METHODS OF TREATING COGNITIVE DISORDERS BY INHIBITION OF Gpr12
AssigneeHelicon Therapeutics, Inc.
InventorsMarco Peters, Roderick Euan Milne Scott, Timothy P. Tully
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Abstract
The present invention provides methods for screening a pharmaceutical agent for its ability to modulate long term memory formation, performance of a hippocampal-dependent cognitive task or Gpr12 function. The present invention also provides methods for modulating long term memory formation or performance of a hippocampal-dependent cognitive task by modulating Gpr12-dependent protein expression. The present invention further provides methods for treating a defect in long term memory formation by inhibiting Gpr12 function and methods for treating a defect in performance of a hippocampal-dependent cognitive task by inhibiting Gpr12 function.
Claims29
A method comprising administering to a mammal an effective amount of a pharmaceutical agent which modulates Gpr12 activity in the mammal.
A method comprising the steps of:
- (a) introducing a pharmaceutical agent of interest into host cells expressing a Gpr12 protein;
- and (b) determining Gpr12 function, wherein a difference in the Gpr12 function determined in (b) compared to the Gpr12 unction of host cells of (a) to which said pharmaceutical agent has not been administered identifies the pharmaceutical agent as one capable of modulating Gpr12 function.
A method comprising the steps of (a) administering to a mammal a pharmaceutical agent which modulates Gpr12 function;
- (b) training the mammal of step (a) and a control mammal of the same species to which said pharmaceutical agent has not been administered under conditions sufficient to produce long term memory formation in said mammal;
- (c) assessing long term memory formation in the mammals trained in step (b);
- and (d) comparing long term memory formation in the mammals assessed in step (c), wherein a difference in long term memory formation assessed in the mammal administered the pharmaceutical agent relative to long term memory formation assessed in the control mammal identifies the pharmaceutical agent as one which is capable of modulating long term memory formation.
Dependencies are inferred from the claim text.