Abstract: Studies in mouse models of Fragile X and preliminary studies in human youth demonstrate that ERK1/2 is biomarker useful to monitoring the treatment of people diagnosed with ASD. Results reported herein demonstrate that acamprosate has the ability to reduce levels of ERK1/2 activation associated with many of the symptoms of ASD. Accordingly, in addition to its utility as a diagnostic marker for ASD ERK1/2 activation levels can be used to monitor patients treated with acamprosate and to screen potentially therapeutic compounds.

Abstract: The present disclosure provides pharmaceutical compositions comprising rationally designed peptide analogs of the p65-TAD binding region of GILZ to selectively sequester activated p65. Structural and functional analyses suggest that select GILZ analog (GA) bind p65-TAD with optimum affinity, exhibit an estimated half minimal lethal dose comparable to known peptide drugs and suppress A?1-42 induced cytotoxicity. Furthermore, the present disclosure provides uses and methods of using the pharmaceutical compositions, and uses and methods of using pharmaceutical formulations comprising the pharmaceutical compositions, for the treatment of neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).

Abstract: The present disclosure provides pharmaceutical compositions comprising rationally designed peptide analogs of the p65-TAD binding region of GILZ to selectively sequester activated p65. Structural and functional analyses suggest that select GILZ analog (GA) bind p65-TAD with optimum affinity, exhibit an estimated half minimal lethal dose comparable to known peptide drugs and suppress A?1-42 induced cytotoxicity. Furthermore, the present disclosure provides uses and methods of using the pharmaceutical compositions, and uses and methods of using pharmaceutical formulations comprising the pharmaceutical compositions, for the treatment of neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).

Abstract: The present disclosure provides pharmaceutical compositions comprising rationally designed peptide analogs of the p65-TAD binding region of GILZ to selectively sequester activated p65. Structural and functional analyses suggest that select GILZ analog (GA) bind p65-TAD with optimum affinity, exhibit an estimated half minimal lethal dose comparable to known peptide drugs and suppress A?1-42 induced cytotoxicity. Furthermore, the present disclosure provides uses and methods of using the pharmaceutical compositions, and uses and methods of using pharmaceutical formulations comprising the pharmaceutical compositions, for the treatment of neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).

Abstract: Studies in mouse models of Fragile X and preliminary studies in human youth demonstrate that ERK1/2 is biomarker useful to monitoring the treatment of people diagnosed with ASD. Results reported herein demonstrate that acamprosate has the ability to reduce levels of ERK1/2 activation associated with many of the symptoms of ASD. Accordingly, in addition to its utility as a diagnostic marker for ASD ERK1/2 activation levels can be used to monitor patients treated with acamprosate and to screen potentially therapeutic compounds.

Abstract: Studies in mouse models of Fragile X and preliminary studies in human youth demonstrate that ERK1/2 is biomarker useful to monitoring the treatment of people diagnosed with ASD. Results reported herein demonstrate that acamprosate has the ability to reduce levels of ERK1/2 activation associated with many of the symptoms of ASD. Accordingly, in addition to its utility as a diagnostic marker for ASD ERK1/2 activation levels can be used to monitory patients treated with acamprosate.

Abstract: The present disclosure provides pharmaceutical compositions comprising rationally designed peptide analogs of the p65-TAD binding region of GILZ to selectively sequester activated p65. Structural and functional analyses suggest that select GILZ analog (GA) bind p65-TAD with optimum affinity, exhibit an estimated half minimal lethal dose comparable to known peptide drugs and suppress A?1-42 induced cytotoxicity. Furthermore, the present disclosure provides uses and methods of using the pharmaceutical compositions, and uses and methods of using pharmaceutical formulations comprising the pharmaceutical compositions, for the treatment of neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).

Abstract: Studies in mouse models of Fragile X and preliminary studies in human youth demonstrate that ERK1/2 is biomarker useful to monitoring the treatment of people diagnosed with ASD. Results reported herein demonstrate that acamprosate has the ability to reduce levels of ERK1/2 activation associated with many of the symptoms of ASD. Accordingly, in addition to its utility as a diagnostic marker for ASD ERK1/2 activation levels can be used to monitory patients treated with acamprosate.

Abstract: The invention relates to the use of NMDA receptor antagonists such as 1-aminocyclohexane derivatives to modify deposition of potentially toxic and fibrillogenic A? peptides in amyloidopathies. Specifically, the invention relates to the ability of memantine to intervene in the processing of APP and decrease the levels of fibrillogenic A? peptides.