Abstract: Methods for treating the animal central nervous system against the effects of spinal cord injury, including associated cognitive, behavioral and physical impairments. Effective amounts of therapeutic agents are administered to the upper third of the patient's nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and/or copper such as iron chelators, copper chelators, and antioxidants. A particular example of a therapeutic agent is the iron chelator deferoxamine (DFO).

Abstract: Methods for treating the animal central nervous system for the effects of traumatic brain injury. Therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and/or copper such as iron chelators, copper chelators, and antioxidants. A particular example of such therapeutic agents is the iron chelator deferoxamine (DFO). An effective amount of DFO may be administered to the upper third of the nasal cavity of a patient suffering from traumatic brain injury. The effective amount of DFO is delivered directly to the patient's central nervous system for treating the traumatic brain injury.

Abstract: Methods for preconditioning and/or providing neuroprotection to the animal central nervous system against the effects of progressive supranuclear palsy. Therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and/or copper such as iron chelators, copper chelators, and antioxidants. A particular example of such therapeutic agents is the iron chelator deferoxamine (DFO). An effective amount of DFO may be administered to the upper third of the nasal cavity of a patient at risk for, or diagnosed with, progressive supranuclear palsy. The effective amount of DFO is delivered directly to the patient's central nervous system for preconditioning, preventing and/or treating the progressive supranuclear palsy.

Abstract: Methods are provided for the prevention and treatment of seizures and epilepsy. It is shown herein that leukocyte recruitment plays a key role in the pathogenesis of epilepsy. Treatment with an agent that inhibits leukocyte recruitment has therapeutic and preventative effects in blocking recurrent seizures and epilepsy.

Abstract: A method of selecting an agent comprising a neuroprotecting activity is disclosed. The method comprises: (a) introducing a plurality of agents into a plurality of cells; and (b) analyzing Vesicular Monoamine Transporter 2 (VMAT2) transcription in the cells; and (c) identifying an agent of the plurality of agents capable of up-regulating DJ-1-dependent VMAT2 transcription in the cells, thereby selecting the agent comprising the neuroprotectingactivity.

Abstract: The present invention provides effective dosing regimes for neural stem cell proliferating agents, kits containing effective dosing regimes for neural stem cell proliferating agents, and uses thereof. In particular, neural stem cell proliferating agents, such as hCG, prolactin and EPO are delivered to mammalian subjects at low doses in a continuous fashion over several days, as opposed to delivery of high doses in a short period of time.

Abstract: The present invention describes materials and methods related to synthetic peptides which block the secretion of neurotransmitters and induce muscle relaxation, and use of said peptides as inhibitors of neurotransmitter secretion and muscle contraction, and as inducers of muscle relaxation.

Abstract: Subjects having autism are treated with a composition that includes gamma-aminobutyric acid agonists. The gamma-aminobutyric acid agonist (GABA) can be a GABA(B) agonist, such as baclofen.

Abstract: Subjects having fragile X syndrome are treated with a composition that includes gamma-aminobutyric acid agonists. The gamma-aminobutyric acid agonist (GABA) can be a GABA(B) agonist, such as baclofen, including racemic and R-baclofen.

Abstract: Non-activated tissue-regeneration polypeptides (TRPs) and their preparation methods are disclosed. The TRPs include: a protein transduction domain (PTD) making the polypeptides to permeate a cell membrane without cell membrane receptors; a furin activation domain (FAD) which has at least one proprotein convertase cleavage site and which can be cleaved by the proprotein convertase and activate a tissue regeneration domain (TRD) in cells; and a tissue regeneration domain (TRD) which can be activated by the proprotein convertase cleavage of the FAD to stimulate the growth or formation of tissues or to induce the regeneration of tissues. The TRPs can be mass-produced by cultured bacteria, such as recombinant E. coli, are in a non-activated state before in vivo administration, and their separation, purification, handling, storage and administration are simple and convenient.

Abstract: The present invention provides a method for detecting or diagnosing in vitro Alzheimer's disease, or memory and/or cognitive disorders, using a human biological sample and the inactivation of STAT3 protein as an indication, and a method for screening for a therapeutic drug for Alzheimer's disease or memory and/or cognitive disorders, using the activation of STAT3 protein as an indication.

Abstract: The present invention relates to a composition comprising a peptide immunogen useful for the prevention and treatment of Alzheimer's Disease. More particularly, the peptide immunogen comprises a main functional/regulatory site, an N-terminal fragment of Amyloid ? (A?) peptide linked to a helper T cell epitope (Th) having multiple class II MHC binding motifs. The peptide immunogen elicits a site-directed immune response against the main functional/regulatory site of the A? peptide and generate antibodies, which are highly cross-reactive to the soluble A?1-42 peptide and the amyloid plaques formed in the brain of Alzheimer's Disease patients. The antibodies elicited being cross reactive to the soluble A?1-42 peptide, promote fibril disaggregation and inhibit fibrillar aggregation leading to immunoneutralization of the “soluble A?-derived toxins”; and being cross-reactive to the amyloid plaques, accelerate the clearance of these plaques from the brain.

Abstract: A method of differentiating embryonic stem cells into oligodendroglial precursor cells and oligodendroglial cells by culturing a population of cells comprising a majority of cells that are characterized by a neural tube-like rosette morphology and are Pax6+/Sox1+ into a population of cells that are PDGFR?+.

Abstract: The invention relates to the MeCP2 protein and its use in protein substitution therapy. More specifically, the invention relates to condon-optimized nucleic acid sequences for the expression of MeCP2 proteins, methods for creating such a nucleic acid sequence and expressing such a protein, fusions of a protein of the invention to a transduction domain, and vectors and host cells comprising a protein of the invention. Further, the invention relates to uses of nucleic acids or proteins of the invention in medicine, pharmaceutical compositions comprising nucleic acid sequences and proteins of the invention, as well as methods for the treatment, prevention, and/or therapy of neurodegenerative or neurodevelopmental diseases including Rett syndrome.

Abstract: The present invention provides methods and compositions for identifying compounds which modulate cellular glycosylation. The invention further provides methods for treating subjects suffering from or at risk of developing a glycosylation associated disorder.

Abstract: The invention provides a method for diagnosing amyotrophic lateral sclerosis (ALS) in a subject, a method for assessing the effectiveness of a drug in treating ALS, and a method for determining the site of onset of ALS in a subject. Each method comprises (a) obtaining a sample from the subject, (b) analyzing the proteins in the sample by mass spectroscopy, and (c) determining a mass spectral profile for the sample. In some embodiments, the method comprises comparing the mass spectral profile of the sample to the mass spectral profile of a positive or a negative standard.

Abstract: Novel bifunctional peptides useful in the treatment and/or diagnosis of EAE or MS. The peptides have a first peptide portion derived from an epitope of myelin proteolipid protein, myelin oligodendrocyte glycoprotein, or oligodendrocyte-specific peptide and a second peptide portion derived from CD11a (LFA-1 alpha subunit), CD18 (LFA-1 beta subunit), CD154 (CD40L), Fas-Ligand, or CTLA4. The carboxy and/or amino termini of the bifunctional peptides may be modified.

Abstract: The present invention discloses anti-histone H1 monoclonal antibodies, hybridomas for the production thereof, and polypeptides, which are useful for suppressing, predicting, or diagnosing transplant rejection in organ transplantation.

Abstract: Neural outgrowth in the central nervous system is achieved by administering chondroitinase AC and/or chondroitinase B to degrade chondroitin sulfate proteoglycans that inhibit or contribute to the inhibition of nervous tissue regeneration.

Abstract: There is disclosed a pharmaceutical composition and method for treating sepsis, including septic shock and ARDS (acute respiratory distress syndrome), comprising administering an effective amount of a HMG1 antagonist. There is further disclosed a diagnostic method for monitoring the severity or potential lethality of sepsis or septic shock, comprising measuring the serum concentration of HMG1 in a patient exhibiting or at risk of exhibiting sepsis or septic shock symptoms. Lastly, there is disclosed a pharmaceutical composition and method for effecting weight loss or treating obesity, comprising administering an effective amount of HMG1 or a therapeutically active HMG1 fragment.