Animal model for schizophrenia

Multicellular living organisms and unmodified parts thereof and – Nonhuman animal – The nonhuman animal is a model for human disease

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C800S003000, C800S021000

Reexamination Certificate

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07902421

ABSTRACT:
The invention is an animal model which exhibits neuropathological and behavioral features associated with human schizophrenia. The invention also encompasses an in vivo method of preparing an animal model of human schizophrenia. Such a model is useful for screening and identifying therapeutic agents for treating human schizophrenia.

REFERENCES:
patent: 5549884 (1996-08-01), Weinberger et al.
patent: WO 00/11943 (2000-03-01), None
Bunney et al., Evidence for a compromised dorsolateral prefrontal cortical parallel circuit in schizophrenia, Brain Res Brain Res Rev. 31(2-3):138-46, 2000.
Eastwood et al., Interstitial white matter neuron density in the dorsolateral prefrontal cortex and parahippocampal gyrus in schizophrenia. Schizophr Res. 79(2-3):181-8, 2005.
Matthaei, Genetically manipulated mice: a powerful tool with unsuspected caveats. J Physiol. 582(Pt 2):481-8, 2007.
Saunders et al., Origin and fate of fetuin-containing neurons in the developing neocortex of the fetal sheep, Anat Embryol (Berl). 186(5):477-86, 1992.
Clapcote et al., Behavioral phenotypes of Disc1 missense mutations in mice, Neuron 54(3):387-402, 2007.
Low et al., What is a schizophrenic mouse? Neuron, 54(3):348-9, 2007.
Rioux et al., Distribution of microtubule-associated protein MAP2-immunoreactive interstitial neurons in the parahippocampal white matter in subjects with schizophrenia, Am J Psychiatry 160:149-153, 2003.
Lazar et al., Injections of NGF into neonatal frontal cortex decrease social interaction as adults: a rat model of schizophrenia, Schizophr Bull. 34(1):127-36, 2008.
Akil, M. et al., “Lamins-Specific alterations in the dopamine innervation of the prefrontal cortex in schizophrenic subjects”,American Journal of Psychiatry, (1999), 156, pp. 1580-1589.
Allendoerfer, K.L. et al., “The Subplate, a transient neocortical Structure: It's role in the development of connections between Thalamus and Cortex”,Annual Review of Neuroscience, (1994), vol. 17, pp. 185-218.
Aloe, L. et al., “Studies in Animal Models and Humans Suggesting a Role of Nerve Growth Factor in Schizophrenia-like Disorders”Behavioral Pharmacology, (2000), vol. 11 (3-4), pp. 235-242.
Anderson, S.A., “Increased Density of Microtubule associated protein 2-immunoreactive neurons in the prefrontal white matter of schizophrenic subjects”,Schizophrenia Research, (1996), vol. 19, pp. 111-119.
Bunney, Blynn Garland et al., “Neuropathological studies of brain tissue in schizophrenia”, Journal of Psychiatric Research, (1997), vol. 31(2), pp. 159-173.
Chua, S.E. et al., “Schizophrenia—a brain disease? A critical review of structural and functional cerebal abnormality in the disorder”,British Journal of Psychiatry, (1995), vol. 166, pp. 563-582.
Frade, JM et al., “Induction of cell death by endogenous nerve growth factor through its p75NTR receptor”, Natture, (1996), vol. 383, pp. 166-168.
Friedman, W.J. et al., “Neurotrophin signaling via Trks and p75”,Experimental Cell Research, (1999), vol. 253, pp. 131-142.
Ghosh, A., “Subplate neurons and the patterning of thalamocortical connections”,Ciba Foundation Symposium, (1995), vol. 193, pp. 150-172.
Harrison, P.J., “The neuropathology of schizophrenia—A critical review of the data and their interpretation”,Brain, (1999), vol. 122, pp. 593-624.
Johnson, D., et al., “Expression and structure of the human NGF receptor”,Cell, (1986), vol. 47(4), pp. 545-554.
Kokkinidis, L. et al., “Amphetamine models of paranoid schizophrenia: an overview and elaboration of animal experimentation”,Psychological Bulletin, (1980), vol. 88, pp. 551-579.
Lee, F.S. et al., “The uniqueness of being a neutrophin receptor”,Current Opinion in Neurobiology, (2001), vol. 11, pp. 281-286.
Lewis DA. Levitt P. et al., “Schizophrenia as a disorder of neurodevelopment”,Annual Review of Neuroscience, (2002), vol. 25, pp. 409-432.
Lipska, B.K. et al., “Postpubertal emergence of hyperresponsiveness to stress and to amphetamine after neonatel excitotoxic hippocampal damage: a potential animal model of schizophrenia”,Neuropsychopharmacology, (1993), vol. 9, pp. 67-75.
Lipska, B.K.et al., “Effects of reversible inactivation of the neonatal ventral hippocampus on behaviour in the adult rat”,Journal of Neuroscience, (2002), vol. 22(7), pp. 2835-2842.
Marenco, S. et al., The neurodevelopmental hypothesis of schizophrenia: following a trail of evidence from cradle to grave,Developmental Psychopathology, (2000), vol. 12(3), pp. 501-527.
McQuillen Patrick S et al. “Selective vulnerability of subplate neurons after early neonatal hypoxia-ischemia”,Journal of Neuroscience, (2003), vol. 23(8), pp. 3308-3315.
Nachman, R.J. et al., “Pseudodipeptide analogs of the pyrokinin/PBAN (FXPRLa) insect neuropeptide family containing carbocyclic Pro-mimetic conformational components”,Regulatory Peptides, (1995), vol. 57(3), pp. 359-370.
Rajakumar B et al. “Ontogeny of schizophrenia: lessons from a novel animal model”,Society for Neuroscience Abstract Viewer and Itinerary Planner(2003) Abstract No. 774.13.
Rajakumar, N. et al., “Effects of intrastriatal infusion of D2 receptor antisense oligonucleotide on apomorphine-induced behaviors in the rat”,Synapse, (1997), vol. 26(3), pp. 199-208.
Rajakumar N et al., “Altered neurotrophin receptor function in the developing prefrontal cortex leads to adult-onset dopaminergic hyperresponsivity and impaired prepulse inhibition of acoustic startle”,Biological Psychiatry, (2004), vol. 55(8), pp. 797-803.
Rajakumar, N., “Nerve growth factor causes apoptosis of subplate cells in developing cerebral cortex via p75 dependent mechanism”,Society for Neuroscience Abstract Viewer and Itinerary Planner(2002) Abstract No. 426. 16.
Rajakumar, N. et al., “Parvalbumin-containing GABAergic neurons in the basal ganglia output system of the rat”,Journal of Comparative Neurology, (1994), vol. 350(2), pp. 324-336.
Roux, P. P. et al., “Neurotrophin signaling through the p75 neurotrophin receptor”,Progress in Neurobiology, (2002), vol. 67, pp. 203-233.
Super, H. et al., “The functions of the preplate in development and evolution of the neocortex and hippocampus”,Brain Research Reviews, (1998), vol. 27, pp. 40-64.
Thome J et al., “Neurotrophic factors and the maldevelopment hypothesis of schizophrenic psychoses”,Journal of Neural Transmission, (1998), vol. 105(1), pp. 85-100.
Uehara, T. et al., “Neonatal lesions of the left entorhinal cortex affect dopamine metabolism in the rat brain”,Brain Research, (2000), vol. 860, pp. 77-86.
Volk D. et al., “GABA transporter-1 mRNA in the prefrontal cortex in schizophrenia: decreased expression in a subset of neurons”,American Journal of Psychiatry, (2001), vol. 158(2), pp. 256-265.
Wang Cheng et al., “Blockade of phencyclidine-induced cortical apoptosis and deficits in prepulse inibition by M40403, a superoxide dismutase mimetic”,Journal of Pharmacology and Experimental Therapeutics, (2003), vol. 304(1), pp. 266-271.
Woo, T.U. et al., “A subclass of prefrontal gamma-aminobutyric acid axon terminals are selectively altered in schizophrenia”,Proceedings of the National Academy of ScienceU.S.A., (1998), vol. 95(9), pp. 5341-5346.

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