Abstract: The invention relates to methods and products for enhancing and improving recovery of lost memories. In particular the methods are accomplished by inhibiting HDAC2 and or selectively inhibiting HDAC1/2 or HDAC1/2/3.

Abstract: The invention relates to methods and products for enhancing and improving recovery of lost memories. In particular the methods are accomplished through the increase of histone acetylation.

Abstract: The invention relates to methods and products for enhancing and improving recovery of lost memories. In particular the methods are accomplished through the increase of histone acetylation.

Abstract: The invention relates to methods and compositions for promoting cognitive function and/or treating cognitive function disorders and impairments. In particular the methods are accomplished by administering to a subject CI-994 or dinaline or a pharmaceutically acceptable salt, ester, prodrug or metabolite thereof.

Abstract: The invention relates to methods and products for treating emotional disorders such as stress induced emotional disorders, as well as related assays and kits. Methods include administering to a subject an effective amount of an agent for targeting the Rac1, Cdk5, p35, PAK-1 pathway to treat the emotional disorder. The agent for targeting the Rac1, Cdk5, p35, PAK-1 pathway may be, for instance a Rac-1 inhibitor, a Cdk5 inhibitor, a PAK-1 activator, or p35 mobilizing agent.

Abstract: The invention provides methods and compounds for the treatment of neurological disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease, ALS (Amyotrophic Lateral Sclerosis), traumatic brain injury, ischemic brain injury or a stroke. In one aspect the compounds are HDAC1 activators. Exemplary HDAC1 activators include metal chelators, iron chelators, deferoxamin, flavonoids, compounds comprising a catechol moity, ginkgetin K, Chembridge 5104434, sciadopilysin, tetrahydrogamboic acid, TAM-11, LY 235959, CGS 19755, SK&F 97541, etidronic acid, levonordefrin, methyldopa, ampicillin trihydrate, D-aspartic acid, gamma-D-glutamylaminomethylsulfonic acid, phenazopyridine to hydrochloride, oxalamine citrate salt, podophyllotoxin, SK&F 97541, (+-)-4-amino-3-(5-chloro-2-thienyl)-butanoic acid, (RS)-(tetrazol-5-yl) glycine, R(+)-SKF-81297, gambogic acid, and derivatives thereof.

Abstract: The invention relates to methods of treating neurological disorders in a subject, by activating a DISC1 pathway. Methods of promoting neurogenesis in adult neural progenitor cells, enhancing nerve generation and treating GSK3 disorders as well as related compositions are also provided.

Abstract: Provided herein are methods and compositions for treating or preventing mood disorders and certain other mental disorders.

Abstract: The invention relates to methods and products for enhancing and improving recovery of lost memories. In particular the methods are accomplished through the increase of histone acetylation.

Abstract: Provided herein are methods and compositions for enhancing the cognitive performance of a subject in need thereof. A method may include administering to a subject an agent that increases the level of protein or activity of a sirtuin, such as SIRT1.

Abstract: The present invention relates to siRNA molecules derived from BACE1 and BACE2 genes. Accordingly, provided herein are siRNA molecules comprising a nucleotide sequence consisting essentially of a BACE1 or BACE2 gene. Also provided are methods for reducing the level of BACE1 protein in a cell. Further provided are methods for preparing a pharmaceutical composition comprising an siRNA with a pharmaceutically acceptable carrier.

Abstract: Disclosed are improved methods of treating individuals with Alzheimer's disease (AD) as well as methods to diagnose AD in an individual. Also included are compounds and methods of identifying compounds to treat AD. The present invention also discloses methods for decreasing the phosphorylation of amyloid precursor protein (APP), including inhibiting phosphorylation of amino acid residue tyrosine 668 of APP and for reducing cleavage of APP. The present invention further discloses transgenic (Tg), non-human animals and cells expressing a p25 transgene that are models of neurodegenerative diseases. Embodiments of the present invention are directed to methods wherein the Tg animals and Tg cells of the invention are used to screen for modulators of neurodegenerative disorders. The Tg animals and cells of the present invention are useful for elucidating the mechanisms of neurodegenerative disorders.

Abstract: Provided herein are methods and compositions for modulating the activity of sirtuin deacetylase protein family members; p53 activity; apoptosis; lifespan and sensitivity to stress of cells and organisms. Exemplary methods comprise contacting a cell with an activating compound, such as a flavone, stilbene, flavanone, isoflavone, catechin, chalcone, tannin or anthocyanidin; or an inhibitory compound, such as a sphingolipid, e.g., sphingosine. Also disclosed herein are methods for treating, preventing or diagnosing a disease associated with neuronal cell death, e.g., a neurodegenerative disease.

Abstract: One aspect of the present invention relates to a method of labeling a peptide or protein comprising a phosphorylated amino acid comprising: a) removing from the peptide or protein the phosphate group via a ?-elimination to form a double bond conjugated to a C?O group; b) reacting the double bond from step a) with a nucleophile comprising a tag on a solid support; and c) removing the solid support from the product of step b) forming the labeled peptide or protein. A second aspect of the invention relates to a solid support comprising a linker and tag between the solid support and a nucleophile, wherein the tag comprises a label.

Abstract: Disclosed are improved methods of treating individuals with Alzheimer's disease (AD) as well as methods to diagnose AD in an individual. Also included are compounds and methods of identifying compounds to treat AD. The present invention also discloses methods for decreasing the phosphorylation of amyloid precursor protein (APP), including inhibiting phosphorylation of amino acid residue tyrosine 668 of APP and for reducing cleavage of APP. The present invention further discloses transgenic (Tg), non-human animals and cells expressing a p25 transgene that are models of neurodegenerative diseases. Embodiments of the present invention are directed to methods wherein the Tg animals and Tg cells of the invention are used to screen for modulators of neurodegenerative disorders. The Tg animals and cells of the present invention are useful for elucidating the mechanisms of neurodegenerative disorders.