Abstract: The present disclosure relates to a novel indenone derivative or an isomer or pharmaceutically acceptable salt thereof, and use thereof. The indenone derivative according to the present disclosure may be effectively used for the prevention or treatment of a neurodegenerative brain disease by (i) inhibiting amyloid-beta aggregation and/or disaggregating amyloid-beta aggregates, (ii) inhibiting tau protein aggregation and/or disaggregating tau protein aggregates, and/or (iii) inhibiting the hyperphosphorylation of tau protein.

Abstract: Provided is a pharmaceutical composition for treating a degenerative brain disease, including a glycine transporter as an active ingredient. A composition including, as an active ingredient, a glycine transporter protein, a fragment thereof or a nucleic acid molecule encoding the protein or the fragment thereof, a vector including the nucleic acid molecule, or a cell transformed with the vector including the nucleic acid molecule, according to an embodiment, not only can achieve excellent effect(s) of inhibiting amyloid-beta aggregation and/or degrading aggregated amyloid-beta, but also degrades tau protein (and/or inhibition of the aggregation thereof), inhibits the hyperphosphorylation of tau protein, and has excellent blood-brain barrier permeability, thus making it possible to successively act on brain tissues.

Abstract: Provided is a method for manufacturing a composition for increasing cognitive function.

Abstract: Provided is a pharmaceutical composition for treating a degenerative brain disease, including a glycine transporter as an active ingredient. A composition including, as an active ingredient, a glycine transporter protein, a fragment thereof or a nucleic acid molecule encoding the protein or the fragment thereof, a vector including the nucleic acid molecule, or a cell transformed with the vector including the nucleic acid molecule, according to an embodiment, not only can achieve excellent effect(s) of inhibiting amyloid-beta aggregation and/or degrading aggregated amyloid-beta, but also degrades tau protein (and/or inhibition of the aggregation thereof), inhibits the hyperphosphorylation of tau protein, and has excellent blood-brain barrier permeability, thus making it possible to successively act on brain tissues.