Lgi, lingo and p75ntr family members: novel modulators of neuronal growth

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to block the action of a myelin-based axon growth inhibitor (MBGI) in order to enhance the ability of neurons of the central nervous system to regenerate.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to inhibit growth cone collapse induced by Nogo66 or myelin.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to reduce the association of p75NTRn, LINGOn, or p75NTRn and LINGOn with the Nogo receptor (NgR).

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to promote the regeneration or repair of the central or peripheral nervous system.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to promote the remyelination of neurons after injury to or disease of to the central or peripheral nervous system.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or derivative thereof, to modulate the action of LINGOn in regulating myelination in the peripheral or central nervous system.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to modulate the action of p75NTRn in regulating myelination in the peripheral or central nervous system.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to promote the regeneration or repair of the peripheral nervous system.

Use of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to facilitate proliferation of oligodendrocyte precursor cells (OPCs) and thereby expand pools of myelin-producing cells.

A method of treating central or peripheral nerve damage comprising the administration of an effective amount of a leucine-rich, glioma-inactivated protein (LGIn), an analog or a derivative thereof, to the site of the damage.

A method of identifying whether an LGIn can reverse the effects of a compound that causes growth cone collapse of primary cerebellar neurons maintained in the presence of myelin, the method comprising:

• Plating central neurons on the compound;
• and
• Measuring neurite outgrowth in the presence and absence of said LGIn to determine whether said LGIn reverses the effects of said test compound.

A method of identifying a compound that interferes with the interaction of a LGIn with LINGOn, the method comprising:

• Providing a cell that expresses LINGOn;
• and
• Contacting the cell with said compound in the presence and absence of said LGIn to determine whether said LGIn competes with said test compound for LINGOn.

A method of identifying a compound that interferes with the interaction of a LGIn with p75NTRn, the method comprising:

• Providing a cell that expresses p75NTRn;
• and
• Contacting the cell with said compound in the presence and absence of said LGIn to determine whether said LGIn competes with said test compound for p75NTRn.

A method of identifying a compound that interferes with the interaction of LGIn and OPCs, the method comprising:

• Contacting the compound with OPCs;
• and
• Measuring whether proliferation of OPCs is increased in the presence of LGIn.

A cultured cell transfected with a vector, wherein the cell expresses LGI1-FLAG.

A cultured cell transfected with vectors, wherein the cell expresses LGI1-FLAG and LINGO-1.

A cultured cell transfected with vectors, wherein the cell expresses LGI1-FLAG and p75NTR.

A cultured cell transfected with vectors, wherein the cell expresses LGI1-FLAG, LINGO-1 and p75NTR.