Methods for treating alzheimer disease and for reducing amyloid beta formation

Abstract

The present invention provides methods for reducing amyloid beta formation and for treating diseases associated with IC the accumulation of amyloid beta, The present invention provides (1) A β aggregation inhibition by A β Oligomer/Fibril formation inhibition, (2) BACE-1 reduced a through β-Amyloidogenic Processing inhibition, (3) cerebral blood flow to the increase of the cell outer Aβ Monomer, Oligomer & Aβ Fibril/Plaque reduction, (4) NO/cGMP/PKG/CREB Pathway to the activation of Neuronal cell Death inhibition and Neurogenesis, Synaptogenesis, Angiogenesis promotion, (5) DKK-1 inhibition by Wnt Signaling in the activation of synaptic plasticity recovery and Aβ production Positive Feedback Loop for inhibition of APP generates reduced and Aβ accumulation suppression, (6) Autophagy activation by cells within Toxic Mirodenafil, Sildenafil, Vardenafil, Tadalafil, Udenafil, Dasantafil, and Avanafil for the treatment of inhibition of Aβ Fibril/Plaque formation through removal of Soluble Aβ Oligomer; and a Pharmaceutically Acceptable Salt, Solvate, and Hydrate in selected compounds key of ingredient containing drug compound composition, and this with the treatment method provided.

1 - 6 . (canceled) 
     
     
         7 . A method for treating Alzheimer comprising:
 administering a pharmaceutical composition comprising a compound selected from the group consisting of mirodenafil, sildenafil, vardenafil, tadalafil, udenafil, dasantafil, and avanafil; and a pharmaceutically acceptable salt, solvate, and hydrate thereof.   
     
     
         8 . The method of  claim 7 , wherein the compound inhibits formation of Aβ aggregation inhibition by reducing formation of Aβ Oligomer or Fibril. 
     
     
         9 . The method of  claim 7 , wherein the compound inhibits β-Amyloidogenic Processing through BACE-1 reduction. 
     
     
         10 . The method of  claim 7 , wherein the compound reduces extracellular formation and accumulation of amyloid beta monomer, oligomer, and/or amyloid beta fibril and plaque by vasolidation. 
     
     
         11 . The method of  claim 7 , wherein the compound reduces neuronal cell death and enhances neurogenesis, synaptogenesis, or angiogenesis by activating NO/cGMP/PKG/CREB Pathway. 
     
     
         12 . The method of  claim 7 , wherein the compound restored Synaptic plasticity by Wnt Signaling activation through DKK-1 inhibition. 
     
     
         13 . The method of  claim 7 , wherein the compound suppresses DKK-1 by inhibiting Positive Feedback Loop of Aβ production to inhibit formation of APP and Aβ accumulation. 
     
     
         14 . The method of  claim 7 , wherein the compound activates Autophagy to remove intracellular Toxic Soluble Aβ Oligomer to suppress formation and accumulation of Aβ Fibril/Plaque. 
     
     
         15 . The method of  claim 7 , wherein compound improves behavioral and cognitive function. 
     
     
         14 - 15 . (canceled)