Abstract: The invention provides a composition comprising SGEF protein or gene as a therapeutic means to clinical or subclinical defects associated with anomalies of at least one from among the macula, corpus callosum, hippocampus, liver or immune system or feverless response to infection. Methods of diagnosis of such disease and development anomalies are based on detection of mutations of the SGEF gene. The SGEF protein is also used as a preventive or curative treatment of atherosclerosis by local or systemic delivery. The invention also provides a composition comprising an inhibitor of the SGEF gene expression or SGEF protein concentration, as a therapeutic means for glaucoma, osteoarthritis, auto-inflammatory diseases, tumors or cancers.

Abstract: This invention provides new therapeutic peptides, i.e. new protracted Exendin-4 compounds, pharmaceutical compositions and the use of such.

Abstract: The present invention is directed to conjugates that include a polypeptide capable of crossing the blood-brain barrier or entering one or more cell types attached to a transport vector, i.e., a composition capable of transporting an agent (e.g., a therapeutic agent). In certain cases, the polypeptides are directly conjugated to a lipid or polymeric vector to allow targeted application of a therapeutic agent to treat, for example, a cancer, a neurodegenerative disease, or a lysosomal storage disorder.

Abstract: Described herein are isolated polypeptides having phosphatase and tensin homolog (PTEN) inhibitory activity, vectors and cells for the expression thereof and methods for their use in treating diseases associated with cytotoxic stress, such as spinal cord injury, stroke, traumatic brain injury, multiple sclerosis, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Huntington's disease.

Abstract: The present invention relates to the field of protein misfolding diseases and thus to diseases which are associated with or induced by abnormal or pathogenic three-dimensional folding of proteins and/or peptides or which are linked to pathogenic conformational changes of proteins and/or peptides, such as Alzheimer's disease. Particularly, the present invention provides novel trimeric pyrazole compounds, which exhibit a therapeutic effectiveness in regard to the aforementioned protein misfolding diseases, and refers to their use for the treatment of such protein misfolding diseases, especially neurodegenerative diseases as well as to medicaments or pharmaceutical compositions comprising these compounds.

Abstract: The present invention relates to apolipoprotein A-1 mimic peptides, and therapeutic agent for treating hyperlipidemia and diseases related to hyperlipidemia comprising the same. More specifically, the apolipoprotein A-1 mimic peptides of the present invention were manufactured by modifying hydrophilic or hydrophobic face of existing 4F amphipathic peptides to produce Apo A-I mimic peptides which specifically bind with cholesterol ester to allow high density lipoprotein content to increase, and the peptide of which phenylalanine in hydrophobic face of 4F is substituted with 2-naphthylalanine has superior cholesterol efflux capability and cognitive function for lipids to the existing 4F peptides, among the mimic peptides. Thus, the Apo A-I mimic peptides of the present invention can be used as Apo A-I mimic peptides and as a therapeutic agent for treating hyperlipidemia and diseases related to hyperlipidemia.

Abstract: An antioxidant compound is disclosed, along with pharmaceutical compositions and methods of treatment which utilize said compound. The compound is characterized by a peptide including at least three amino acid residues of which at least two are cysteine residues, and a first hydrophobic or non-charged moiety being attached to an amino terminal of the peptide via a first bond and a second hydrophobic or non-charged moiety being attached to a carboxy terminal of the peptide via a second bond, as described herein. Cleavage of the peptide by an intracellular peptidase results in generation of a plurality of antioxidant species, each including one of the cysteine residues, thereby providing for a plurality of different antioxidant species acting in synergy in exerting antioxidation.

Abstract: Fragments of snapin important for interaction with cypin and thus regulating microtubule assembly are provided. Also provided are methods of use of said fragments and kits to facilitate said methods.

Abstract: The invention pertains to a liquid composition for preventing and/or treating memory decline and/or cognitive dysfunction, Alzheimer's, Parkinson's and/or dementia, said composition comprising: (i) at least 50 mg nucleoside and/or nucleotide per 100 ml; (ii) between 0.2 and 10 grams protein per 100 ml; (iii) between 0.05 and 3 wt. % of 5 thickener, based on total weight of the composition. The thickener is preferably selected from the group consisting of cellulose, xanthan gum, gellan gum, alginate, guar gum, locust bean gum, gum karaya, gum tragacanth, carrageenan, and mixtures thereof. The composition preferably has a loss factor tan ? between 0.1 and 100, as measured at any strain in the range of 1 100% at 0.1 Hz and 20° C. It is particularly found that a thickener selected from the group consisting of gellan gum, xanthan gum and cellulose greatly reduces sedimentation.

Abstract: The invention relates to novel polypeptide analogues of GLP-1 and exendin-4. The polypeptide, in a preferred embodiment, is insulinotropic and long-acting. Preferably, the polypeptide's insulinotropic effect is comparable to or exceeds the effect of an equimolar amount of GLP-1 or exendin-4. The invention also relates to a method of treating a subject with diabetes, comprising administering to the subject the polypeptide of the invention in an amount that has an insulinotropic effect. The invention also relates to methods of using GLP-1, exendin-4, and polypeptide analogues thereof for neuroprotective and neurotrophic effects.

Abstract: Neurotrophin binding to its specific receptors Trk A and p75 leads to the activation of multiple signalling cascades, culminating in neuroprotective and regenerative effects, including neuronal survival and neurite outgrowth. Neurotrophic factors have been used for the treatment of several neurodegenerative diseases. However, their use is limited by their inability to cross the blood-brain barrier, their short half life and their side effects. Small molecule neurotrophin mimetics may be beneficial in treating a number of neurodegenerative disorders. The present invention shows the capacity of nerve growth factor agonist molecules of Formulae I-IV, as defined in the specification, to induce differentiation in PC 12 cells, promote survival in RN22 cells and activate Trk A, IkBa and SAPK/JNK phosphorylation to various extents in both cell lines.

Abstract: Various embodiments provide methods for the detection, the diagnosis, and/or the prediction of disease onset of Alzheimer's disease. Methods for determining a state of Alzheimer's disease are provided. Accordingly, these methods can comprise the steps of placing a sample comprising at least one blood component onto a substrate, labeling the sample to identify at least one epigenetic marker and at least one of an inflammation marker and a cellular stress marker; determining an amount of the markers; performing a multivariate statistical analysis to produce an output value; comparing the output value to a reference value; and determining a state of Alzheimer's disease.

Abstract: The invention provides Sp35 polypeptides and fusion proteins thereof, Sp35 antibodies and antigen-binding fragments thereof and nucleic acids encoding the same. The invention also provides compositions comprising, and methods for making and using, such Sp35 antibodies, antigen-binding fragments thereof, Sp35 polypeptides and fusion proteins thereof.

Abstract: The subject invention relates to the cloning, expression and isolation of recombinant forms of beta-amyloid protein containing a N-terminal methionine (or one or more amino acids) as well as to methods of using this recombinant protein in the production of therapeutic antibodies, in the identification of therapeutic small molecules, and in the performance of diagnostic assays.

Abstract: The present invention relates to a novel use of substance P. The substance P of the present invention exhibits effects of decreasing microglia activity, decreasing proinflammatory cytokines, inhibiting apoptosis, etc. The substance P of the present invention effectively treats degenerative central nervous system diseases or disorders such as a spinal cord injury caused by a traumatic injury (flexion injury, vertical compression injury, hyperextension injury, flexion-rotation injury) and by a non-traumatic injury (vascular dysfunction, arthritis, or degenerative arthritis), Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, depressive disorder, epilepsy, etc.

Abstract: Isolated DJ-1 related peptides are disclosed and pharmaceutical compositions comprising same for treating oxidative stress-related disorder.

Abstract: The present invention provides a method of detecting or diagnosing a neurodegenerative disease or condition in a subject. Further aspects of the invention provide a method of monitoring a subject over a period of time to detect the development or progress of a neurodegenerative disease or condition. Methods of treating, detecting or diagnosing a neurodegenerative disease or condition in a subject are also provided.

Abstract: This invention relates to methods of treating diseases involving accumulation of A? plaques, including Alzheimer's Disease by the peripheral administration of soluble Nogo receptor polypeptides. The invention also provides methods of increasing the plasma to brain ratio of A? peptide and enhancing A? peptide clearance via peripheral administration of soluble Nogo receptor polypeptides. This invention also provides methods of improving memory function or inhibiting memory loss via the peripheral administration of soluble Nogo receptor polypeptides. The invention also provides methods of decreasing the size and number of A? plaques in a mammal via peripheral administration of soluble Nogo receptor polypeptides.

Abstract: A GABA (gamma-aminobutyric acid) release-inhibiting agent in the cerebellum and a composition for treating pathological symptoms caused by over-release of GABA in the cerebellum, each comprising a Bestrophin 1(Best1) channel inhibitor as an active ingredient; a GABA release-promoting agent in the cerebellum and a composition for treating pathological symptoms caused by the deficit of GABA in the cerebellum, each comprising a Best1 channel activator as an active ingredient; and a method for screening a GABA release-regulating agent in the cerebellum, which uses Best1 channel as target, are provided.

Abstract: The present invention is related to chimeric and humanized antibody and to methods and compositions for the therapeutic and diagnostic use in the treatment of amyloidosis, a group of disorders and abnormalities associated with amyloid protein such as Alzheimer's disease.

Abstract: Disclosed are peptides for augmenting the expression of BDNF (brain-derived neurotrophic factor) and a pharmaceutical composition for the prevention and treatment of Alzheimer's disease or Parkinson's disease, comprising the same. The peptides can induce the expression of BDNF in dopamine-reactive human cells, pass easily through the blood-brain barrier thanks to their low molecular weights and are almost free of cytotoxicity. Thus, they are useful in the prevention and treatment of neuropathies such as Alzheimer's disease or Parkinson's disease.

Abstract: The invention relates to methods of regulating complement. In particular, the inventors have identified a relationship between a particular gene, CFHR5, and irregularities in complement regulation. The invention provides a method for diagnosing a complement related disease, comprising identifying a mutation in the CFHR5 gene in a sample obtained from a subject.

Abstract: The present invention provides peptide-based peroxidase inhibitors having the formula AA1-AA2-AA3, wherein AA1 is a positively charged, negatively charged or neutral amino acid, AA2 is a redox active amino acid, and AA3 is an amino acid possessing a reducing potential such that AA3 is capable of undergoing a redox reaction with a radical of amino acid AA2 or a retro or retro-inverso analog thereof. The result of such a combination is a highly effective inhibitor of peroxidase activity that has potent anti-inflammatory properties in widely diverse models of vascular disease and injury. Exemplary tripeptides effectively inhibit peroxidase mediated LDL oxidation, increase vasodilation in SCD mice, inhibit eosinophil infiltration and collagen deposition in asthma mice, inhibit acute lung injury, and decrease ischemic injury of the heart.

Abstract: The present invention relates to a pharmaceutical composition for the prevention or treatment of neurological disorders, comprising an ICAM-1 (intercellular adhesion molecule-1) protein, or a fragment or a variant thereof as an active ingredient, which can increase the expression of neprilysin to remove amyloid-beta (A?), a cause of dementia, and is thus useful in preventing or treating a neurological disease including Alzheimer's disease.

Abstract: The present invention relates to a method for identifying an inhibitor of the aggregation of amyloid-? peptide (A?), comprising the steps of a) contacting at least one A?-peptide and/or the nitrated forms thereof with at least one candidate inhibitor that potentially specifically binds to a region in said A?-peptide capable of being nitrated, and b) detecting said inhibitor specifically binding to said region in said A?-peptide through detecting a lack of or a reduced aggregation of said at least one A?-peptide. The present invention is further directed at improved methods for treating neuronal degradation and particularly Alzheimer's disease, based on said inhibitor. The present invention is further directed at methods for diagnosing the aggregation of A?-peptide in the context of neuronal degradation and particularly Alzheimer's disease.

Abstract: The present invention provides a peptide which functions as a mimic peptide of an amyloid ? peptide and is capable of inhibiting the fibrillogenesis of an amyloid ? peptide. The present invention relates to an 8- to 30-amino acid residue peptide comprising an amino acid sequence represented by the following formula (I): X1-Asp-X2-X3-X4-Pro-X5-X6 (SEQ ID NO: 28) (I), wherein X1 represents a branched chain amino acid, and X2, X3, X4, X5, and X6 are the same or different and each represents an ?-amino acid, and to a pharmaceutical composition and an amyloid ? fibrillogenesis inhibitor comprising the peptide.

Abstract: The invention is directed to a method of treating a patient suffering from Alzheimer's disease comprising administering to said patient an agent that reduces the activity of the IGF-1 signaling pathway.

Abstract: The present invention relates to methods for treating, preventing, or diagnosing the pathology of progressive cognitive disorders resulting from accumulation of an amyloid peptide, in particular, Alzheimer's disease, Down's syndrome and cerebral amyloid angiopathy, in mammalian subjects using a composition comprising therapeutically effective amount of a leptin, leptin mimic, leptin derivative, leptin agonist, or AMP-dependent protein kinase activator, alone, or in combination with, one or more lipolytic/antilipogenic compounds. It further relates to methods for improving cognitive function using a composition comprising a therapeutically effective amount of leptin, a leptin mimic, a leptin derivative, an AMP-dependent protein kinase activator, a leptin agonist, a leptin blocker, a mimic of a leptin blocker, a leptin antagonist, an AMP-dependent protein kinase inhibitor; or a pharmaceutically acceptable salt thereof.

Abstract: This invention relates to grassystatins A, B and C, and their isolated or purified forms. The compounds of the invention are useful as aspartic protease, gamma secretase, or metalloprotease inhibitors. Methods of using the compounds and compositions thereof are also disclosed.

Abstract: A chaperone protein Q2 and ?-amyloid can form a complex. This complex can be detected in a biological sample, such as, for example, tissues or fluids from a mammal. Q2 levels can also be detected in a biological sample. A method for determining the Q2 level in a biological sample and comparing that level to a normal Q2 level can be used to detect, screen, diagnose, or otherwise determine a person's susceptibility to Alzheimer's disease such as, for example, the presence or absence of Alzheimer's disease, of symptoms of this disease, of factors leading to or associated with this disease, of likelihood of developing this disease, and the like. In one embodiment, a decline in Q2 level correlates to an increased likelihood of developing Alzheimer's disease. In another embodiment, a decline in Q2 level correlates to an increase in ?-amyloid aggregation. The method may further include screening for an apolipoprotein E genotype, which is associated with Alzheimer's disease.

Abstract: Disclosed are the novel glycolipoprotein gintonin isolated and identified from ginseng, a method for preparing the same, and uses thereof. Gintonin causes a transient increase in intracellular free Ca2+ level, which in turn activates endogenous Ca2+-activated chloride channel to elevate intracellular calcium levels. Therefore, the novel glycolipoproteins are useful in the therapy and prophylaxis of calcium deficiency-associated diseases as well as effectively inducing calcium-dependent physiological activities, including adaptogenic activity, immunostimulatory activity, aphrodisiac activity, neuroprotection and neuroactivation, angiogenesis, and antidiabetic activity.

Abstract: The present invention generally relates to methods, compositions and materials for treatment of and promotion of neurological functional recovery from neurological conditions including central nervous system injuries and/or diseases.

Abstract: This invention discloses CN2097-like compositions that facilitate the induction of long-term potentiation (LTP). In one embodiment the method comprises inducing long-term potentiation in a subject by the method of administering a therapeutically effective dose of a CN2907-like compound.

Abstract: A method for delivering a biologic pharmaceutical, comprising: administering an effective amount of a biologic pharmaceutical to a patient in need thereof by perispinal injection, without direct intrathecal or direct epidural injection.

Abstract: Methods of suppressing the activation of microglial cells in the Central Nervous System (CNS), methods of ameliorating or treating the neurological effects of cerebral ischemia or cerebral inflammation, and methods of combating specific diseases that affect the CNS by administering a compound that binds to microglial receptors and prevents or reduces microglial activation are described. Also described are methods of screening compounds for the ability to suppress or reduce microglial activation.

Abstract: The use of the HIP/PAP protein or a protein derivative thereof for manufacturing a medicament for preventing or treating: a neonatal brain injury, which includes a neonatal brain injury caused by a brain hypoxia, an adult or child brain injury, which includes an adult or child brain injury caused by a brain hypoxia, an adult or child or neonatal traumatic brain injury, a cerebellar disease or disorder, and a disease involving a defect in the production or in the phosphorylation of Gap-43.

Abstract: The present invention relates to multimeric (e.g., dimeric, trimeric) forms of peptide vectors that are capable of crossing the blood-brain barrier (BBB) or efficiently entering particular cell types. These multimeric peptide vectors, when conjugated to agents (e.g., therapeutic agents) are capable of transporting the agents across the BBB or into particular cell types. These compounds are therefore particularly useful in the treatment of neurological diseases.

Abstract: Methods are disclosed for determining progression of a condition, onset of a condition, or efficacy of treatment of a condition characterized by an adipocyte imbalance in a patient. In addition, methods are disclosed of treating diabetes, abnormal adipocyte activity, and insulin resistance using monomeric, homodimeric, and heterodimeric forms of certain C-terminal fragments of adiponectin receptor. In addition, methods of treating abnormal adipocyte activity, treating metabolic syndrome, causing insulin secretion, increasing insulin levels, inhibiting insulin degradation enzyme, treating Alzheimer's disease, treating cardiovascular disease associated with adiponectin levels, inhibiting ADAM-17 enzyme, inhibiting a protease, treating a condition associated with TNF-alpha, and treating a condition associated with HER2-neu are disclosed. Compositions, dosage forms, and kits are also disclosed.

Abstract: The application describes several mutant amyloid beta peptides and specific regions which are useful in the therapeutic and diagnostic of neurological diseases. The application further describes methods of using these mutant peptides as treatment and reagents for diagnosis of diseases. The application further describes diagnostic kits and pharmaceutical compositions for use in therapy to treat neurological diseases including but not limited to Alzheimer's disease and various forms of mild cognitive impairments.

Abstract: The present invention relates generally to the field of brain health, brain protection, maintenance of cognitive function, prevention of cognitive decline and cognitive disorders. Neuronal cells in the brain can be protected. Also cognitive performance can be increased.

Abstract: The present invention provides methods for treating apoE-related disorders. The methods generally involve administering an effective amount of an agent that inhibits activity of an enzyme that cleaves apoE.

Abstract: An isolated protein selected from the group consisting of (i) proteins comprising an amino acid sequence having at least 70% identity to the C-terminal domain of lung surfactant protein C precursor (CTproSP-C, “CTC”) from a mammal; and (ii) proteins comprising an amino acid sequence having at least 70% identity to the Brichos domain of CTproSP-C from a mammal, is disclosed for treatment of Alzheimer's disease in a mammal, including man.

Abstract: S-protected cysteine analogs and related compounds and methods of using these compounds for the treatment of diseases and/or conditions, including but not limited to diseases and/or conditions of Central Nervous System (CNS).

Abstract: S-t-butyl protected cysteine di-peptide analogs and related compounds and methods of using these compounds for the treatment of diseases and/or conditions, including but not limited to diseases and/or conditions of Central Nervous System (CNS).

Abstract: The invention relates to a method of co-administering a peptide or protein drug with an enzyme-resistant PGA-complexone compound orally so to mitigate enzyme attack in the gastrointestinal tract of an animal subject.

Abstract: The present invention provides novel tetrahydrocarbazole compounds according to formula (I) as ligands of G-protein coupled receptors (GPCR) which are useful in the treatment and/or prophylaxis of physiological and/or pathological conditions in mammals mediated by GPCR or of physiological and/or pathological conditions which can be treated by modulation of these receptors.

Abstract: The present disclosure relates to methods and compositions for promoting the extension of a neural cell by increasing the expression of activity of cofilin in the cell. The increase can be local to the end of the neural cell in need of extension and the neural cell can be a cell in an individual. By extending the neural cell to reach its synaptic target, the methods and compositions of the present disclosure can also be used for treating neurological diseases characterized by damaged or degenerated neurons.

Abstract: Apoptosis inducing factor (“AIF”) contains a PAR-binding motif (“PBM”) that binds to Poly(ADP-ribose) (“PAR”). Binding of PAR to AIF via the PBM is required for AIF release from the mitochondria to occur, and that this PAR-related release is a key step in the programmed cell death process known as parthanatos, both in vitro and in vivo. Preventing or disrupting this release can inhibit parthanatos and thus be the basis for treatments for patients suffering from diseases or medical conditions during which parthanatos commonly occurs, including Parkinson's disease or diabetes, or patients who have had and are recovering from heart attack, stroke and other ischemia reperfusion-related injuries. Alternatively, agents could be identified that enhance the release of AIF, thereby promoting parthanatos and serving as potential anti-tumor chemotherapeutic agents.

Abstract: The present invention relates to pharmaceutical formulations of Aviptadil and its derivatives. The stability of the Aviptadil formulation was shown to be improved by a formulation having a defined concentration of Aviptadil prepared in a buffer having a defined pH range.

Abstract: Methods are provided for the preparation of conjugates of a variety of bioactive components, especially proteins, with water-soluble polymers (e.g., poly(ethylene glycol) and derivatives thereof), which conjugates have reduced antigenicity and immunogenicity compared to similar conjugates prepared using poly(ethylene glycol) containing a methoxyl or another alkoxyl group. The invention also provides conjugates prepared by such methods, compositions comprising such conjugates, kits containing such conjugates or compositions and methods of use of the conjugates and compositions in diagnostic and therapeutic protocols.