request reprint [Drug development for tauopathy and Alzheimer's disease]
    Akihiko Takashima
    Brain Science Institute, RIKEN, Wako, Japan
    Nihon Shinkei Seishin Yakurigaku Zasshi 30:177-80. 2010
    ..Therefore, inhibition of oligomer tau, and granular tau aggregation is expected to block the progression of AD symptoms by preventing synapse loss and neuronal loss...
  3. ncbi request reprint GSK-3 is essential in the pathogenesis of Alzheimer's disease
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN, Brain Science Institute, 2 1 Hirosawa, Wako si, Saitama 351 0198, Japan
    J Alzheimers Dis 9:309-17. 2006
    ..Therefore, therapeutics targeted to inhibiting GSK-3 may be beneficial in the treatment of this devastating disease...
  4. doi request reprint Amyloid-beta, tau, and dementia
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako, Saitama, Japan
    J Alzheimers Dis 17:729-36. 2009
    ....
  5. ncbi request reprint Activation of tau protein kinase I/glycogen synthase kinase-3beta by amyloid beta peptide (25-35) enhances phosphorylation of tau in hippocampal neurons
    A Takashima
    Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan
    Neurosci Res 31:317-23. 1998
    ..Treatment with TPK I/GSK-3beta antisense oligonucleotide inhibited the enhancement of tau phosphorylation induced by Abeta(25-35) exposure. Thus, TPK I/GSK-3beta activation by Abeta(25-35) may lead to extensive tau phosphorylation...
  6. ncbi request reprint Involvement of cyclin dependent kinase5 activator p25 on tau phosphorylation in mouse brain
    A Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, 2 1 Hirosawa, Wako Shi, 351 0198, Saitama, Japan
    Neurosci Lett 306:37-40. 2001
    ..The feature of these mice was the progression of cell growth in pituitary gland. These results suggest that overexpression of p25 lead to the activation of cell cycle but not to the direct phosphorylation of tau...
  7. ncbi request reprint Direct association of presenilin-1 with beta-catenin
    M Murayama
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, Saitama, Japan
    FEBS Lett 433:73-7. 1998
    ..These results indicate that PSI plays a role as inhibitor of the beta-catenin signal, which may be connected with the AD dysfunction...
  8. ncbi request reprint Familial Alzheimer's disease-associated mutations block translocation of full-length presenilin 1 to the nuclear envelope
    T Honda
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 351 0198, Saitama, Japan
    Neurosci Res 37:101-11. 2000
    ..However, PS1 with familial Alzheimer's disease-associated mutations could not translocate to the nuclear envelope, and both the full-length and processed mutants were co-localized in the ER...
  9. ncbi request reprint Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100
    X Sun
    Lab for Alzheimer s Disease, The Brain Science Institute of RIKEN, 2 1 Hirosawa, Wako, 351 0198 Saitama, Japan
    Neurosci Lett 321:61-4. 2002
    ....
  10. pmc Presenilin 1 associates with glycogen synthase kinase-3beta and its substrate tau
    A Takashima
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 350 01, Japan
    Proc Natl Acad Sci U S A 95:9637-41. 1998
    ..We propose that the increased association of GSK-3beta with mutant PS1 leads to increased phosphorylation of tau...
  11. ncbi request reprint Characterization of tau phosphorylation in glycogen synthase kinase-3beta and cyclin dependent kinase-5 activator (p23) transfected cells
    G Michel
    Mitsubishi Kasei Institute of Life Sciences, 11 Minamiooya, Machida shi, Tokyo 194, Japan
    Biochim Biophys Acta 1380:177-82. 1998
    ..Triplicated transfection resulted in phosphorylation of tau at 8 observed sites (Ser-199, Ser-202, Thr-205, Thr-231, Ser-235, Ser-396, Ser-404, and Ser-413)...
  12. ncbi request reprint Impaired proteolytic processing of presenilin-1 in chromosome 14-linked familial Alzheimer's disease patient lymphocytes
    H Takahashi
    Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan
    Neurosci Lett 260:121-4. 1999
    ..This result suggests that impaired proteolysis of PS1 may be associated with the pathogenesis of FAD. Moreover, our simple test using lymphocytes from FAD patients might be useful from a diagnostic point of view...
  13. ncbi request reprint New insights on how metals disrupt amyloid beta-aggregation and their effects on amyloid-beta cytotoxicity
    Y Yoshiike
    Laboratory for Alzheimer's Disease, Brain Science Institute, RIKEN, Wako, Saitama 351-0198, Japan
    J Biol Chem 276:32293-9. 2001
    ....
  14. ncbi request reprint Formation of filamentous tau aggregations in transgenic mice expressing V337M human tau
    K Tanemura
    Laboratory for Alzheimer's Disease, Neural Architecture, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama, 351-0198, Japan
    Neurobiol Dis 8:1036-45. 2001
    ..These mice, therefore, provide a preclinical model for the testing of therapeutic drugs for the treatment of neurodegenerative disorders that exhibit NFTs...
  15. ncbi request reprint Tau oligomerization: a role for tau aggregation intermediates linked to neurodegeneration
    N Sahara
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama 351 0198, Japan
    Curr Alzheimer Res 5:591-8. 2008
    ..Here, we review the latest developments in tracking the structural changes of tau protein and discuss the utility improving our understanding of tau aggregation pathway leading to human tauopathies...
  16. ncbi request reprint Cloning of cDNA and expression of the gene encoding rat presenilin-2
    H Takahashi
    Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan
    Gene 197:383-7. 1997
    ..During brain development, the expression level of both PS-2 and PS-1 increased but decreased in the adult. No remarkable change was observed in neural differentiation of PC12 cells...
  17. ncbi request reprint Nontoxic amyloid beta peptide 1-42 suppresses acetylcholine synthesis. Possible role in cholinergic dysfunction in Alzheimer's disease
    M Hoshi
    Mitsubishi Kasei Institute of Life Sciences, 11 Minamiooya, Machida shi, Tokyo 194, Japan
    J Biol Chem 272:2038-41. 1997
    ..H., Ball, M. J., and Roher, A. E. (1996) J. Biol. Chem. 271, 4077-4081). This increase in soluble Abeta1-42 may disturb cholinergic function, leading to the deterioration of memory and cognitive function that is characteristic of AD...
  18. ncbi request reprint Possible role of tau protein kinases in pathogenesis of Alzheimer's disease
    K Imahori
    Mitsubishi Kasei Institute of Life Sciences, Machida, Tokyo, Japan
    Neurobiol Aging 19:S93-8. 1998
    ..Indeed, when septum cells were treated with Abeta, the level of acetyl choline decreased dramatically...
  19. ncbi request reprint [Significance of tau in the development of Alzheimer's disease]
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN, Brain Science Institute, Wako Shi, Saitama, Japan
    Brain Nerve 62:701-8. 2010
    ..Therefore, inhibition of tau aggregation and tau phosphorylation is expected to prevent synapse loss and neuron loss, which may halt progressive dementia in AD...
  20. ncbi request reprint Hyperphosphorylated tau is a cause of neuronal dysfunction in tauopathy
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama, Japan
    J Alzheimers Dis 14:371-5. 2008
    ..Recent studies suggest that, before forming fibrils but after becoming hyperphosphorylated, tau is involved in neurodegenerative disease...
  21. doi request reprint Active c-jun N-terminal kinase induces caspase cleavage of tau and additional phosphorylation by GSK-3beta is required for tau aggregation
    Naruhiko Sahara
    Laboratory for Alzheimer Disease, RIKEN Brain Science Institute, Wako Shi, Saitama 351 0198, Japan
    Eur J Neurosci 27:2897-906. 2008
    ....
  22. pmc Hyperphosphorylated tau in parahippocampal cortex impairs place learning in aged mice expressing wild-type human tau
    Tetsuya Kimura
    Laboratorty for Alzheimer s Disease, RIKEN Brain Science Institute, Wako, Saitama, Japan
    EMBO J 26:5143-52. 2007
    ..Thus, the accumulation of hyperphosphorylated tau that occurs before NFT formation in entorhinal cortex may contribute to the memory problems seen in Alzheimer's disease (AD)...
  23. ncbi request reprint Molecular chaperone-mediated tau protein metabolism counteracts the formation of granular tau oligomers in human brain
    N Sahara
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama, Japan
    J Neurosci Res 85:3098-108. 2007
    ..This is expressed pathologically as an early sign of NFT formation. The molecular basis of chaperone-mediated protection against neurodegeneration might lead to the development of therapeutics for tauopathies. (c) 2007 Wiley-Liss, Inc...
  24. doi request reprint Microtubule destruction induces tau liberation and its subsequent phosphorylation
    Tomohiro Miyasaka
    Laboratory for Alzheimer s Disease, Brain Science Institute, The Institute of Physical and Chemical Research RIKEN, Wako Shi, Saitama, Japan
    FEBS Lett 584:3227-32. 2010
    ..In contrast, c-Jun N-terminal kinase activation, or phosphatase inhibition, led to significant tau phosphorylation without affecting MT structure. These findings suggest that MT disruption induces subsequent tau phosphorylation...
  25. pmc Aggregation of detergent-insoluble tau is involved in neuronal loss but not in synaptic loss
    Tetsuya Kimura
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako, Saitama 351 0198, Japan
    J Biol Chem 285:38692-9. 2010
    ..Finally, increasing concentrations of insoluble tau aggregates leads to the formation of fibrillar tau, which causes NFTs to form...
  26. pmc Tau filament formation and associative memory deficit in aged mice expressing mutant (R406W) human tau
    Yoshitaka Tatebayashi
    Laboratory for Alzheimer s Disease and Neural Architecture, Brain Science Institute, Institute of Physical and Chemical Research RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 351 0198, Japan
    Proc Natl Acad Sci U S A 99:13896-901. 2002
    ....
  27. ncbi request reprint Formation of tau inclusions in knock-in mice with familial Alzheimer disease (FAD) mutation of presenilin 1 (PS1)
    Kentaro Tanemura
    Laboratory for Alzheimer Disease and Neural Architecture, Brain Science Institute, RIKEN, Wako, Saitama 351 0198, Japan
    J Biol Chem 281:5037-41. 2006
    ....
  28. ncbi request reprint Aberrant tau phosphorylation by glycogen synthase kinase-3beta and JNK3 induces oligomeric tau fibrils in COS-7 cells
    Shinji Sato
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako Shi, Saitama 351 0198, Japan
    J Biol Chem 277:42060-5. 2002
    ..These results suggest that aberrant tau phosphorylation by the combination of these kinases may be involved in "pretangle," oligomeric tau fibril formation in vivo...
  29. ncbi request reprint Mitochondrial dysfunction and tau hyperphosphorylation in Ts1Cje, a mouse model for Down syndrome
    Ebrahim Abdul Shukkur
    Laboratory for Neurogenetics, RIKEN Brain Science Institute, Saitama, Japan
    Hum Mol Genet 15:2752-62. 2006
    ....
  30. ncbi request reprint Three-dimensional structures of the amyloid beta peptide (25-35) in membrane-mimicking environment
    T Kohno
    Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan
    Biochemistry 35:16094-104. 1996
    ..The structural comparison of amyloid beta peptide (25-35), its non-neurotoxic mutant and substance P gives a structural basis to understand the mechanism of neurotoxicity caused by amyloid beta peptide...
  31. ncbi request reprint Molecular cloning and expression of the rat homologue of presenilin-1
    H Takahashi
    Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan
    Neurosci Lett 206:113-6. 1996
    ..We found one transcript of the PS-1 gene in embryonic day 12 (E12)-E15 rat brain and two transcripts in E18-adult rat brain. Therefore, PS-1 may play a role in neurogenesis...
  32. ncbi request reprint Granular tau oligomers as intermediates of tau filaments
    Sumihiro Maeda
    Lab for Alzheimer s Disease, RIKEN Brain Science Institute, 2 1 Hirosawa, Wako, Saitama 351 0198, Japan
    Biochemistry 46:3856-61. 2007
    ..Thus, granular tau aggregates may be a relevant marker for the early diagnosis of tauopathy. Reducing the level of these aggregates may be a promising therapy for tauopathies and for promoting healthy brain aging...
  33. ncbi request reprint [Neurofibrillary tangles and neurodegenerative disease]
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosawa, Wako, Saitama 358 0198
    Seikagaku 74:461-70. 2002
  34. ncbi request reprint Aluminum induces tau aggregation in vitro but not in vivo
    Tatsuya Mizoroki
    Laboratory for Alzheimer Disease, Brain Science Institute, RIKEN, Wako, Saitama 351 0198, Japan
    J Alzheimers Dis 11:419-27. 2007
    ..These results indicate that Al has no direct link to AD pathology...
  35. ncbi request reprint Increased levels of granular tau oligomers: an early sign of brain aging and Alzheimer's disease
    Sumihiro Maeda
    Lab for Alzheimer s Disease, Brain Science Institute, RIKEN, 2 1 Hirosaswa, Wako, Saitama 351 0198, Japan
    Neurosci Res 54:197-201. 2006
    ..Thus, increases in granular tau oligomer levels may represent a very early sign of NFT formation and AD...
  36. ncbi request reprint In vivo evidence of CHIP up-regulation attenuating tau aggregation
    Naruhiko Sahara
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Saitama, Japan
    J Neurochem 94:1254-63. 2005
    ..If confirmed, this would indicate that the quality-control machinery in a neuron might play an important role in retarding the pathogenesis of tauopathies...
  37. ncbi request reprint Drug development targeting the glycogen synthase kinase-3beta (GSK-3beta)-mediated signal transduction pathway: role of GSK-3beta in adult brain
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Japan
    J Pharmacol Sci 109:174-8. 2009
    ..Further analysis indicated that GSK+/- mice had impaired memory reconsolidation but normal memory consolidation. Therefore, we concluded that GSK-3beta activation is required for memory reconsolidation in the adult brain...
  38. pmc GABA(A) receptor-mediated acceleration of aging-associated memory decline in APP/PS1 mice and its pharmacological treatment by picrotoxin
    Yuji Yoshiike
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama, Japan
    PLoS ONE 3:e3029. 2008
    ....
  39. ncbi request reprint Loss of M5 muscarinic acetylcholine receptors leads to cerebrovascular and neuronal abnormalities and cognitive deficits in mice
    Runa Araya
    Yamada Research Unit, RIKEN Brain Science Institute, Saitama 351 0198, Japan
    Neurobiol Dis 24:334-44. 2006
    ..The M5 receptor may represent an attractive novel therapeutic target to ameliorate memory deficits caused by impaired cerebrovascular function...
  40. ncbi request reprint c-jun N-terminal kinase hyperphosphorylates R406W tau at the PHF-1 site during mitosis
    Yoshitaka Tatebayashi
    Laboratory for Alzheimer s Disease, Brain Science Institute, The Institute of Physical and Chemical Research RIKEN, Saitama, Japan
    FASEB J 20:762-4. 2006
    ....
  41. ncbi request reprint Failure to support a genetic contribution of AKT1 polymorphisms and altered AKT signaling in schizophrenia
    Masayuki Ide
    Laboratory for Molecular Psychiatry, RIKEN Brain Science Institute, Saitama, Japan
    J Neurochem 99:277-87. 2006
    ..Collectively, this study failed to support reduced signaling of the AKT-GSK3beta molecular cascade in schizophrenia...
  42. ncbi request reprint Amino- and carboxyl-terminal mutants of presenilin 1 cause neuronal cell death through distinct toxic mechanisms: Study of 27 different presenilin 1 mutants
    Yuichi Hashimoto
    Department of Pharmacology, Keio University School of Medicine, Tokyo, Japan
    J Neurosci Res 75:417-28. 2004
    ....
  43. ncbi request reprint Insulin dysfunction induces in vivo tau hyperphosphorylation through distinct mechanisms
    Emmanuel Planel
    Laboratory for Alzheimer s Disease, The Institute of Physical and Chemical Research, Saitama 351 0198, Japan
    J Neurosci 27:13635-48. 2007
    ....
  44. pmc GSK-3beta is required for memory reconsolidation in adult brain
    Tetsuya Kimura
    Lab for Alzheimer s Disease, RIKEN Brain Science Institute, Wako, Saitama, Japan
    PLoS ONE 3:e3540. 2008
    ..Intraperitoneal injection of a GSK-3 inhibitor before memory reactivation impaired memory reconsolidation in WT mice. These results suggest that memory reconsolidation requires activation of GSK-3beta in the adult brain...
  45. ncbi request reprint Assembly of two distinct dimers and higher-order oligomers from full-length tau
    Naruhiko Sahara
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama, Japan
    Eur J Neurosci 25:3020-9. 2007
    ..The levels of these dimers may be used to gauge the potential for tau assembly...
  46. ncbi request reprint Intracellular Abeta is increased by okadaic acid exposure in transfected neuronal and non-neuronal cell lines
    Xiaoyan Sun
    Laboratory for Alzheimer s Disease, Brain Science Institute of the RIKEN, 2 1 Hirosawa, Wako, 351 0198, Saitama, Japan
    Neurobiol Aging 23:195-203. 2002
    ..The increased full-length APP and decreased APPC99 were also observed. This is the first study to demonstrate that OA treatment significantly increases intracellular Abeta...
  47. ncbi request reprint Specific compositions of amyloid-beta peptides as the determinant of toxic beta-aggregation
    Yuji Yoshiike
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, 2 1 Hirosawa, Wako Shi, Saitama, 351 0198, Japan
    J Biol Chem 278:23648-55. 2003
    ..These results may introduce a new therapeutic approach through the disruption of this balance...
  48. doi request reprint Enzymatic characteristics of I213T mutant presenilin-1/gamma-secretase in cell models and knock-in mouse brains: familial Alzheimer disease-linked mutation impairs gamma-site cleavage of amyloid precursor protein C-terminal fragment beta
    Masafumi Shimojo
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama 351 0198, Japan
    J Biol Chem 283:16488-96. 2008
    ..Our results also provide novel insight into how enhancing the generation of longer Abetas may contribute to Alzheimer disease onset...
  49. ncbi request reprint [Animal model for Alzheimer's disease]
    Akihiko Takashima
    Laboratory for Alzheimer s Disease, Brain Science Institute, RIKEN
    Nihon Rinsho 62:240-7. 2004
  50. ncbi request reprint Decreased Abeta secretion by cells expressing familial Alzheimer's disease-linked mutant presenilin 1
    Masafumi Shimojo
    Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Wako Shi, Saitama, Japan
    Neurosci Res 57:446-53. 2007
    ..The elevated Abeta42/Abeta40 ratio observed with mutant PS1-expressing cells may be due to reduced Abeta40 production not increased Abeta42 production...
  51. ncbi request reprint Electrical stimulation modulates fate determination of differentiating embryonic stem cells
    Masahisa Yamada
    Laboratory for Cell Culture Development, Yamada Research Unit, Molecular Neuropathology Group, Institute of Physical and Chemical Research, Saitama 351 0198, Japan
    Stem Cells 25:562-70. 2007
    ..This phenomenon opens up possibilities for understanding novel mechanisms underlying cellular differentiation and early development, and, perhaps more importantly, suggests possibilities for treatments in medical contexts...
  52. pmc Beneficial effects of estrogen in a mouse model of cerebrovascular insufficiency
    Naohito Kitamura
    Yamada Research Unit, RIKEN Brain Science Institute, Saitama, Japan
    PLoS ONE 4:e5159. 2009
    ....