89 results about "Neuronal degeneration" patented technology

The present invention relates generally to methods for promoting regeneration, outgrowth and survival of dopaminergic neurons comprising contacting said dopaminergic neurons with an effective amount of a composition comprising an Sp35 antagonist. Additionally, the invention is related generally to methods of treating various diseases, disorders or injuries associated with dopaminergic neuronal degeneration or death by administration of an Sp35 antagonist.

Oligosaccharides, and in particular disaccharides, which are degradation products of chondroitin sulfate proteoglycan are effective for use in treating, inhibiting, or ameliorating the effects of injuries or diseases or disorders that result in or are caused by neuronal degeneration or of disorders resulting in mental and cognitive dysfunction. They are also useful for promoting neurogenesis.

An anionic fluorescein homologue capable of selectively staining degenerating neurons in brain slices, the method of making the anionic fluorescein homologue, and the method of using the same for detecting neuronal degeneration. Two anionic fluorescein based fluorescent stains are the water soluble tribasic salt of a mixture of the fluorescein isomers 5-carboxyfluorescein and 6-carboxyfluorescein, and the water soluble tetrabasic salt of 5,6 dicarboxyfluorescein.

Methods and compositions are provided for preventing or inhibiting neuronal degeneration, or for promoting nerve regeneration, in the central nervous system (CNS) or peripheral nervous system (PNS), or for protecting nerves from glutamate toxicity, which comprises administering to an individual in need thereof an effective amount of the copolymer poly-Glu,Tyr.

The invention relates to a biotechnology and especially relates to a construction method of a glial cell line-derived neurotrophic factor gene-modified embryo neural stem cell. The construction method comprises the following steps of 1, plasmid transformation, 2, plasmid digestion purification, 3, target gene and vector cloning, 4, recombinant plasmid packaging, 5, recombinant plasmid identification, 6, virus titer determination, 7, stem cell culture, 8, virus infection of the stem cells, 9, transgenic stem cell identification, 10, transgenic stem cell target-protein content determination, and 11, transgenic stem cell biological-activity detection. The glial cell line-derived neurotrophic factor gene-modified embryo neural stem cell has strong effects of promoting survival of dopaminergic neurons and retains characteristics of the original neural stem cell. The glial cell line-derived neurotrophic factor gene-modified embryo neural stem cell has good effects of treating motor neuron damage diseases and neuronal degeneration diseases.

The invention relates to T. cruzi trans-sialidase (TS) and to the neurotrophic and IL-6 secretion-inducing activities of the protein. TS, neurotrophic variants and/or neurotrophic peptides based upon the sequence of TS can be administered to a mammal to directly or indirectly provide neurotrophic support for neurons. A mammalian neurotrophic factor (e.g., CNTF, LIF) can be co-administered with the TS, neurotrophic variant and/or neurotrophic peptide. TS, IL-6 secretion-inducing variants and/or IL-6 secretion-inducing peptides based upon the sequence of TS can be administered to a mammal to induce the secretion of IL-6. TS, active variants and/or active peptides can be administered to a mammal having an acquired or congenital condition characterized by neuronal degeneration or to a mammal that has experienced trauma to the brain, spinal cord or peripheral nerves. The invention also relates to neurotrophic and IL-6 secretion-inducing variants of TS and to neurotrophic and IL-6 secretion-inducing peptides. The invention also relates to compositions comprising TS, active variants thereof and/or active peptides and a physiologically acceptable carrier.

A synthetic composition is provided comprising (a) one or more compounds selected from the group consisting of flavanols and hydroxystilbenes; and (b) one or more compounds selected from the group consisting of flavanones, flavones, flavonols, proanthocyanidins and anthocyanidins. Also provided is a method of reducing neuronal degeneration in an individual which method comprises administering to the individual said composition.

This invention provides a composition of herbs comprising Radix angelica sinensis (DangGui) 15–60%, Ligusticum chuanxiong (ChuanXiong) 5–20%, Hirudo (ShuiZhi) 3–7%, Polygonatum sibiricum (HuangJing) 4–15%. This invention further provides various uses of this composition.

The invention relates to T. cruzi trans-sialidase (TS) and to the neurotrophic and IL-6 secretion-inducing activities of the protein. TS, neurotrophic variants and/or neurotrophic peptides based upon the sequence of TS can be administered to a mammal to directly or indirectly provide neurotrophic support for neurons. A mammalian neurotrophic factor (e.g., CNTF, LIF) can be co-administered with the TS, neurotrophic variant and/or neurotrophic peptide. TS, IL-6 secretion-inducing variants and/or IL-6 secretion-inducing peptides based upon the sequence of TS can be administered to a mammal to induce the secretion of IL-6. TS, active variants and/or active peptides can be administered to a mammal having an acquired or congenital condition characterized by neuronal degeneration or to a mammal that has experienced trauma to the brain, spinal cord or peripheral nerves. The invention also relates to neurotrophic and IL-6 secretion-inducing variants of TS and to neurotrophic and IL-6 secretion-inducing peptides. The invention also relates to compositions comprising TS, active variants thereof and/or active peptides and a physiologically acceptable carrier.

This invention relates to methods and compositions for detection and treatment of neurodegenerative diseases. In particular, the invention relates to polypeptides that can protect against neuron degeneration, nucleic acid molecules that encode such polypeptides, and antibodies that recognize said polypeptides.

The neuronal activity in the brain of demented subject becomes non-uniform over the cortical surface and this non-uniformity is sensitively detected by properly analyzing observed scalp potentials. The present invention is related to the computer algorithm and apparatus for numerically detecting the degree of such neuronal degeneration. A proper frequency component of EEG is selected so that its scalp potential becomes smooth in a normal subject. When the brain function is impaired, non-uniformity of neuronal activity is detected in spatial as well as temporal fluctuations in the observed scalp potential of properly filtered EEG (usually the alpha component). The statistical parameters derived from dipolarity values of such a properly selected EEG component determine the state of the brain, in which whether the subject is normal or demented is Judged in the early stage of dementia by comparing the obtained parameters with their threshold values. This invention presents a reliable, inexpensive, easy-to-handle and non-invasive method for sensitive screening of dementia and monitoring progress of dementia which also allows optimizing medication and treatment for dementia.

Mutations in the leucine-rich repeat kinase (LRRK2) gene cause late-onset autosomal dominant Parkinson's disease (PD) with pleiomorphic pathology. Previously, we and others found that expression of mutant LRRK2 causes neuronal degeneration in cell culture. Here we used the GAL4/UAS system to generate transgenic Drosophila expressing either wild-type (WT1) human LRRK2 or LRRK2-G2019S, the most common mutation associated with PD. Expression of either WT1 human LRRK2 or LRRK2-G2019S in the photoreceptor cells caused retinal degeneration. Expression of WT1 LRRK2 or LRRK2-G2019S in neurons produced adult-onset selective loss of dopaminergic neurons, locomotor dysfunction, and early mortality. Expression of mutant G2019S-LRRK2 caused a more severe parkinsonism-like phenotype than expression of equivalent levels of WT1 LRRK2. Treatment with L-DOPA improved mutant LRRK2-induced locomotor impairment but did not prevent the loss of tyrosine hydroxylase (TH)-positive neurons. To our knowledge, this is the first in vivo “gain-of-function” model which recapitulates several key features of LRRK2-linked human parkinsonism. These flies may provide a useful model for studying LRRK2-linked pathogenesis and for future therapeutic screens for PD intervention.

Provided is a method of treating and/or preventing Wolfram Syndrome (WS)-related neurodegeneration (i.e. of Wolfram Syndrome-Associated Neuronal Degeneration), by increasing the expression and/or functional activity of p21. A method of screening for pharmacological agents useful in treating and/or preventing such conditions is also provided.

Methods and compositions for the downregulation of P2X7 receptor expression or activity are disclosed. Preferred compositions comprise siNA. The methods and compositions are useful in the treatment of diseases characterised by increased P2X7 receptor activity, such as neuronal degeneration, Alzheimer's disease, inflammatory diseases, and some cancers.

The present invention provides methods and compositions comprising compounds useful for stimulating neurogenesis. The methods and compositions comprising compounds are also useful for inhibiting neuronal degeneration. Thus, the present invention can be used in the treatment of diseases and conditions characterized by neuronal loss and reduced neurogenesis including Alzheimer's disease, stroke, traumatic brain injury, and depression. This invention could also be used for research products including single agents or mixtures of agents to promote, proliferate, differentiate, or maintain neurons from stem or progenitor cells.