A compound represented by the general formula (V)

##STR00001##

wherein all the symbols are as defined in the specification, has an improved balance of the agonist activity against the S1P.sub.5 receptor relative to the S1P.sub.1 receptor, and can thus serve as a therapeutic agent for S1P.sub.5-mediated diseases such as schizophrenia and Binswanger's disease and other neurodegenerative diseases.

A compound represented by the general formula (V)

##STR00001##

wherein all the symbols are as defined in the specification, has an improved balance of the agonist activity against the S1P.sub.5 receptor relative to the S1P.sub.1 receptor, and can thus serve as a therapeutic agent for S1P.sub.5-mediated diseases such as schizophrenia and Binswanger's disease and other neurodegenerative diseases.

Provided herein are curcumin analogues that are able to interact with amyloid β (Aβ) and to attenuate the copper-induced crosslinking of Aβ. Also provided herein are methods of using the compounds in the treatment of Alzheimer's Disease or a related disorder.

Provided herein are curcumin analogues that are able to interact with amyloid β (Aβ) and to attenuate the copper-induced crosslinking of Aβ. Also provided herein are methods of using the compounds in the treatment of Alzheimer's Disease or a related disorder.

A compound represented by the general formula (V) ##STR00001##
wherein all the symbols are as defined in the specification, has an improved balance of the agonist activity against the S1P.sub.5 receptor relative to the S1P.sub.1 receptor, and can thus serve as a therapeutic agent for S1P.sub.5-mediated diseases such as schizophrenia and Binswanger's disease and other neurodegenerative diseases.

A compound represented by the general formula (V) ##STR00001##
wherein all the symbols are as defined in the specification, has an improved balance of the agonist activity against the S1P.sub.5 receptor relative to the S1P.sub.1 receptor, and can thus serve as a therapeutic agent for S1P.sub.5-mediated diseases such as schizophrenia and Binswanger's disease and other neurodegenerative diseases.

Provided herein are curcumin analogues that are able to interact with amyloid beta (Aβ) and to attenuate the copper-induced crosslinking of Aβ. Also provided herein are methods of using the compounds as imaging agents of amyloid beta and for the treatment of diseases associated with amyloid beta. Methods of preparing unlabeled and radiolabeled compounds useful for interacting with amyloid beta and pharmaceutical compositions are also provided.

Provided herein are curcumin analogues that are able to interact with amyloid beta (Aβ) and to attenuate the copper-induced crosslinking of Aβ. Also provided herein are methods of using the compounds as imaging agents of amyloid beta and for the treatment of diseases associated with amyloid beta. Methods of preparing unlabeled and radiolabeled compounds useful for interacting with amyloid beta and pharmaceutical compositions are also provided.

Provided herein are curcumin analogues that are able to interact with amyloid beta (Aβ) and to attenuate the copper-induced crosslinking of Aβ. Also provided herein are methods of using the compounds as imaging agents of amyloid beta and for the treatment of diseases associated with amyloid beta. Methods of preparing unlabeled and radiolabeled compounds useful for interacting with amyloid beta and pharmaceutical compositions are also provided.

Provided herein are curcumin analogues that are able to interact with amyloid beta (Aβ) and to attenuate the copper-induced crosslinking of Aβ. Also provided herein are methods of using the compounds as imaging agents of amyloid beta and for the treatment of diseases associated with amyloid beta. Methods of preparing unlabeled and radiolabeled compounds useful for interacting with amyloid beta and pharmaceutical compositions are also provided.