74 results about "Neuron survival" patented technology

The invention discloses a family of peptides termed NRP compounds or NRPs that can promote neuronal migration, neurite outgrowth, neuronal proliferation, neural differentiation and / or neuronal survival, and provides compositions and methods for the use of NRPs in the treatment of brain injury and neurodegenerative disease. NRP compounds can induce neurons and neuroblasts to proliferate and migrate into areas of damage caused by acute brain injury or chronic neurodegenerative disease, such as exposure to toxins, stroke, trauma, nervous system infections, demyelinating diseases, dementias, and metabolic disorders. NRP compounds may be administered directly to a subject or to a subject's cells by a variety of means including orally, intraperitoneally, intravascularly, and directly into the nervous system of a patient. NRP compounds can be formulated into pharmaceutically acceptable dose forms for therapeutic use. Methods for detecting neural regeneration, neural proliferation, neural differentiation, neurite outgrowth and neural survival can be used to develop other neurally active agents.

This invention relates to methods for promoting neuronal survival and regeneration using LINGO-1 antagonists and TrkB agonists. Additionally, the invention relates to methods for treating pressure induced optic neuropathies using LINGO-1 antagonists. The invention also relates generally to methods for increasing TrkB activity and inhibiting JNK pathway signaling using a LINGO-1 antagonist.

An implantable microstimulator, or equivalent neural stimulator, generates a relatively simple signal containing temporally challenging information and delivers such signal to the middle or outer portion of the ear contra-lateral to an ear having a cochlear implant of a bilaterally deafened patient. Such stimulation delivered to the contra lateral ear advantageously increases the survival rate of neurons therein, and further helps maintain or extend the plasticity of the higher auditory pathways of the contra-lateral ear, thereby allowing a cochlear implant to be more effectively used in such ear at a later date. The stimulation provided by the microstimulator, or equivalent simple neural stimulator, need not be continuous, but may be provided only during limited periods of time each day, or only on selected days. Further, such stimulation preserves whatever residual hearing may be left in the contra lateral ear.

A method of post-stroke treatment at delayed timepoints with sigma receptor agonists. Sigma receptors are promising targets for neuroprotection following ischemia. One of the key components in the demise of neurons following ischemic injury is the disruption of intracellular calcium homeostasis. The sigma receptor agonist, DTG, was shown to depress [Ca2+]i elevations observed in response to ischemia induced by sodium azide and glucose deprivation. Two sigma receptor antagonists, metaphit and BD-1047, were shown to blunt the ability of DTG to inhibit ischemia-evoked increases in [Ca2+]i. DTG inhibition of ischemia-induced increases in [Ca2+]i was mimicked by the sigma-1 receptor-selective agonists, carbetapentane, (+)-pentazocine and PRE-084, but not by the sigma-2 selective agonist, ibogaine, showing that activation of sigma-1 receptors is responsible for the effects. Activation of sigma receptors can ameliorate [Ca2+]i dysregulation associated with ischemia in cortical neurons, providing neuroprotective properties. The effects of 1,3-di-o-tolyguanidine (DTG), a high affinity sigma receptor agonist, as a potential treatment for decreasing infarct area at delayed time points was further examined in rats. DTG treatment significantly reduced infarct area in both cortical / striatal and cortical / hippocampal regions by >80%, relative to control rats. These findings were confirmed by immunohistochemical experiments using the neuronal marker, mouse anti-neuronal nuclei monoclonal antibody (NeuN), which showed that application of DTG significantly increased the number of viable neurons in these regions. Furthermore, DTG blocked the inflammatory response evoked by MCAO, as indicated by decreases in the number of reactive astrocytes and activated microglia / macrophages detected by immunostaining for glial fibrillary acidic protein (GFAP) and binding of isolectin IB4, respectively. Thus, the sigma receptor-selective agonist, DTG, can enhance neuronal survival when administered 24 hr after an ischemic stroke. In addition, the efficacy of sigma receptors for stroke treatment at delayed time points is likely the result of combined neuroprotective and anti-inflammatory properties of these receptors.

The invention discloses a primer and a probe for screening spinal muscular atrophy (SMA) genes and a using method of the primer and probe, belonging to the technical field of biology. The invention discloses eight combinations of the primer and probe for screening survival motor neuron genes 1 (SMN1), and the primer and probe can be effectively applied to screening the SMN1. Meanwhile, the invention also discloses sixteen groups of combinations of the primer and probe for screening survival motor neuron genes 2 (SMN2), as well as application in fetal SMA gene screening by utilizing the primer and probe for screening the SMN1 and the primer and probe for screening the SMN2. According to the primer and probe provided by the invention, the SMA genotypes of adults and fetuses can be detected at high efficiency.

The present invention relates to neurological and physiological dysfunction associated with neuron disorders. In (particular, the invention relates to the involvement of vascular endothelial growth factor (VEGF) and homologues in the aetiology of motor neuron disorders. The invention further concerns a novel, mutant transgenic mouse (VEGFm / m) with a homozygous deletion in the hypoxia responsive element (HRE) of the VEGF promoter which alters the hypoxic upregulation of VEGF. These mice suffer severe adult onset muscle weakness due to progressive spinal motor neuron degeneration which is reminiscent of amyotrophic lateral sclerosis (ALS)-a fatal disorder with unknown aetiology. Furthermore, the neuropathy of these mice is not caused by vascular defects, but is due to defective VEGF-mediated survival signals to motor neurons. The present invention relates in particular to the isoform VEGF165 which stimulates survival of motor neurons via binding to neuropilin-1, a receptor known to bind semaphorin-3A which is implicated in axon retraction and neuronal death, and the VEGF Receptor-2. The present invention thus relates to the usage of VEGF, in particular VEGF165, for the treatment of neuron disorders and relates, in addition, to the usage of polymorphisms in the VEGF promotor for diagnosing the latter disorders.

The present invention relates to the discovery of a composition including a seven-amino acid peptide that promotes neuronal survival, inhibits inflammation, and is a potent inhibitor of sPL2A, and uses thereof.

A system and method uses an electrical stimulator to stimulate the auditory system with a relatively simple signal that contains temporally challenging information in order to preserve neuronal survival and plasticity of the auditory system, and also to preserve residual hearing. The stimulation provided need not be continuous, but may be provided only during limited periods of time each day, or only on selected days. The system or method is particularly suited for very young children who acquire hearing impairment or deafness early in life and who may not yet be ready for a cochlear implant. The invention requires only minimal surgical intervention, if any, and may be carried out without the need for intra-cochlear electrodes. Under special circumstances, the invention may also be used with older children or adults with a hearing impairment or deafness.

The present invention provides, inter alia, methods for identifying a candidate agent that may be effective to treat or ameliorate an effect of a neurodegenerative disease in a subject. These methods include: (a) contacting a wildtype neuron and a mutant neuron with a stressor which is effective to accelerate the degeneration of the mutant neuron; (b) further contacting the wildtype neuron and the mutant neuron from step (a) with a candidate agent; and (c) determining whether the candidate agent lowers a wildtype to mutant survival ratio or increases both wildtype and mutant neuron survival.

The invention relates to an isolated nucleic acid encoding a eukaryotic Survival of Motor Neuron-Interacting Protein 1 (SIP1), compositions comprising SIP1 and SIP1 and the spinal muscular atrophy (SMA) disease gene product Survival of Motor Neuron protein (SMN), and diagnostic and therapeutic assays directed to SMA. The invention also relates to another protein that specifically interacts with SMN and is a component of gems, designated Gemin3, and the nucleic acid encoding the protein. Additionally, the invention relates to a novel cell line wherein the endogenous SMN genes have been deleted and where an exogenous nucleic acid encoding SMN has been inserted into the cell such that expression of SMN in the cell is under the control of an inducible promoter. This novel cell line provides a stable genetic system for the study of SMA and for the development of SMA therapeutics.

Disclosed herein are compositions and methods for treatment of spinal muscular atrophy (SMA). In certain embodiments, compounds are provided that increase full-length survival of motor neuron (SMN) protein production by an SMN2 gene.

The invention relates to the field of genetic testing, and specifically relates to a kit used for detecting the copy number of survival genes of human motor neurons. According to the kit used for detecting the copy number of the survival genes of the human motor neurons, a multifluorescent polymerase chain reaction (PCR) method is adopted for detecting the copy number of the survival genes of thehuman motor neurons; and specific primers and probes for exons 7 and 8 of SMN1 gene, exons 7 and 8 of SMN2 gene, exon 6 of SMN gene and internal reference gene cystic fibrosis transmembrane regulator(CFTR) are separately designed. The kit is smartly designed, so that, relative quantifying can be separately performed on the copy number of the exons 7 and 8 of the SMN1 gene, the exons 7 and 8 of the SMN2 gene as well as the exon 6 of the SMN gene by adopting 3 independent PCR reactions. The kit is easy to operate, strong in specificity and excellent in sensitivity. Thus, the result of the copynumber of the exon 6 of the SMN gene can be improved in terms of accuracy; so that, the kit is more suitable for clinical classifying of patients with spinal muscular atrophy and screening of carriers.

The invention relates to an isolated nucleic acid encoding a eukaryotic Survival of Motor Neuron-Interacting Protein 1 (SIP1), compositions comprising SIP1 and SIP1 and the spinal muscular atrophy (SMA) disease gene product Survival of Motor Neuron protein (SMN), and diagnostic and therapeutic assays directed to SMA. The invention also relates to another protein that specifically interacts with SMN and is a component of gems, designated Gemin3, and the nucleic acid encoding the protein. Additionally, the invention relates to a novel cell line wherein the endogenous SMN genes have been deleted and where an exogenous nucleic acid encoding SMN has been inserted into the cell such that expression of SMN in the cell is under the control of an inducible promoter. This novel cell line provides a stable genetic system for the study of SMA and for the development of SMA therapeutics.

Disclosed herein are compositions and methods for treatment of spinal muscular atrophy (SMA). In certain embodiments, compounds are provided that increase full-length survival of motor neuron (SMN) protein production by an SMN2 gene.

The present invention relates to novel chimeric C3-like Rho antagonists and their use for promoting repair and neuron survival in injured mammalian central and peripheral nervous system and for treating or preventing cancer.

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.

The invention discloses a detection kit for human survival motor neuron genes SMN1 and SMN2, and a method. The kit comprises an SMN1 main reaction liquid, an SMN2 main reaction liquid, an enzyme mixed liquid, 0-copy quality control, SMN1 single-copy quality control, SMN1 two-copy quality control, SMN2 single-copy quality control and SMN2 two-copy quality control, wherein the SMN1 main reaction liquid comprises a detection primer of the gene SMN1 and an inner reference primer of the SMN1; and the SMN2 main reaction liquid comprises a detection primer of the gene SMN2 and an inner reference primer of the SMN2. According to the kit, a PCR melting curve method is adopted, the change of a fluorescence signal value during a double-strand DNA melting process is detected in real time, target genes and inner reference genes generate different dissolution peaks according to the difference of different amplification product quantities, and then the copy numbers of the genes SMN1 and SMN2 are judged through software processing. The kit and the method which are disclosed by the invention are high in detection result accuracy, high in sensitivity, less in detection time consumption and low in cost.

Disclosed herein are compositions and methods for treatment of spinal muscular atrophy (SMA). In certain embodiments, compounds are provided that increase full-length survival of motor neuron (SMN) protein production by an SMN2 gene.

The present invention relates to novel chimeric C3-like Rho antagonists and their use for promoting repair and neuron survival in injured mammalian central and peripheral nervous system and for treating or preventing cancer.

The present invention relates to novel chimeric C3-like Rho antagonists and their use for promoting repair and neuron survival in injured mammalian central and peripheral nervous system and for treating or preventing cancer.

The disclosure provides compounds, compositions, and methods for promoting motor neuron survival, and for treating or preventing neurodegenerative disorders, such as spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS).

The present invention provides a method for treating patients with spinal cord injury by administering germination activated Ganoderma lucidium spores (GASP) to the patients. The GASP are sporoderm-broken. The GASP promote axon regeneration and improve motor neuron survival in the injured spinal cord.

The present invention includes assays and kits for detecting the assembly of an RNA binding protein-RNA complex and for detecting the activity of an RNA binding protein.

The present invention relates to methods for promoting motor neuron survival, treating or preventing neurodegenerative disorders, identifying agents that promote survival of motor neurons, identifying agents that are useful for treating neurodegenerative disorders, diagnosing neurodegenerative disorders, predicting the progression of a neurodegenerative disorder in a subject, and monitoring the effectiveness of a therapy in reducing the progression of a neurodegenerative disorder in a subject.

The present inventions relate to methods and compositions useful for improving the efficiency of inducing the generation of neurons from non-neuronal cell types, for example, by contacting the cell or cell culture medium with one or more agents which inhibit Activin and / or PLK1 signaling. Also disclosed are methods for promoting neuron survival, for example, by inhibiting Activin and / or PLK1 signaling, and methods for promoting the survival of intermediates in a cell differentiation pathway, for example, by inhibiting Activin and / or PLK1 signaling.

Nucleic acids encoding the neurotrophic protein known as pigment epithelium-derived factor (PEDF), a truncated version of PEDF referred to as rPEDF, and equivalent proteins, vectors comprising such nucleic acids, host cells into which such vectors have been introduced, recombinant methods for producing PEDF, rPEDF, and equivalent proteins, the rPEDF protein and equivalent proteins of rPEDF and PEDF-BP, -BX and BA, and the PEDF protein produced by recombinant methods. Effects and uses of these variants on 1) neuronal differentiation (neurotrophic effect) 2) neuron survival (neuronotrophic effect) and 3) glial inhibition (gliastatic effect) are described.

Devices useful in the delivery of DNA encoding neurotrophic agents, anti-fibrotic agents, and related compositions are disclosed herein for use in the treatment of central and / or peripheral nervous system injury. Methods of making and using the disclosed devices and DNA are also described. In various embodiments, the invention also discloses compositions and devices that may further include a targeting agent, such as a polypeptide that is reactive with an FGF receptor (e.g., bFGF), or another ligand that binds to cell surface receptors on neuronal cells, or a support cell. The invention also discloses methods of promoting neuronal survival and regeneration via transfection of an axon as it grows through a device or composition of the present invention, or via transfection of a repair cell.