Purdue Research Foundation

US Government As Represented by the Secretary of the Army

The University of Chicago

Indiana University

National Science Foundation

Richard B Borgens

Riyi Shi

Stephen Robert Byrn

Daniel T Smith

Scott A Shapiro

Raphael C Lee

Michael E McGinnis

To achieve, an in vivo repair of injured mammalian nerve tissue, an effective amount of a biomembrane fusion agent is administered to the injured nerve tissue. The application of the biomembrane fusion agent may be performed by directly contacting the agent with the nerve tissue at the site of the injury. Alternatively, the biomembrane fusion agent is delivered to the site of the injury through the blood supply after administration of the biomembrane fusion agent to the patient. The administration is preferably by parenteral administration including including intravascular, intramuscular, subcutaneous, or intraperitoneal injection of an effective quantity of the biomembrane fusion agent so that an effective amount is delivered to the site of the nerve tissue injury.

Methods and compositions for treating mammalian nerve tissue injuries

To achieve, an in vivo repair of injured mammalian nerve tissue, an effective amount of a biomembrane fusion agent is administered to the injured nerve tissue. The application of the biomembrane fusion agent may be performed by directly contacting the agent with the nerve tissue at the site of the injury. Alternatively, the biomembrane fusion agent is delivered to the site of the injury through the blood supply after administration of the biomembrane fusion agent to the patient. The administration is preferably by parenteral administration including intravascular, intramuscular, subcutaneous, or intraperitoneal injection of an effective quantity of the biomembrane fusion agent so that an effective amount is delivered to the site of the nerve tissue injury.

Embodiments of the present disclosure provide a novel pyridine, pharmaceutical compositions comprising such pyridine, and the use of such compositions in treating injured mammalian nerve tissue, including but not limited to an injured spinal cord. In at least one embodiment of the method, the method comprises the step of administering to the mammal in need thereof with a pharmaceutical composition, or pharmaceutically acceptable salt, comprising 4-aminopyridine-3-methanol.

Pyridines for treating injured mammalian nerve tissue

The invention provides novel pyridines, pharmaceutical compositions comprising such pyridines, and the use of such compositions in treating injured mammalian nerve tissue, including but not limited to an injured spinal cord, in one embodiment, the compounds, compositions, and methods of the instant invention treat a mammalian nerve tissue injury by restoring action potential or nerve impulse conduction through a nerve tissue lesion. Significantly, in vivo application of compounds of the instant invention established, on the basis of SSEP testing, that the compounds provide longer lasting effects at lower concentrations than comparable treatment with the known agent 4-aminopyridine (4 AP).

To achieve, an in vivo repair of injured mammalian nerve tissue, an effective amount of a biomembrane fusion agent is administered to the injured nerve tissue. The application of the biomembrane fusion agent may be preformed by directly contacting the agent with the nerve tissue at the site of the injury. Alternatively, the biomembrane fusion agent is delivered to the site of the injury through the blood supply after administration of the biomembrane fusion agent to the patient. The administration is preferably by parenteral administration including intravascular, intramuscular, subcutaneous, or intraperitoneal injection of an effective quantity of the biomembrane fusion agent so that an effective amount is delivered to the site of the nerve tissue injury.

Injuries to the central nervous system, particularly spinal cord injuries, are treated by administering a purine nucleoside or analog to the patient and, optionally, electrically stimulating the site of injury.

Method of treatment for central nervous system injury

Methods of treating an injured vertebrate spinal cord are described. In one aspect of the invention, a method of treating an injured vertebrate spinal cord includes contacting the spinal cord with a biomembrane fusion agent such as a polyalkylene glycol, especially polyethylene glycol. In alternative embodiments of the invention, methods of treating an injured vertebrate spinal cord include contacting the cord with a biomembrane fusion agent and a potassium channel blocker. Other aspects of the invention include compositions for treating a vertebrate nervous system. A preferred composition includes a biomembrane fusion agent, such as a polyalkylene glycol, and a potassium channel blocker, such as an amino-substituted pyridine.

Methods and compositions for treating mammalian spinal cord injuries

The invention provides novel pyridines, pharmaceutical compositions comprising such pyridines, and the use of such compositions in treating injured mammalian nerve tissue, including but not limited to an injured spinal cord. In one embodiment, the compounds, compositions, and methods of the instant invention treat a mammalian nerve tissue injury by restoring action potential or nerve impulse conduction through a nerve tissue lesion. Significantly, in vivo application of compounds of the instant invention established, on the basis of SSEP testing, that the compounds provide longer lasting effects at lower concentrations than comparable treatment with the known agent 4-aminopyridine (4 AP).

Method of treatment for spinal cord injury

A method and apparatus for stimulating nerves in the central nervous system of a mammal to regenerate within the central nervous system applies an oscillating electrical field to the central nervous system across a lesion in the central nervous system. The polarity reversal period of the electrical field is long enough to stimulate growth of cathodally facing axons of the nerve cells in the central nervous system but is shorter than a die back period of anodally facing axons of the nerve cells.

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Delphi, IN, United States of America

Richard B Borgens