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Method for treating neurological deficits

A nerve and central nervous system technology, applied in nervous system diseases, pharmaceutical formulations, resistance to vector-borne diseases, etc., can solve problems such as undetermined nutritional effects

Inactive Publication Date: 2000-11-15
RGT UNIV OF CALIFORNIA
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0013] Compared with EGF, although TGFα has stronger activity in vitro, its nutritional role in vivo - especially in animals with neurological deficits, including humans is undetermined

Method used

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  • Method for treating neurological deficits
  • Method for treating neurological deficits
  • Method for treating neurological deficits

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0124] Example 1: Expression of TGFα and EGF receptor mRNAS in the normal developing and adult nigrostriatal system

[0125] As described in the Detailed Description of the Invention, mRNAs encoding EGF-family neurotrophic factors are developmentally regulated in the nigrostriatal system. In the studies described below, the expression of TGF[alpha] and EGF receptor mRNAs were examined in normal developing and adult rodent systems.

[0126] A. Animal and Tissue Preparation

[0127] Adult male and female Sprague-Dawley pregnant mice (250-350 g) were purchased from Simonsen (Gilroy, CA). In these experiments, and in all other experiments described here, animals were maintained in room temperature and humidity controlled zoos. The use of animals in all experimental procedures was approved by the Animal Research Institute at the University of California, Irvine, in accordance with the guidelines of the National Institutes of Health.

[0128] Neonatal (P0), postnatal day 1 (P1) a...

Embodiment 2

[0140] Example 2: Modulation of TGFα and TGF receptor mRNA expression by 6-hydroxydopamine injury and striatal TGFα infusion.

[0141] In situ hybridization was used to determine whether nigrostriatal TGFα or EGF receptor mRNA was affected by intrastriatal infusion of TGFα. In addition, the effect of unilateral 6-OHDA injury on receptor expression in infused and non-infused animals was also examined.

[0142] A. Treatment group

[0143] Adult male Sprague-Dawley rats weighing 250-300 g were purchased from Simonsen (Gilroy, CA) and assigned to each of the five treatment groups:

[0144] (1) Striatal TGFα infusion, substantia nigra 6-OHDA injury (hereinafter referred to as “injury”); (2) TGFα infusion, no injury; (3) artificial cerebrospinal fluid (aCSF) infusion, injury; (4) aCSF infusion, no injury; (5) no infusion, no injury. Each experimental group used 4 to 8 animals. Animals were monitored after each surgery until full recovery, at all other times animals were housed in ...

Embodiment 3

[0189] Example 3: Properties of striatal cristae

[0190] As noted above, striatal infusion of TGFα in combination with substantia nigra 6-OHDA induced the formation of striatal body cell crests expressing EGF receptor mRNA in abundance, but not TGFα more than surrounding tissue. The cristae consisted of a large number of dense cells, making it clearly detectable using a simple sulfur stain. The identity of the abnormal striatal cristae is unclear, but three possibilities are considered.

[0191] Gliosis in response to injury is a hallmark of brain tissue damaged by injury and neurotoxicity. In general, both types of brain injury promote astrogliosis and infiltration of injured tissue by astrocytes and microglia (Fernaud-Espinoza et al., Glia 8:277-291, 1993 ). Astrocytes have been shown to express EGF receptor immunoreactivity, particularly in response to brain injury (Gomez-Pinilla et al., Neurosci. Lett. 91:276-282, 1988). Furthermore, TGF itself stimulates astrogliosis...

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Abstract

The present invention features methods and compositions for treating a patient who has a neurological deficit. The method can be carried out, for example, by contacting (in vivo or in culture) a neural progenitor cell of the patient's central nervous system (CNS) with a polypeptide that binds the epidermal growth factor (EGF) receptor and directing progeny of the proliferating progenitor cells to migrate en masse to a region of the CNS in which they will reside and function in a manner sufficient to reduce the neurological deficit. The method may include a further step in which the progeny of the neural precursor cells are contacted with a compound that stimulates differentiation.

Description

[0001] This application claims priority to provisional application serial number 60 / 055,383, filed August 4, 1997, the entire contents of which are incorporated herein by reference. [0002] The field of the invention is the treatment of neurological deficits resulting from injuries, diseases or developmental disorders affecting the central nervous system. Background of the invention [0003] Neurotrophic factors are peptides that multifacetedly support the survival, proliferation, differentiation, size and function of nerve cells (for review, see Loughlin and Fallon, Neurotrophic Factors, Academic Press, San Diego, Chem. Abstracts (CA), 1993). As the number of trophic or growth factors identified continues to increase, most can be assigned to one or another defined family based on their structure or binding affinity. Growth factors from various families, including the epidermal growth factor (EGF) family, have been shown to support dopamine neurons in the nigrostriatal syste...

Claims

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Application Information

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IPC IPC(8): A61K38/00A61K38/18A61K45/06A61K38/22A61P25/28A61P27/02
CPCA61K38/1841A61K38/185A61P25/00A61P25/28A61P27/02Y02A50/30A61K38/02
Inventor 詹姆斯·S·里德詹姆斯·H·法伦
Owner RGT UNIV OF CALIFORNIA
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