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Researcher Profile - Hans W. Moises |
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| First Name: | Hans W. | | Last Name: | Moises | | Title: | Professor | | Advanced Degrees: | M.D. | Country/Territory: | Germany |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 24 January 2006]
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View all comments by Hans W. Moises
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Attention-deficit hyperactivity disorder (ADHD, ADD) , Bipolar disorder , Borderline personality disorder, Anxiety disorders , Psychology, Schizophrenia
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Bioinformatics/Statistics, Genetics, Animal models, Neuroanatomy/Systems Neuroscience, Glia/myelin
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Master of Medicine, University of Heidelberg (Germany); Pre- and postdoctoral Research Fellow, Central Institute of Mental Health (Germany); Doctor of Medicine, University of Heidelberg (Germany), Postdoctoral Fellow in Genetics - Molecular Genetics at the Department of Genetics, Stanford University, Stanford (USA); Director of Molecular Genetics Laboratory at the Department of Psychiatry, Kiel University Hospital (Germany); Professor of Psychiatry, University of Kiel (Germany).
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Moises HW, Gottesman II. Does glial asthenia predispose to schizophrenia? Arch Gen Psychiatry. 2004;61:1170. PMID: 15520365
Moises HW, Zoega T, Gottesman II. The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia. BMC Psychiatry. 2002 ;2:8. PMID: 12095426 http://www.biomedcentral.com/1471-244X/2/8
Moises HW, Frieboes RM, Spelzhaus P, Yang L, Kohnke M, Herden-Kirchhoff O, Vetter P, Neppert J, Gottesman II. No association between dopamine D2 receptor gene (DRD2) and human intelligence.
J Neural Transm. 2001;108:115-21. PMID: 11261743
Folster-Holst R, Moises HW, Yang L, Fritsch W, Weissenbach J, Christophers E. Linkage between atopy and the IgE high-affinity receptor gene at 11q13 in atopic dermatitis families. Hum Genet. 1998;102:236-9. PMID: 9521597
Moises HW, Yang L, Kristbjarnarson H, Wiese C, Byerley W, Macciardi F, Arolt V, Blackwood D, Liu X, Sjogren B, et al. An international two-stage genome-wide search for schizophrenia susceptibility genes. Nat Genet. 1995;11: 321-4. PMID: 7581457
Moises HW, Gelernter J, Giuffra LA, Zarcone V, Wetterberg L, Civelli O, Kidd KK, Cavalli-Sforza LL, Grandy DK, Kennedy JL, et al. No linkage between D2 dopamine receptor gene region and schizophrenia. Arch Gen Psychiatry. 1991;48:643-7. PMID: 2069495
Kennedy JL, Giuffra LA, Moises HW, Cavalli-Sforza LL, Pakstis AJ, Kidd JR, Castiglione CM, Sjogren B, Wetterberg L, Kidd KK. Evidence against linkage of schizophrenia to markers on chromosome 5 in a northern Swedish pedigree. Nature. 1988; 336: 167-70. PMID: 2903450
Moises HW, Schindler L, Leroux M, Kirchner H.
Decreased production of interferon alpha and interferon gamma in leucocyte cultures of schizophrenic patients.Acta Psychiatr Scand. 1985; 72:45-50. PMID: 3929565 |
Reif A, Fritzen S, Finger M, Strobel A, Lauer M, Schmitt A, Lesch KP. Neural stem cell roliferation is decreased in schizophrenia, but not in depression. Mol Psychiatry. 2006; PMID: 16415915
Hood L, Heath JR, Phelps ME, Lin B. Systems biology and new technologies enable predictive and preventative medicine.Science. 2004;306:640-3. PMID: 15499008
Heath JR, Phelps ME, Hood L. NanoSystems biology.Mol Imaging Biol. 2003;5 :312-25. Review. PMID: 14630511 |
Resources are always limited. |
Moises HW, Zoega T, Gottesman II. The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia. BMC Psychiatry. 2002 Jul 3;2:8. PMID: 12095426 http://www.biomedcentral.com/1471-244X/2/8
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(1) Biochemical evidence of glia asthenia in relatives of schizophrenia, e.g. by microarray technology.
(2) In vivo imaging of viral gene expression in the human CNS, e.g by PET. References: Molecular Imaging Central at http://www.mi-central.org/
(3) Double-blind studies to prove clinical efficacy of growth factors such as IGF-I in schizophrenia; including prolactin and insulin. Because prolactin is elevated by traditional and insulin by atypical antipsychotic treatments.
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The genetic studies and numerous other findings in schizophrenia research are so far all in agreement with the glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia first proposed in 2002(reference: http://www.biomedcentral.com/1471-244X/2/8/). Since the influence of glia cells on synaptic transmission has been termed tripartite synapse model, our hypothesis might briefer be called the weakened tripartite-synapse hypothesis of schizophrenia.
However, besides reactivation of the numerous latent viruses in the human brain other factors might also weaken glia cells causing inefficient synaptic transmission in schizophrenia.
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