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Method and composition for treating neuronal hyper-excitability

A treatment plan and technology for subjects, applied in the direction of receptors of neurotransmitters, drug combinations, nervous system diseases, etc., can solve problems such as not allowing spinal cord segments to limit therapeutic effects

Active Publication Date: 2018-11-23
RGT UNIV OF CALIFORNIA
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Furthermore, currently available spinal drug delivery systems (such as epidural or intrathecal delivery) do not allow for spinal cord segment-limiting therapeutic effects

Method used

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  • Method and composition for treating neuronal hyper-excitability
  • Method and composition for treating neuronal hyper-excitability
  • Method and composition for treating neuronal hyper-excitability

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Embodiment 1

[0102] AAV9 virus encoding GAD65 (glutamate decarboxylase 65) and VGAT (vesicular GABA transporter) was injected into the targeted segment using the subpial delivery method ( figure 1 ). Animals (rats) with spinal cord injury-induced muscle spasm were used. The distribution of transgene expression achieved after lumbar subpial AAV9-UBI-GFP delivery as figure 2 shown. Extensive GFP expression can be seen in interneurons across the gray matter.

[0103] Following gene delivery, spastic responses were measured up to 8 weeks after GAD65 and VGAT gene delivery. In control spastic animals, control AAV9-UBI-GFP was used. Figure 3A-3D showed a gradual decrease in the spasm response in animals injected with AAV9-UBI-GAD65+VGAT. Significant antispasmodic effects persist for at least 8 weeks after gene delivery ( Figure 3A and 3B ). Measures of rate-dependent depression (representing an indicator of altered spinal cord inhibition) showed significant recovery if compared to ani...

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Abstract

The present invention provides a therapy for treating loss of GABA-mediated pre-synaptic inhibition after spinal injury. The therapeutic regimen includes spinal segment-specific upregulation of GAD65(glutamate decarboxylase) and VGAT (vesicular GABA transporter) to modulate chronic spasticity in patients after spinal traumatic or ischemic injury.

Description

[0001] Cross-references to related literature [0002] This application claims priority under 35 U.S.C. §119(e) to U.S. Serial No. 62 / 314,128 filed March 28, 2016, the entire contents of which are incorporated herein by reference. [0003] Funding Information [0004] This invention was made with Government support under Grant No. NS051644-02A2 awarded by the National Institutes of Health. The US Government has certain rights in this invention. technical field [0005] The present invention relates generally to treating spinal cord injuries, and more particularly to combination therapy regimens for modulating chronic spasticity in patients following spinal cord trauma or ischemic injury. Background technique [0006] Spinal cord injury (traumatic or ischemic) can lead to the development of clinically defined spasticity and stiffness. One of the mechanisms underlying spasticity after SCI is thought to be loss of local segmental inhibition, and thus: i) increased tonic moto...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): C07C233/69C07C235/34C07C235/42
CPCC07C233/69C07C235/34C07C235/42A61K48/005A61K48/0075C12Y401/01015C12N9/88C12N2750/14143C12N2710/00C07K14/70571A61P25/14A61P21/00
Inventor 马丁·马尔萨拉
Owner RGT UNIV OF CALIFORNIA