C Behl

Summary

Affiliation: Max Planck Institute of Psychiatry
Country: Germany

Publications

  1. ncbi The female sex hormone oestrogen as a neuroprotectant
    C Behl
    Max Planck Institute of Psychiatry, Kraepelinstr 2 10, 80804 Munich, Germany
    Trends Pharmacol Sci 20:441-4. 1999
  2. ncbi Vitamin E protects neurons against oxidative cell death in vitro more effectively than 17-beta estradiol and induces the activity of the transcription factor NF-kappaB
    C Behl
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, Munich, Federal Republic of Germany
    J Neural Transm 107:393-407. 2000
  3. ncbi Apoptosis and Alzheimer's disease
    C Behl
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, Munich, Federal Republic of Germany
    J Neural Transm 107:1325-44. 2000
  4. ncbi Alzheimer's disease and oxidative stress: implications for novel therapeutic approaches
    C Behl
    Max Planck Institute of Psychiatry, Munich, Germany
    Prog Neurobiol 57:301-23. 1999
  5. ncbi Effects of glucocorticoids on oxidative stress-induced hippocampal cell death: implications for the pathogenesis of Alzheimer's disease
    C Behl
    Max Planck Institute of Psychiatry, Munich, Germany
    Exp Gerontol 33:689-96. 1998
  6. ncbi [Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection]
    C Behl
    Max Planck Institut fur Psychiatrie, Klinisches Institut, Munchen
    Fortschr Neurol Psychiatr 66:113-21. 1998
  7. ncbi Sex hormones, neuroprotection and cognition
    Christian Behl
    Max-Planck-Institute of Psychiatry, 80804 Munich, Germany
    Prog Brain Res 138:135-42. 2002
  8. ncbi Amyloid beta-protein toxicity and oxidative stress in Alzheimer's disease
    C Behl
    Max Planck Institute of Psychiatry, Clinical Institute, Kraepelinstr 2 10, D 80804 Munich, Germany
    Cell Tissue Res 290:471-80. 1997
  9. ncbi Oestrogen as a neuroprotective hormone
    Christian Behl
    Max Planck Institute of Psychiatry, 80804 Munich, Germany
    Nat Rev Neurosci 3:433-42. 2002
  10. ncbi Neuroprotection against oxidative stress by estrogens: structure-activity relationship
    C Behl
    Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany
    Mol Pharmacol 51:535-41. 1997

Collaborators

Detail Information

Publications43

  1. ncbi The female sex hormone oestrogen as a neuroprotectant
    C Behl
    Max Planck Institute of Psychiatry, Kraepelinstr 2 10, 80804 Munich, Germany
    Trends Pharmacol Sci 20:441-4. 1999
    ..Thus, oestrogen might represent a potential 'chemical shield' for neurones. In this article, some recent advances in the elucidation of oestrogen's beneficial activities on nerve cell survival are discussed...
  2. ncbi Vitamin E protects neurons against oxidative cell death in vitro more effectively than 17-beta estradiol and induces the activity of the transcription factor NF-kappaB
    C Behl
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, Munich, Federal Republic of Germany
    J Neural Transm 107:393-407. 2000
    ..These results may have implications regarding the prevention and treatment of oxidative stress-related degenerative disorders such as Alzheimer's disease...
  3. ncbi Apoptosis and Alzheimer's disease
    C Behl
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, Munich, Federal Republic of Germany
    J Neural Transm 107:1325-44. 2000
    ....
  4. ncbi Alzheimer's disease and oxidative stress: implications for novel therapeutic approaches
    C Behl
    Max Planck Institute of Psychiatry, Munich, Germany
    Prog Neurobiol 57:301-23. 1999
    ..reserved..
  5. ncbi Effects of glucocorticoids on oxidative stress-induced hippocampal cell death: implications for the pathogenesis of Alzheimer's disease
    C Behl
    Max Planck Institute of Psychiatry, Munich, Germany
    Exp Gerontol 33:689-96. 1998
    ..Therefore, age-related alterations of glucocorticoid homeostasis appear to enhance GR activation and may render hippocampal neurons more vulnerable to oxidative insults...
  6. ncbi [Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection]
    C Behl
    Max Planck Institut fur Psychiatrie, Klinisches Institut, Munchen
    Fortschr Neurol Psychiatr 66:113-21. 1998
    ....
  7. ncbi Sex hormones, neuroprotection and cognition
    Christian Behl
    Max-Planck-Institute of Psychiatry, 80804 Munich, Germany
    Prog Brain Res 138:135-42. 2002
  8. ncbi Amyloid beta-protein toxicity and oxidative stress in Alzheimer's disease
    C Behl
    Max Planck Institute of Psychiatry, Clinical Institute, Kraepelinstr 2 10, D 80804 Munich, Germany
    Cell Tissue Res 290:471-80. 1997
    ..The toxicity of the AD-associated amyloid beta-protein (Abeta), the induction of oxidative stress by Abeta in neurons, and potential sources of oxidative events in brain tissue are discussed...
  9. ncbi Oestrogen as a neuroprotective hormone
    Christian Behl
    Max Planck Institute of Psychiatry, 80804 Munich, Germany
    Nat Rev Neurosci 3:433-42. 2002
    ..Understanding the mechanisms of oestrogen action will be crucial to determine its potential as a therapeutic agent, particularly in the elderly...
  10. ncbi Neuroprotection against oxidative stress by estrogens: structure-activity relationship
    C Behl
    Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany
    Mol Pharmacol 51:535-41. 1997
    ..The neuroprotective antioxidant activity of estrogens is dependent on the presence of the hydroxyl group in the C3 position on the A ring of the steroid molecule but is independent of an activation of estrogen receptors...
  11. ncbi Antioxidant neuroprotection in Alzheimer's disease as preventive and therapeutic approach
    Christian Behl
    Max Planck Institute of Psychiatry, Munich, Germany
    Free Radic Biol Med 33:182-91. 2002
    ....
  12. ncbi Glucocorticoids enhance oxidative stress-induced cell death in hippocampal neurons in vitro
    C Behl
    Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany
    Endocrinology 138:101-6. 1997
    ..Our data suggest that changes in hippocampal GR homeostasis and regulation may render hippocampal neurons more vulnerable to oxidative stress-induced neuronal degeneration...
  13. ncbi Differential induction of NF-kappaB activity and neural cell death by antidepressants in vitro
    A Post
    Max Planck Institute of Psychiatry, Kraepelinstrasse 2 10, D 80804 Munich, Germany
    Eur J Neurosci 12:4331-7. 2000
    ..These results indicate that some antidepressant drugs may cause both oxidative stress and changes in cellular antioxidative capacity, resulting in altered NF-kappaB activity and, ultimately, cell death...
  14. ncbi Protective activity of aromatic amines and imines against oxidative nerve cell death
    B Moosmann
    Max-Planck-Institute of Psychiatry, Munich, Germany
    Biol Chem 382:1601-12. 2001
    ..We conclude that bridged bisarylimines with a single free NH-bond, such as iminostilbene, are superior neuroprotective antioxidants, and may be promising lead structures for rational drug development...
  15. ncbi Oxidative stress-resistant cells are protected against haloperidol toxicity
    C Behl
    Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany
    Brain Res 717:193-5. 1996
    ..This data strongly supports the causative involvement of free radicals in haloperidol-induced cell death...
  16. ncbi Estrogen induces a rapid secretion of amyloid beta precursor protein via the mitogen-activated protein kinase pathway
    D Manthey
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, Munich, Germany
    Eur J Biochem 268:4285-91. 2001
    ....
  17. ncbi Bcl-2 prevents hippocampal cell death induced by the neuroleptic drug haloperidol
    F Lezoualc'h
    Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany
    Brain Res 738:176-9. 1996
    ..We found that clonal mouse hippocampal cells stably transfected with the antioxidant Bcl-2 are protected against haloperidol toxicity. This data strongly supports the causative involvement of free radicals in haloperidol toxicity...
  18. ncbi [Estrogens against Alzheimer disease? The female sexual hormone as a protective neurohormone]
    C Behl
    Max Planck Institut fur Psychiatrie, Munchen
    MMW Fortschr Med 143:33-5. 2001
    ..But on the basis of the current knowledge, estrogen is not a drug for the treatment of an already ongoing Alzheimer's disease process...
  19. ncbi Expression of the trefoil polypeptide ITF in PC12 cells
    J C Probst
    Max Planck Institute of Psychiatry, Department of Neuroendocrinology, Munich, Germany
    Biochem Mol Biol Int 42:425-32. 1997
    ....
  20. ncbi Soluble tumor necrosis factor receptor (p75) does not attenuate the sleep changes induced by lipopolysaccharide in the rat during the dark period
    M Lancel
    Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany
    Brain Res 770:184-91. 1997
    ....
  21. ncbi Human Nck-associated protein 1 and its binding protein affect the metabolism of beta-amyloid precursor protein with Swedish mutation
    A Yamamoto
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, D-80804 Munich, Germany
    Neurosci Lett 316:50-4. 2001
    ..Furthermore, neither human Nap1 nor hNap1BP influenced the ratio of Abeta42/43 to total Abeta. Taken together, human Nap1 and hNap1BP may play a role in regulation of beta-secretase activity in the processing of betaAPP...
  22. ncbi The orthologous human and murine semaphorin 6A-1 proteins (SEMA6A-1/Sema6A-1) bind to the enabled/vasodilator-stimulated phosphoprotein-like protein (EVL) via a novel carboxyl-terminal zyxin-like domain
    A Klostermann
    MPI of Psychiatry, Independent Research Group Neurodegeneration, Kraepelinstrasse 2, 80804 Munich, Germany
    J Biol Chem 275:39647-53. 2000
    ..In addition these findings suggest a completely new role for transmembranous semaphorins such as SEMA6A-1/Sema6A-1 in retrograde signaling...
  23. ncbi Brain region-specific neuroprotective action and signaling of corticotropin-releasing hormone in primary neurons
    Nadhim Bayatti
    Independent Research Group Neurodegeneration, Max Planck Institute of Psychiatry, 80804 Munich, Germany Chemistry and Pathobiochemistry, Johannes Gutenberg University Mainz, 55099 Mainz, Germany
    Endocrinology 144:4051-60. 2003
    ..Differences in signaling were found to be independent of receptor expression levels because RT-PCR analysis indicated no region-specific differences in CRHR1 mRNA expression...
  24. ncbi Concepts for the treatment of Alzheimer's disease: molecular mechanisms and clinical application
    Claus Pietrzik
    Department of Molecular Neurodegeneration, Institute for Physiological Chemistry and Pathochemistry, Johannes Gutenberg-University Mainz, Medical School, 55099 Mainz, Germany
    Int J Exp Pathol 86:173-85. 2005
    ..Additionally, we summarize some of the experimental approaches in AD therapy, which might lead to the development of more promising drugs in the future...
  25. ncbi Estrogen can protect neurons: modes of action
    Christian Behl
    MPI of Psychiatry, D 80804 Munich, Germany
    J Steroid Biochem Mol Biol 83:195-7. 2002
    ..The various modes of action of estrogen via receptor activation and in a non-receptor fashion are currently under intensive investigation...
  26. ncbi Neuroprotective strategies in Alzheimer's disease
    Christian Behl
    Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany
    Adv Exp Med Biol 513:475-96. 2002
  27. ncbi Oxidative nerve cell death in Alzheimer's disease and stroke: antioxidants as neuroprotective compounds
    Christian Behl
    Max-Planck-Institute of Psychiatry, Munich, Germany
    Biol Chem 383:521-36. 2002
    ..Finally, an outlook is given on the neuroprotective potential of aromatic amines and imines, which may comprise novel lead structures for antioxidant drug design...
  28. ncbi Oestrogen receptor subtype-specific repression of calpain expression and calpain enzymatic activity in neuronal cells--implications for neuroprotection against Ca-mediated excitotoxicity
    Martin Gamerdinger
    Department of Pathobiochemistry, Medical School, Johannes Gutenberg University, Mainz, Germany
    J Neurochem 97:57-68. 2006
    ....
  29. ncbi Neuroprotective properties of cannabinoids against oxidative stress: role of the cannabinoid receptor CB1
    Giovanni Marsicano
    Department of Molecular Genetics of Behavior, Max Planck Institute of Psychiatry, Munich, Germany
    J Neurochem 80:448-56. 2002
    ..The results strongly suggest that CB1 is not involved in the cellular antioxidant neuroprotective effects of cannabinoids...
  30. ncbi Oxidative stress in Alzheimer's disease: implications for prevention and therapy
    Christian Behl
    Institute for Physiological Chemistry and Pathobiochemistry, Faculty of Medicine, Johannes Gutenberg University, Mainz, D-55099 Mainz, Germany
    Subcell Biochem 38:65-78. 2005
    ..Nevertheless, the exact molecular mechanisms and the real impact of oxidative stress on the development and progression of Alzheimer's Disease as well as of other neurodegenerative disorders still needs to be further investigated...
  31. ncbi The search for novel avenues for the therapy and prevention of Alzheimer's disease
    Christian Behl
    Institute for Physiological Chemistry and Pathobiochemistry, Johannes Gutenberg University Mainz, Medical School, Mainz, Germany
    Drug News Perspect 19:5-12. 2006
    ....
  32. ncbi The neuroprotective actions of corticotropin releasing hormone
    Nadhim Bayatti
    Neural Development, Plasticity and Repair, Sir James Spence Institute (Child Health, School of Clinical Medical Sciences, University of Newcastle-upon-Tyne, Newcastle-upon-Tyne, NE1 4LP, UK
    Ageing Res Rev 4:258-70. 2005
    ..Taken together, an impressive amount of evidence has accumulated recently, highlighting this new and potentially important function of CRH...
  33. ncbi O-glycosylation of the tail domain of neurofilament protein M in human neurons and in spinal cord tissue of a rat model of amyotrophic lateral sclerosis (ALS)
    Nina Lüdemann
    Department of Neurobiology, University of Osnabruck, Barbarastrasse 11, D 49076 Osnabrück
    J Biol Chem 280:31648-58. 2005
    ....
  34. ncbi Cholesterol-like effects of selective cyclooxygenase inhibitors and fibrates on cellular membranes and amyloid-beta production
    Martin Gamerdinger
    Department of Pathobiochemistry, Medical School, Johannes Gutenberg University, Mainz, Germany
    Mol Pharmacol 72:141-51. 2007
    ....
  35. ncbi Corticotropin-releasing hormone-mediated induction of intracellular signaling pathways and brain-derived neurotrophic factor expression is inhibited by the activation of the endocannabinoid system
    Nadhim Bayatti
    Department of Pathobiochemistry, Johannes Gutenberg University Mainz Medical School, 55099 Mainz, Germany
    Endocrinology 146:1205-13. 2005
    ..Thus, these data highlight an interaction between the CRH and the cannabinoid system in the regulation of BDNF expression by influencing cAMP and Ca2+ signaling pathways...
  36. ncbi High-throughput functional genomics identifies genes that ameliorate toxicity due to oxidative stress in neuronal HT-22 cells: GFPT2 protects cells against peroxide
    Jürgen Zitzler
    Xantos Biomedicine AG, Max Lebsche Platz 31, D 81377 Munich, Germany
    Mol Cell Proteomics 3:834-40. 2004
    ..Thus, GFPT appears to be conserved among yeast and men as a critical target of methylmercury and ROS-induced cytotoxicity...
  37. ncbi Inhibition of glycogen synthase kinase 3 beta is involved in the resistance to oxidative stress in neuronal HT22 cells
    Monika Schäfer
    Independent Research Group Neurodegeneration, Max Planck Institute for Psychiatry, Munich, Germany
    Brain Res 1005:84-9. 2004
    ....
  38. ncbi CB1 cannabinoid receptors and on-demand defense against excitotoxicity
    Giovanni Marsicano
    Molecular Genetics of Behaviour, Max Planck Institute of Psychiatry, Kraepelinstrabetae 2 10, 80804 Munich, Germany
    Science 302:84-8. 2003
    ..These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons...
  39. ncbi Functional interaction of estrogen receptor alpha and caveolin isoforms in neuronal SK-N-MC cells
    Jürgen Zschocke
    Institute of Physiological Chemistry and Pathobiochemistry, Johannes Gutenberg University, 55099 Mainz, Germany
    J Steroid Biochem Mol Biol 84:167-70. 2003
    ..In conclusion, our observations provide a possible mechanism of negative feedback regulation of ERalpha co-activator caveolin by the steroid receptor itself in this cellular model...
  40. ncbi Antioxidants as treatment for neurodegenerative disorders
    Bernd Moosmann
    Center for Neuroscience and Aging, The Burnham Institute, La Jolla, CA 92037, USA
    Expert Opin Investig Drugs 11:1407-35. 2002
    ..Finally, an outlook as to which direction antioxidant drug development and clinical practice may be leading to in the near future will be provided...
  41. ncbi Estrogen receptor alpha-mediated silencing of caveolin gene expression in neuronal cells
    Jürgen Zschocke
    Neurodegeneration Group, Max Planck Institute of Psychiatry, 80804 Munich, Germany
    J Biol Chem 277:38772-80. 2002
    ..The observed mechanism of gene silencing by ER alpha may have implications for the transcriptional regulation of further ER alpha target genes...
  42. ncbi Secretory peptide hormones are biochemical antioxidants: structure-activity relationship
    Bernd Moosmann
    Max Planck Institute of Psychiatry, Munich, Germany
    Mol Pharmacol 61:260-8. 2002
    ....
  43. ncbi Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption
    Christoph R W Kuhlmann
    Institute of Physiology and Pathophysiology, Johannes Gutenberg University of Mainz, Mainz, Germany
    J Neurochem 102:501-7. 2007
    ..Furthermore, ML-7 and apocynin blocked hypoxia-dependent phosphorylation of MLC. Our data demonstrate that hypoxia causes a breakdown of the BBB in vitro and in vivo involving ROS and the contractile machinery...