38 results about "Neuronal organization" patented technology

The invention is directed to a method for accelerating the cell cycle by delivering to a cell an effective amount of electromagnetic energy. The invention also provides a method for activating a cell cycle regulator by delivering to a cell an effective amount of electromagnetic energy. Also provided by the invention is a method for activating a signal transduction protein; a method for activating a transcription factor; a method for activating a DNA synthesis protein; and a method for activating a Receptor. A method for inhibiting an angiotensin receptor as well as a method for reducing inflammation also are provided by the present invention. The invention also is directed to a method for replacing damaged neuronal tissue as well as a method for stimulating growth of administered cells.

The invention is directed to methods of promoting neurogenesis by contacting neuronal tissue with neurogenesis increasing agents. Novel methods for treating neurological disorders using neurogenesis increasing agents are disclosed.

The invention is directed to methods of promoting neurogenesis by contacting neuronal tissue with neurogenesis modulating agents. Novel methods for treating neurological disorders using neurogenesis modulating agents are disclosed.

The present invention describes methods involving the use of muscle derived cells (MDCs), preferably obtained from skeletal muscle, to support the innervation and repair of damaged tissues and organs, particularly associated with nerve damage or neuropathy. The invention relates to MDCs for use in methods for promoting or enhancing innervation of nerve cells, particularly in the peripheral nervous system, and their ability to contribute to the development of neuronal tissue when MDCs are introduced at or near a tissue or organ site in need of repair due to injury, damage, disease, or dysfunction. Such methods are useful for the treatment of central and peripheral nervous system disorders and to alleviate, abate, or eliminate the symptoms of neurologic or neurodegenerative diseases in animals, particularly mammals, including humans. The methods are also useful for treating both nerve and muscle tissue following injury, damage, or dysfunction to these tissue types.

The present invention relates to methods and compositions for modulating levels of amyloid-β peptide (Aβ) exhibited by non-neuronal (i.e., peripheral) cells, fluids, or tissues. The invention also relates to modulation of Aβ levels via selective modulation (e.g., inhibition) of γ-secretase activity. The invention also relates to methods of preventing, treating or ameliorating the symptoms of a disorder, including but not limited to an Aβ-related disorder, by administering a compound that result in the modulation of γ-secretase in a non-neuronal tissue, either directly or indirectly to prevent, treat or ameliorate the symptoms of a brain Aβ disorder, such as Alzheimer's disease.

Formulations and methods of use thereof for restoring neuronal tissue function in children and adults afflicted with chronic neurodegenerative diseases, such as neurodegenerative movement disorders and ataxias, seizure disorders, motor neuron diseases, and inflammatory demyelinating disorders. Examples of disorders include Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). The method involves administering a pharmaceutical composition containing an effective amount of a tetrahydrobenzathiazole, preferably a formulation consisting substantially of the R(+) enantiomer of pramipexole. R(+) pramipexole is generally administered in doses ranging from 0.1-300 mg / kg / daily, preferably 0.5-50 mg / kg / daily, and most preferably 1-10 mg / kg / daily for oral administration. Daily total doses administered orally are typically between 10 mg and 500 mg. Alternatively, R(+) pramipexole can be administered parenterally to humans with acute brain injury in single doses between 10 mg and 100 mg, and / or by continuous intravenous infusions between 10 mg / day and 500 mg / day.

Neuregulin, a known neuroprotein, has been found to ameliorate or prevent damage caused by mechanical or chemical assault to blood vessels and, when administered into the cerebral spinal fluid, can ameliorate damage to neuronal tissue caused by stroke, inflammation or organophosphate neurotoxins. Additionally, neuregulin has been found to be useful for enhancement of stem cell migration from the ventricle to the site of injury to the brain.

Use of antagonists to IL-31 are used to treat inflammation and pain by inhibiting, preventing, reducing, minimizing, limiting or minimizing stimulation in neuronal tissues. Such antagonists include antibodies and fragments, derivative, or variants thereof. Symptoms such as pain, tingle, sensitization, tickle associated with neuropathies are ameliorated.

The invention is directed to methods of promoting neurogenesis by contacting neuronal tissue with neurogenesis modulating agents. Novel methods for treating neurological disorders using neurogenesis modulating agents are disclosed.

The present disclosure describes novel hybrid soluble ActRIIB-ECD polypeptides which fully retain binding affinity for myostatin and activin A but demonstrate significantly reduced binding to BMPs, especially BMP-9. The novel compositions described herein can be used to prepare novel hybrid ActRIIB ligand trap proteins, which can be used for modulating the growth of muscle, bone, cartilage, fat, fibroblast, blood and neuronal tissue to counteract muscle wasting, bone loss, anemia, inflammation and fibrosis in a therapeutically meaningful manner. Because these novel next-generation myostatin / activin inhibitors are safer and more effective molecules than the currently available myostatin inhibitors, they are useful in a wide variety of clinical indications.

The present invention relates to biologically active peptides derived from the neurite outgrowth-promoting domain of luminin-1, i.e. the γ1-chain of laminin-1. These peptides include the decapeptide RDIAEIIKDI (SEQ ID NO: 1) and the truncated peptides derived therefrom comprising the biologically active domain thereof, the tripeptide KDI. The invention is directed to the biologically active tripeptide motifKDI, and to its use in promoting regeneration of neuronal or non-neuronal tissues and, in specific, to its use in the treatment of spinal cord injuries.

A catheter system and method for selectively cooling or freezing target neuronal tissue to induce lesions along the neuroaxis and produce cryoanalgesia by impairing nerve conduction of the targeted neuronal tissue. The system includes a catheter that has cryogenic capability for variable cooling or freezing of neuronal tissue. The catheter also includes temperature sensing and electrodiagnostic capabilities. A pressurized fluid source is included for inflating a portion of the catheter body. The system includes electrodiagnostic equipment for stimulating and monitoring sensory evoked potentials in the patient. The method involves placement of the catheter tip in the subarachnoid space of the spinal canal and location of the tip on the neuronal target using imaging and electrodiagnostic techniques.

Neuregulin, a known neuroprotein, has been found to ameliorate or prevent damage caused by mechanical or chemical assault to blood vessels and, when administered into the cerebral spinal fluid, can ameliorate damage to neuronal tissue caused by stroke or inflammation. Additionally, neuregulin has been found to be useful for enhancement of stem cell migration from the ventricle to the site of injury to the brain.

Method and system for determining a cognitive enhancement and / or anti-epileptic effect comprising: detecting synchronized neuronal activity in neuronal tissue (601), monitoring spreading of the synchronized neuronal activity (602), determining a parameter (604, 605) indicative of the closeness of the synchronized neuronal activity to the critical state and comparing (613) the parameter to a predetermined value.

The present invention provides a composition based on poly-1-lactic acid (PLLA) and polylactic-co-glycolic-acid (PLGA) scaffold on which neuronal tissue can ex-vivo grow. Further, more the invention provides a method for making cellular vasculature networks and a method for treating a neuronal injury in a subject, by implanting the current composition.

The present invention provides compositions and methods for alleviation or reduction of the symptoms and signs associated with damaged neuronal tissues whether resulting from tissue trauma, or from chronic or acute degenerative changes. In particular, some embodiments of the present invention provide one or more pharmaceutical compositions comprising as an active ingredient a BMP2A inhibitor further comprising a pharmaceutically acceptable diluent or carrier. An additional embodiment provides a method for reducing damage to the central nervous system in a patient who has suffered an injury to the central nervous system, comprising administering to the patient a pharmaceutical composition in a dosage sufficient to reduce the damage. Yet another embodiment provides of the use of a BMP2A inhibitor for the preparation of a medicament for promoting or enhancing recovery in a patient who has suffered an injury to the central nervous system. Preferable inhibitors according to some embodiments of the invention are siRNA molecules and neutralizing antibodies. An additional embodiment provides a method for identifying a chemical compound that modulates apoptosis. Further, a process for diagnosing a neurodegenerative disease or an ischemic event in a subject is provided. The preferred methods, materials, and examples that will now be described are illustrative only and are not intended to be limiting; materials and methods similar or equivalent to those described herein can be used in practice or testing of the invention. Other features and advantages of the invention will be apparent from the following detailed description, and from the claims.

Novel neuroprotectant compositions and methods are described. β-Lactamase inhibitors are used to prevent or reduce loss of neuronal cells and neuronal cell function in patients afflicted with or susceptible to disease states or conditions known to result in or cause neuronal tissue insult.

The present disclosure describes novel hybrid soluble ActRIIB-ECD polypeptides which fully retain binding affinity for myostatin and activin A but demonstrate significantly reduced binding to BMPs, especially BMP-9. The novel compositions described herein can be used to prepare novel hybrid ActRIIB ligand trap proteins, which can be used for modulating the growth of muscle, bone, cartilage, fat, fibroblast, blood and neuronal tissue to counteract muscle wasting, bone loss, anemia, inflammation and fibrosis in a therapeutically meaningful manner. Because these novel next-generation myostatin / activin inhibitors are safer and more effective molecules than the currently available myostatin inhibitors, they are useful in a wide variety of clinical indications.

This invention relates to methods and devices for the detection and characterization of psychoactive compounds by analyzing alterations of network level physiological characteristics before and after the introduction of a candidate sample onto an in vitro neuronal tissue sample. The invention further provides a software package that enables an operator to deliver a timed electrical pulse to neuronal samples at a specific point in their spontaneous or induced oscillations. Such temporal stimulations trigger unexpected and useful network level physiological responses.

This invention relates to neuronal tissue which is suitable to restore neuronal deficits following transplantation. To reduce immunological side effects and to increase the microbiological and genetic safety of the tissue we propose tissue that does not contain glial cells and is maintained in vitro for prolonged periods. The method to generate expandable determined neuronal progenitor cell cultures includes the following procedures: dissection of appropriate mammalian brain regions, isolation of progenitor cells, expansion of progenitor cells, selection and expansion of individual cells and priming.

A real-time detection technique and a real-time, adaptive, model-independent control technique for detecting and stabilizing pathological physiological rhythms, such as repolarization alternans, on the basis of the rate dependence of excitable tissue such as cardiac and neuronal tissue is presented. Unlike other control methods, which require a number of beats to locate the period-1 fixed point, the technique locates the period-1 fixed point almost instantaneously, rapidly eliminating any higher-period or aperiodic rhythms.

The invention relates to the use of a pharmaceutical composition containing nicotinamide (NAM) and / or pyruvate as a neuroprotective medicament or gene therapy in the treatment of neurodegenerative disorders, in particular axon degeneration of neuronal tissue in ocular-related neurodegeneration diseases including glaucoma.

The invention discloses an in-vitro neural network construction system based on robotization. Neuron tissues to be constructed are arranged in a biological culture dish. A laser subsystem comprises alaser source, a laser conduction device and a focusing objective lens. The laser source is connected with the laser conduction device through an energy supply cable and used for conducting laser energy, the focusing objective lens is connected with the laser conduction device through a laser optical fiber, the focusing objective lens is arranged above the biological culture dish, and the focusingobjective lens is used for focusing conducted laser. The focusing objective lens is fixed on the displacement control platform, the biological culture dish is arranged below the focusing objective lens by controlling the displacement control platform to move, and laser ablation or optical stimulation is carried out on target point cells or tissues in the biological culture dish. According to the method, specific activation can be carried out on a single neuron, meanwhile, responses of other neurons in the neural network can be recorded, integration is easy, the integration cost is low, and very high flexibility and operability are achieved.

The present invention relates to methods and compositions for modulating levels of amyloid-β peptide (Aβ) exhibited by non-neuronal (i.e., peripheral) cells, fluids, or tissues. The invention also relates to modulation of Aβ levels via selective modulation (e.g., inhibition) of γ-secretase activity. The invention also relates to methods of preventing, treating or ameliorating the symptoms of a disorder, including but not limited to an Aβ-related disorder, by administering a compound that results in the modulation of γ-secretase in a non-neuronal tissue, either directly or indirectly to prevent, treat or ameliorate the symptoms of a brain Aβ disorder, such as Alzheimer's disease.

The present invention relates to the field of diagnosis and treatment of neurodegenerative diseases, ischemic events, and central nervous system injury, and provides compositions and methods for alleviation or reduction of the symptoms and signs associated with damaged neuronal tissues whether resulting from tissue trauma, or from chronic or acute degenerative changes.The present invention in particular relates to the discovery that the expression of Annexin II is involved in apoptosis induced by oxidative stress, and that anti-sense Annexin II RNA and Annexin II siRNA protected the cells from this apoptosis. Thus Annexin II inhibitors prevent the damage caused by said ischemic event.