Use of VEGF and homologues to treat neuron disorders

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Peptide containing doai

Reexamination Certificate

Rate now

  [ 0.00 ] – not rated yet Voters 0   Comments 0

Details

C514S002600, C530S399000, C530S350000

Reexamination Certificate

active

10257423

ABSTRACT:
The present invention relates to neurological and physiological dysfunction associated with neuron disorders. In (particular, the invention relates to the involvement of vascular endothelial growth factor (VEGF) and homologues in the aetiology of motor neuron disorders. The invention further concerns a novel, mutant transgenic mouse (VEGFm/m) with a homozygous deletion in the hypoxia responsive element (HRE) of the VEGF promoter which alters the hypoxic upregulation of VEGF. These mice suffer severe adult onset muscle weakness due to progressive spinal motor neuron degeneration which is reminiscent of amyotrophic lateral sclerosis (ALS)—a fatal disorder with unknown aetiology. Furthermore, the neuropathy of these mice is not caused by vascular defects, but is due to defective VEGF-mediated survival signals to motor neurons. The present invention relates in particular to the isoform VEGF165which stimulates survival of motor neurons via binding to neuropilin-1, a receptor known to bind semaphorin-3A which is implicated in axon retraction and neuronal death, and the VEGF Receptor-2. The present invention thus relates to the usage of VEGF, in particular VEGF165, for the treatment of neuron disorders and relates, in addition, to the usage of polymorphisms in the VEGF promotor for diagnosing the latter disorders.

REFERENCES:
patent: 5332671 (1994-07-01), Ferrara et al.
patent: 5350836 (1994-09-01), Kopchick et al.
patent: 6455283 (2002-09-01), Ferrara et al.
patent: WO 98/31395 (1998-07-01), None
patent: WO 99/46364 (1999-09-01), None
patent: WO 99/47677 (1999-09-01), None
patent: WO 00/62798 (2000-10-01), None
Miller, G. (2002). Breaking down barriers. Science 297:1116-1118.
Pettit et al. (1998). The development of site-specific drug-delivery systems for protein and peptide biopharmaceuticals. Trends Biotechnol. 16:343-349.
Lambrechts et al. (2004). VEGF: necessary to prevent motoneuron degeneration, sufficient to treat ALS? Trends in Molecular Medicine. 10(6):275-282.
Wells, J.A. (1990). Additivity of mutational effects in proteins. Biochemistry. 29(37):8509-8517.
Ngo et al. (1994). Computational complexity, protein structure prediction, and the Levinthal paradox. In Merz and Le Grand (Eds.) The Protein Folding Problem and Tertiary Structure Prediction. Birkhauser:Boston, pp. 492-495.
Storkebaum et al. (2005). Treatment of motoneuron degeneration by intracerebroventricular delivery of VEGF in a rat model of ALS. Nature Neuroscience. 8(1):85-92.
Jin et al., “Vascular endothelial growth factor: Direct neuroprotective effect in in vitro ischemia”, 2000, PNAS 97:10242-10247.
Jin et al., “Vascular Endothelial Growth Factor Rescues HN33 Neural Cells from Death Induced by Serum Withdrawal”, 2000, J. Mol. Neurosci.14:197-203.
Kilpatrick et al., “Molecular Mechanisms Regulating Motor Neuron Development and Degeneration”, 1999, Mol. Neurobiol. 19:205-228.
Owens et al., “VEGF Promoter Polymorphisms and the Risk of Ischaemic Heart Disease”, 2000, J. Amer. Coll. Cardiol. 35, suppl. A:306A.
Samii et al., “Vascular endothelial growth factor expression in peripheral nerves and dorsal root ganglia in diabetic neuropathy in rats”, 1999, Neurosci. Lett. 3:159-162.
Schratzberger et al., “Favorable effect of VEGF gene transfer on ischemic peripheral neuropathy”, 2000, Nature Med., 6:405-413.
Silverman et al., “Vascular, Glial and Neuronal Effects of Vascular Endothelial Growth Factor in Mesencephalic Explant Cultures”, 1999, Neurosci. 90:1529-1541.
Soker et al., “Neuropilin-1 Is Expressed by Endothelial and Tumor Cells as an Isoform-Specific Receptor for Vascular Endothelial Growth Factor”, 1998, Cell 92: 735-745.
Sondell et al., “Vascular Endothelial Growth Factor Has Neurotrophic Activity and Stimulates Axonal Outgrowth, Enhancing Cell Survival and Schwann Cell Proliferation in the Peripheral Nervous System”, 1999, J. Neurosci. 19:5731-5740.
Chen, W et al., entitled “Lack of association of VEGF promoter polymorphisms with sporadic ALS,” Neurology 2006;67; pp. 508-510.

LandOfFree

Say what you really think

Search LandOfFree.com for the USA inventors and patents. Rate them and share your experience with other people.

Rating

Use of VEGF and homologues to treat neuron disorders does not yet have a rating. At this time, there are no reviews or comments for this patent.

If you have personal experience with Use of VEGF and homologues to treat neuron disorders, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Use of VEGF and homologues to treat neuron disorders will most certainly appreciate the feedback.

Rate now

     

Profile ID: LFUS-PAI-O-3860918

  Search
All data on this website is collected from public sources. Our data reflects the most accurate information available at the time of publication.