60 results about "Neuron cell death" patented technology

A therapeutic and / or cosmetic formulation comprising at least one anti-sense polynucleotide to a connexin protein together with a pharmaceutically acceptable carrier or vehicle is useful in site specific down regulation of connexin protein expression, particularly in reduction of neuronal cells death, wound healing, reduction of inflammation, decrease of scar formation and skin rejuvenation and thickening.

This invention relates generally to stimulating neurogenesis (e.g., post-natal neurogenesis, e.g., post-natal hippocampal neurogenesis) and protection from neuron cell death.

This invention relates generally to stimulating neurogenesis (e.g., post-natal neurogenesis, e.g., post-natal hippocampal neurogenesis) and protection from neuron cell death.

The present invention makes available a method for inducing neuronal differentiation and preventing the death or degeneration of neuronal cells both in vitro and in vivo. The subject method stems from the unexpected finding that, contrary to traditional understanding of neural induction, the default fate of ectodermal tissue is neuronal rather than mesodermal and / or epidermal. In particular, it has been discovered that preventing or antagonizing a signaling pathway in a cell for a growth factor of the TGF-β family can result in neuronal differentiation of that cell.

This invention relates generally to stimulating neurogenesis (e.g., post-natal neurogenesis, e.g., post-natal hippocampal neurogenesis) and protecting from neuron cell death.

This invention relates to a method for reducing a condition associated with fetal alcohol syndrome in a subject who is exposed to alcohol in utero with an ADNF polypeptide. In particular, the present invention relates to a method of reducing a condition associated with fetal alcohol syndrome in a subject who is exposed to alcohol in utero with a combination of ADNF I and ADNF III polypeptides. The present invention further relates to a method for reducing neuronal cell death by contacting neuronal cells with a combination of ADNF I and ADNF III polypeptides. Still further, the present invention relates to a pharmaceutical composition comprising a combination of ADNF I and ADNF III polypeptides.

The present invention is based on the discovery that oligodendrocyte-myelin glycoprotein (OMgp), which is ex-pressed by oligodendrocytes and CNS myelin, negatively regulates oligodendrocyte and neuronal differentiation and survival. Based on these discoveries, the invention relates generally to methods of promoting neuronal and oligodendrocyte survival and differentiation by administration of an OMgp anatagonist. Additionally, the invention generally relates to methods of treating various diseases, disorders or injuries associated with demyelination, dysmyelination, oligodendrocyte / neuronal cell death, axonal injury and / or differentiation by the administration of an OMgp antagonist.

The present invention relates to methods and compositions for inhibiting proliferation and inducing cell death in a population of cancer cells by (i) increasing the amount of the differentiation associated protein MDA-7, and (ii) decreasing RAS activity within the population. It is based, at least in part, on the discovery that decreasing expression of a mutated, activated K-ras gene, together with introducing an expressible mda-7 gene, in pancreatic cancer cells had a synergistic growth-inhibitory and anti-survival effect, and abolished tumorigenicity of the cells in athymic nude mice. The methods of the invention may be directed to the therapy of pancreatic cancer and other malignancies.

This invention relates generally to stimulating neurogenesis (e.g., post-natal neurogenesis, e.g., post-natal hippocampal neurogenesis) and protecting from neuron cell death.

This invention relates generally to stimulating neurogenesis (e.g., post-natal neurogenesis, e.g., post-natal hippocampal neurogenesis) and protection from neuron cell death.

A neuronal cell death inhibitor comprising a compound having an inhibitory activity on the production and / or release of glutamic acid in a microglia; by inhibiting the production and / or release in a microglia, neurite bead-like degeneration or neuronal cell death can be inhibited.

This invention relates to Activity Dependent Neurotrophic Factor I complex (ADNF I complex) and polypeptides of this complex, which produce their neurotrophic effects through multiple proteases intrinsic to the ADNF I complex. The invention also relates to pharmaceutical compositions comprising ADNF I complex polypeptides, as well as methods for reducing neuronal cell death in vitro and in vivo, methods for treating oxidative stress in a patient, methods for reducing a condition associated with fetal alcohol syndrome in a subject, and methods of enhancing learning and memory both pre- and post-natally, all of which methods use the ADNF I complex polypeptides of the invention.

The present invention relates to a pharmaceutical composition for the treatment and / or prevention of a neurodegenerative disease, comprising the following polypeptide shown in any of (a) to (c): (a) a polypeptide comprising the amino acid sequence represented by Ser-Ala-Leu-Leu-Arg-Ser-Ile-Pro-Ala-Pro-Ala-Gly-Ala-Ser-Arg-Leu-Leu-Leu-Leu-Thr-Gly-Glu-Ile-Asp-Leu-Pro (SEQ ID NO: 1); (b) a polypeptide comprising an amino acid sequence having a deletion, substitution, insertion, and / or addition of one or several amino acids in the amino acid sequence consisting of Ser-Ala-Leu-Leu-Arg-Ser-Ile-Pro-Ala-Pro-Ala-Gly-Ala-Ser-Arg-Leu-Leu-Leu-Leu-Thr-Gly-Glu-Ile-Asp-Leu-Pro (SEQ ID NO: 1), and having an activity that inhibits neuronal cell death associated with neurodegenerative disease; and (c) a modified polypeptide from the polypeptide (a) or (b), or a pharmaceutically acceptable salt thereof, as an effective ingredient.

The pharmaceutical composition comprising the compound of the invention having 8-azaprostaglandin skeleton represented by formula (I) (wherein, all the symbols have the same meanings as that of the specification.) a salt thereof, a solvate thereof or a cyclodextrin clathrate thereof, or a prodrug thereof and them as active ingredient have EP4 agonistic action and thus are considered useful for the prevention and / or treatment of immunological diseases, asthma, neuronal cell death, arthritis, lung failure, pulmonary fibrosis, pulmonary emphysema, bronchitis, chronic obstructive pulmonary disease, liver damage, acute hepatitis, nephritis, renal insufficiency, hypertension, myocardial ischemia, systemic inflammatory response syndrome, sepsis, hemophagous syndrome, macrophage activation syndrome, Still's disease, Kawasaki disease, burn, systemic granulomatosis, ulcerative colitis, Crohn's disease, hypercytokinemia at dialysis, multiple organ failure, shock and glaucoma, etc. Furthermore, the compounds also have an action of accelerating bone formation, so it is expected to be useful for the prevention and / or treatment of diseases associated with loss in bone mass, for example, primary osteoporosis, secondary osteoporosis, bone metastasis of cancer, hypercalcemia, Paget's disease, bone loss, osteonecrosis, bone formation after bone operation, alternative treatment for bone grafting.

An object of the present invention is to provide an agent effective for the treatment and / or prevention of motor neuron disease such as amyotrophic lateral sclerosis (ALS). The present invention provides a therapeutic and / or preventive agent for motor neuron disease comprising the following oligopeptide shown in any of (a) to (c) or a pharmaceutically acceptable salt thereof as an active ingredient: (a) an oligopeptide consisting of the amino acid sequence represented by Ser-Ala-Leu-Leu-Arg-Ser-Ile-Pro-Ala (SEQ ID NO: 1); (b) an oligopeptide consisting of an amino acid sequence having a deletion, substitution, insertion, or addition of one or several amino acids in Ser-Ala-Leu-Leu-Arg-Ser-Ile-Pro-Ala (SEQ ID NO: 1), and having an activity that inhibits neuronal cell death caused by a mutant superoxide dismutase-1 gene; and (c) a modified oligopeptide from the oligopeptide (a) or (b).

This invention provides compounds, compositions, and methods for treating Parkinson's disease. In particular, there is provided GM1 ganglioside analogs that are capable of penetrating the blood brain barrier and entering the cytoplasm of neurons. Endogenous GM1 interacts with the with GFRα1 / RET, the GDNF receptor complex involved in GDNF signaling which is essential for neuron survival. In neurons that are deficient in endogenous GM1, the GM1 analog compounds of the invention are capable of restoring GDNF signaling thereby preventing neuron cell death.

It is intended to provide antibodies having a higher reactivity with amylospheroid than a reactivity with amyloid ss-fiber and so on. Some of these antibodies have an activity of inhibiting amylospheroid formation or an activity of inhibiting the induction of nerve cell death by amylospheroid. Such antibodies are usable in remedies / preventives for Alzheimer's disease, screening these drugs, detecting an individual suffering from Alzheimer's disease, reagents and so on.

Provided herein are compositions and methods for reducing one or both of axonal degeneration and neuronal cell death associated with a disease or traumatic brain injury. An aminopropyl carbazole agent with potent neuroprotective properties is described. Specifically, (−)-(S)—N-(3-(3,6-dibromo-9H-carbazol-9-yl)-2-fluoropropyl)-6-methoxypyridin-2-amine, is proposed as a new pharmacological agent for protecting patients against axonal degeneration and chronic consequences of TBI.

The present invention is directed to providing an antibody having greater reactivity with amylospheroid than with amyloid β fibers, and the like. The aforementioned antibody includes an antibody having activity of inhibiting amylospheroid formation or activity of inhibiting neuronal cell death induced by amylospheroid. The antibody can be used for a therapeutic and / or preventive agent for Alzheimer's disease, or a screening thereof, a method and reagent for detecting individuals with Alzheimer's disease, and the like.

The present invention provides for a double stranded RNA comprising a first RNA sequence and a second RNA sequence wherein the first and second RNA sequence are substantially complementary, wherein the first RNA sequence has a sequence length of at least 19 nucleotides and is substantially complementary to SEQ ID NO. 1. Said double stranded RNA is for use in inducing RNAi against Huntingtin exon 1sequences. The double stranded RNA of to the invention was capable of reducing neuronal cell death and huntingtin aggregates in an animal model.

This invention provides novel neuroprotective 4-pyrimidineamine derivatives and neuroprotective pharmaceutical compositions comprising 4-pyrimidinamines. This invention also provides methods of using these compositions to prevent ischemic cell death, particularly neuronal cell death, and reduce the likelihood of neuronal cell death in a subject due to a traumatic event. Finally, this invention provides an apparatus for administering to a subject the instant pharmaceutical compositions.

Macromolecule intracellular transduction technology based on improved cell-permeable Parkin recombinant protein (iCP-Parkin) has been developed as a protein-based anti-neurodegenerative agent for efficient BBB-penetration to effectively deliver the recombinant protein into the brain. Parkin protein, a dopaminergic neuronal cell death inhibitor, has been fused with a newly developed advanced macromolecule transduction domain (aMTD) and solubilization domain (SD) to increase the solubility / yield and cell- / tissue-permeability of the recombinant protein. In addition, our newly developed aMTD / SD-fused recombinant iCP-Parkin protein has shown BBB-permeability. Both in vitro and in vivo, our iCP-Parkin recombinant protein improved motor skills, a typical phenotype of Parkinson's disease, by increasing dopamine level in the brain by suppressing apoptosis of dopaminergic neuron cells. In conclusion, iCP-Parkin could be applicable in clinical studies as a protein-based anti-neurodegenerative agent to treat Parkinson's disease by protecting dopaminergic neuron cells and regulating the secretion of dopamine.

The invention discloses an application of miR-214 (microRNA) to preparation of a product for preventing or treating an alzheimer disease, and provides an application of the miR-214 to preparation of 1) a product for preventing and / or treating the alzheimer disease, and / or 2) a product for reducing the neuron cell death quantity of the alzheimer disease. A nucleotide sequence of the miR-214 is Sequence 1 as shown in a sequence table. An experiment of the application proves that neurodegenerative diseases, such as the alzheimer disease, can be prevented and / or treated through improving substances expressed by the miR-214. In clinical diagnosis at an earlier stage, the miR-214 can also serve as a biological index for diagnosing the neurodegenerative diseases, and a doctor can perform early diagnosis of the neurodegenerative diseases timely on a patient through detecting an miR-214 level in the patient and combining with other effective indexes, and further effectively controls the neurodegenerative diseases and the loss of a cognition level.

Methods and compositions involving a class of boron-protected phenylphosphine agents having increased cell permeability and having improved chemical stability for treating or for preventing neuronal cell death-related diseases or conditions in a human or a non-human animal.

Methods and compositions for identifying an agent (e.g., a gene product or small molecule compound that modulates neuronal cell death in a Parkinson's disease animal model are provided. In practicing the subject methods, a non-mammalian animal model, such as Drosophila melanogaster, that includes a mutant parkin gene and at least one other mutant gene are evaluated for neuronal cell death. Also provided are kits and systems for practicing the subject methods, as well as methods of use of agents identified in the screening method of the invention.

An antibody provided by the present invention has a low reactivity with amyloid precursor proteins, and has a higher reactivity with amylospheroids than with amyloid β fibrils or monomeric amyloid β-proteins. According to the present invention, an antibody is provided that has a higher reactivity with amylospheroids than with amyloid precursor proteins, and has any one or more of the following properties: (i) a higher activity with amylospheroids than with amyloid β fibrils; (ii) a higher reactivity with amylospheroids than with monomeric amyloid β-proteins; and (iii) an activity of inhibiting neuronal cell death induced by amylospheroids.

The invention provides methods of inhibiting Aβ-induced neuronal cell death. The invention further provides methods of providing neuroprotection to a subject and methods of treating a disease state characterized by Aβ-induced neuronal cell death in a subject. Methods of inhibiting p75 receptor mediated neuronal cell death, as well as methods of treating a disease state in a subject characterized by p75 receptor mediated neuronal cell death are provided.

Small molecule agonists, partial agonists, and antagonists for the TrkA receptor are described. The compounds are gambogic amines, where the carboxylic acid group of gambogic acid (CO2H) has been replaced by an amine group (CH2NR1R2). In some embodiments, the compounds selectively bind to TrkA but not TrkB or C, robustly induce its tyrosine phosphorylation and downstream signaling activation including Akt and MAP kinases. Further, they can strongly prevent glutamate-induced neuronal cell death and provoke prominent neurite outgrowth in PC12 cells. Gambogic amines specifically interact with the cytoplasmic juxtamembrane domain of TrkA receptor and trigger its dimerization. Administration of these compounds in can substantially diminishes Kainic acid-triggered neuronal cell death and decrease infarct volume in transient middle cerebral artery occlusion (MCAO) model of stroke. Thus, these compounds can provide effective treatments for debilitating neurodegenerative diseases and provide neuroprotection from patients suffering from stroke or other ischemic events.

Human serum paraoxonase enzyme and DNA (RNA) encoding such serum paraoxonase enzymes are disclosed. Also provided is the procedure for producing such polypeptides by recombinant techniques. Uses of such polypeptides include their use as an antidote for organophosphate poisoning and to prevent neuronal cell death.