38 results about "Nerve degeneration" patented technology

The present invention relates to multipotent stem cells derived from the interstitial tissues of skeletal muscle. The multipotent stem cell of the present invention is capable of differentiating into skeletal muscle cells, smooth muscle cells, cardiomyocytes, blood cells, vascular endothelial cells, adipocytes, osteoblasts, nervous cells, hepatocytes and pancreatic cells, and is useful for regeneration of tissues and cells and treatment for cardiac failure, hepatic insufficiency, renal insufficiency, leukemia, nerve degeneration disease, arthritis, diabetes, arteriosclerosis, and the like.

Antibodies and fragments thereof have high affinity for human α-synuclein protofibrils and low binding of α-synuclein monomers, wherein the antibodies or fragments have specified Complementarity Determining Region (CDR) sequences. Compositions comprise such an antibody or fragment and methods of detecting α-synuclein protofibrils use such an antibody or fragment. In further embodiments, methods of preventing, delaying onset of or treating a neurodegenerative disorder with α-synuclein pathology comprise administering such an antibody or fragment, and such an antibody or fragment is used in the manufacture of a pharmaceutical composition for treatment of a neurodegenerative disorder with α-synuclein pathology. Such an antibody or fragment is used in the diagnosis or monitoring of the development of a neurodegenerative disorder with α-synuclein pathology, and in methods for reducing or inhibiting α-synuclein aggregation by administration of such an antibody or fragment.

The invention provides a drug combination for treating progressive nerve degradation or inhabiting the happening of the progressive nerve degradation of a high risk curer. The drug combination at least comprises the agent of a granulocyte colony stimulating factor receptor in effective quantity, thereby moving hematopoietic stem cells to peripheral blood from bone marrow. The combination can also be used for inhibiting the happening of the progressive nerve degradation on the high risk curer. In addition, a choice of the methods is provided for treating the agent of the granulocyte colony stimulating factor receptor of the progressive nerve degradation.

A compound represented by the formula: wherein X represents a sulfur atom or an oxygen atom; Y represents an optionally oxidized sulfur atom or an oxygen atom; Z represents a bond or a divalent hydrocarbon group; R1 represents an optionally substituted hydrocarbon group; R2 represents an optionally amidated or esterified carboxyl group; ring A represents an optionally substituted aromatic 5-membered heterocyclic ring; or a salt thereof. A compound of the above formula possesses cell differentiation inducing factor action-enhancing activity and anti-matrix metalloprotease activity and that is useful in the prevention and treatment of bone diseases such as osteoporosis, bone fractures, osteoarthritis and rheumatoid arthritis, arteriosclerosis, cancer metastasis, and diseases based on nerve degeneration.

The invention relates to the field of gene engineering, in particular to a target protein for Alzheimer's disease (AD) and a coding gene and application thereof. The symptoms of patients with the AD can be obviously improved or delayed by ribonucleic acid interference (RNAi) of expression of the target protein Zip1 which can be used for treating human neurodegenerative diseases, particularly the AD. The target protein for human AD has an amino acid sequence shown as SEQ ID NO.3 or 5, and the gene has a nucleotide sequence shown as SEQ ID NO.4 or 6. Through the RNAi of the target gene, the early cognitive ability of the patients with the AD can be improved, the deposition of an amyloid beta (A beta) protein in a brain and nerve degeneration caused thereby are slowed down or depressed, athletic ability is improved and life is prolonged. The invention is expected to provide a new treatment strategy and a key target for treating the AD.

The invention relates to gene chip used for detecting functional central nervous damage diagnosis and the preparing method. said gene chip is equipped with oligonucleotide gene probe array, the oligonucleotide biomolecule of said probe array is the special biological gene factor playing improtant role in multiple central nervous system damage process simutaneously, relating to netural cell death and tissue necrosis, inflammation, irritated response, ion dysequilibrium inside cell, signal transmission, abnormal control of cell cycle, abnormal cell construction and nerve degeneration damage morbid physiology and molecular biology active gene, respectively. The gene chip can be used to check the conditioning way, expression level and change rule of biological factor relative to cerebral ischemia damage inside body in the beginning of clinic for high risk group of cerebral apoplexy, and to predict possibility of cerebral apoplexy; and used to conditioning way and change rule of special biological factor relative to nerve damage inside nerve cell after central nervous system damage, and relationship between cell death and disease occurancy, and provides checking criterion for cilinical treatment.

Provided are compounds for the treatment of neurological diseases or injuries, including neurodegenerative diseases, stroke, trauma, epilepsy, acute and chronic kidney injuries, diabetes mellitus, and/or seizures. In some embodiments, derivatives of vitamin K are provided.

A specific clinical protocol for use toward therapy of defective, diseased and damaged neurons in the mammalian brain, of particular usefulness for treatment of neurodegenerative conditions such as Parkinson's disease. The protocol is practiced by directly delivering a definite concentration of a nerve growth factor via delivery of the protein, an expression vector operably encoding the nerve growth factor, or grafting a donor cell containing such an expression vector into the substantia nigra and preferably also the striatum. The method stimulates growth of targeted neurons, and reversal of functional deficits associated with the neurodegenerative disease being treated.

The invention relates to the field of gene engineering and especially relates to Huntingdon disease (HD)-targeted proteins and their coding genes and use. The HD-targeted genes provided by the invention comprise Ctrl, ATP7A and ATP7B, and through gene silencing interference of Ctrl or overexpression of ATP7A and ATP7B, HD patient symptoms are obviously relieved or HD occurrence is delayed. According to the invention, the human HD-targeted proteins have amino acid sequences shown in the formulas of SEQ ID No.5, SEQ ID No.6, SEQ ID No.7, SEQ ID No.8 and SEQ ID No.9. The genes have nucleotide sequences shown in the formulas of SEQ ID No.10, SEQ ID No.11, SEQ ID No.12, SEQ ID No.13 and SEQ ID No.14. Through gene silencing or gene overexpression, the targeted genes can be used for improving HD patient athletic ability, prolonging a HD patient life, and relieving or preventing cut huntingtin (htt) deposition in the brain and htt deposition-caused nerve degeneration. The invention provides a novel treatment approach and key target positions for HD.

The present invention provides an active substance of Lactic Acid Bacteria, a composition comprising thereof and its use for promoting longevity, especially for increasing Cisd2 gene expression, reducing mitochondrial damage and delaying aging conditions such as nerve degeneration and sarcopenia.

An application of tuduranine in treating the nervous degenerations of rectina, such as age-related macular degeneration, pigmentary degeneration of retina, etc is disclosed.

The present invention discloses a double transgenic fly that expresses both Tau protein and the human Aβ42 peptide of human amyloid-β precursor protein (APP). The double transgenic flies of the present invention display a synergistic altered phenotype as compared to the altered phenotype displayed by transgenic flies expressing either Tau or human Aβ42 alone, and thus provide for an improved model for neurodegenerative disorders, such as Alzheimer's disease. The invention further discloses methods for identifying for therapeutic compounds to treat neurodegenerative disorders using the double transgenic flies.

The present invention relates to a ternary fused ring nicotine analogues and its intermediate product. Said invention provides its molecular formula, and said compound is high in chemical stability, good in water soluble property, and can be used for preparing the medicines for curing the diseases (such as senile dementia, etc.) due to nerve degeneration and disturbance.

Disclosed is a novel use of xCT protein and gene coded by same in generation of nerve degeneration diseases. It is discovered for the first time that xCT protein and gene coded by same relates to generating mechanism of nerve degeneration diseases. A novel gene causing nerve degeneration diseases is discovered. Significance of the invention lies in that medicine improving expression quantity of Slc7a11 gene and xCT is screened by using Slc7a11 gene and xCT as targets, to improve expression quantity of Slc7a11 gene(normal gene) and xCT(normal protein), so to improve oxidation damage resistance ability of neurocyte, and as a result to prevent and slow down generation of nerve degeneration diseases. Animal models with the nerve degeneration disease of low expression quantity of Slc7a11 gene and xCT can be used to screen protein, nucleic acid, small organic molecule, and etc. which can improve expression quantity of Slc7a11 gene and xCT and use as candidate medicine.

The present invention provides an active substance of Lactic Acid Bacteria, a composition comprising thereof and its use for promoting longevity, especially for increasing Cisd2 gene expression, reducing mitochondrial damage and delaying aging conditions such as nerve degeneration and sarcopenia.

The present invention provides a Bifidobacterium lactis having active substances, a composition comprising the same, and a method of promoting longevity using the same by subjecting the composition to a subject, thereby increasing Cisd2 gene expression, reducing damage of mitochondria, delaying aging-related symptoms including nerve degeneration and sarcopenia, and so on.