352 results about "Neuroinflammation" patented technology

Methods and devices are disclosed for the non-invasive treatment of neurodegenerative diseases through delivery of energy to target nervous tissue, particularly the vagus nerve. The devices include a magnetic stimulator having coils with toroidal windings, which are in contact with an electrically conducting medium that is adapted to conform to the contour of a target body surface of a patient. The coils induce an electric current and/or an electric field within the patient, thereby stimulating nerve fibers within the patient. The stimulation brings about reduction of neuroinflammation in patients suffering from conditions comprising Alzheimer's Disease, Parkinson's Disease, Multiple Sclerosis, postoperative cognitive dysfunction and postoperative delirium. Reduction in inflammation is effected by enhancing the anti-inflammatory competence of cytokines such as TGF-beta, wherein a retinoid or components of the retinoic acid signaling system provide an anti-inflammatory bias, by enhancing anti-inflammatory activity of a neurotrophic factor such as NGF, GDNF, BDNF, or MANF, and/or by inhibiting the activity of pro-inflammatory cytokines such as TNF-alpha.

Devices, systems and methods are disclosed for treating or preventing dementia, such as Alzheimer's disease. The methods comprise transmitting impulses of energy non-invasively to selected nerve fibers, particularly those in a vagus nerve, that modulate the activity of a patient's locus ceruleus. The transmitted energy impulses, comprising magnetic and/or electrical energy, stimulate the selected nerve fibers to cause the locus ceruleus to release norepinephrine into regions of the brain that contain beta-amyloids. The norepinephrine counteracts neuroinflammation that would damage neurons in those regions and the locus ceruleus, thereby arresting or slowing the progression of the disease in the patient.

The present invention is directed generally to systems, devices and methods for direct delivery of agents, e.g., pharmaceutical agents, to target spinal and neuronal anatomies, e.g., the dorsal root ganglia (DRG), for the treatment of various disorders, particularly pain and pain related disorders, such as chronic itch, sensory disorders, multiple sclerosis, post-herpetic neuralgia and the like. The system, devices and methods of the invention encompass the agents to be delivered to the target anatomy alone or in combination with electrical stimulation. The delivery device and systems and methods as disclosed herein place the distal end of the delivery element, which comprises at least one agent delivery structure, and optionally at least one electrode, in close proximity, or in contact with or next to the target spinal anatomy, e.g., DRG. A variety of agents can be delivered using the device, including sodium channel blockers, biologics, neuroinflammatory modulators, toxins etc., to selectively neuromodulate the neurons. Agent delivery and/or electrical stimulation can be automated and/or can be controlled automatically or by a pre-determined program, or by a patient control pump (PCA).

Methods for the production of monoclonal antibodies specific to conformational epitope(s) of a prefibrilar aggregate(s) which contribute to amyloid fibril formation in human or animal subjects who suffer from amyloid diseases (e.g. Alzheimer's Disease) and the hybridomas and monoclonal antibodies produced therefrom. Also, the use of such monoclonal antibodies in the immunization of human or animal subjects against Alzheimer's Disease or other amyloid diseases and/or for the diagnosis or detection of Alzheimer's Disease or other amyloid diseases. The monoclonal antibodies may be administered concomitantly or in combination with anti-inflammatory agents, such as gold or gold containing compounds, to decrease neural inflammation associated with amyloid diseases (e.g. Alzheimer's Disease).

A method for repairing animal tissue damage due to an inflammatory reaction in an animal has the steps of providing umbilical cord blood cells (UCBCs) in a pharmaceutically acceptable form; and administering a sufficient dose of UCBC at an optimal time thereby reducing the injury from the inflammatory reaction. Also provided are method of treating cerebrovascular accident, acute central nervous inflammation, multiple sclerosis, myocardial ischemia, and neonatal bronchopulmonary distress. For determining the optimal time of UCBCs administration, there is provided a kit containing antibodies for IL-8 and MCP-1.

Novel compounds of the structural formula (I) are antagonists and/or inverse agonists of the Cannabinoid-1 (CB1) receptor and are useful in the treatment, prevention and suppression of diseases mediated by the CB1 receptor. The compounds of the present invention are useful as centrally acting drugs in the treatment of psychosis, memory deficits, cognitive disorders, migraine, neuropathy, neuro-inflammatory disorders including multiple sclerosis and Guillain-Barre syndrome and the inflammatory sequelae of viral encephalitis, cerebral vascular accidents, and head trauma, anxiety disorders, stress, epilepsy, Parkinson's disease, movement disorders, and schizophrenia. The compounds are also useful for the treatment of substance abuse disorders, the treatment of obesity or eating disorders, as well as the treatment of asthma, constipation, chronic intestinal pseudo-obstruction, and cirrhosis of the liver.

Provided are central nervous system (CNS)-targeted antibody or therapeutic Fc-fusion polypeptide conjugates having modified Fc regions, and related methods of use thereof, for instance, to facilitate delivery of therapeutic and/or diagnostic polypeptides across the blood-brain barrier (BBB), and thereby treat and/or diagnose conditions associated with the CNS, including cancer, pain, and various neuropathologies, such as neuroinflammatory, auto-immune, and/or neurodegenerative disorders.

The present invention relates to novel methods for combating cell degeneration or dysfunction resulting from neuroinflammatory conditions. The invention especially relates to the use, in the preparation of a medicament for the treatment of neurodegenerative disease associated with neuroinflammation, of an immunogenic compound which is capable of inducing an immune response against a proapoptotic neurotrophin, or an effective amount of a hapten combined with appropriate carriers and/or adjuvants to render the resulting combination capable of inducing an immune response against a proapoptotic neurotrophin. Also disclosed are compositions for the active or passive immunization against neuronal or glial cell apoptosis caused by neuroinflammation as well as methods and means useful for said active or passive immunization.

Novel compounds of the structural formula (I) are antagonists and/or inverse agonists of the Cannabinoid-1 (CB1) receptor and are useful in the treatment, prevention and suppression of diseases mediated by the CB1 receptor. The compounds of the present invention are useful as centrally acting drugs in the treatment of psychosis, memory deficits, cognitive disorders, migraine, neuropathy, neuro-inflammatory disorders including multiple sclerosis and Guillain-Barre syndrome and the inflammatory sequelae of viral encephalitis, cerebral vascular accidents, and head trauma, anxiety disorders, stress, epilepsy, Parkinson's disease, movement disorders, and schizophrenia. The compounds are also useful for the treatment of substance abuse disorders, the treatment of obesity or eating disorders, as well as the treatment of asthma, constipation, chronic intestinal pseudo-obstruction, and cirrhosis of the liver.

Methods, uses, agents and compositions useful for the diagnosis, prevention and/or treatment of inflammatory conditions, such as neuroinflammatory conditions such as multiple sclerosis, and for the identification and selection of inflammatory cytokine-secreting T cell or a precursor thereof, based on the expression and/or modulation of melanoma cell adhesion molecule (MCAM) are disclosed.

The invention relates to a preparation method and application of a marine fungi aspergillus terreus butyrolactone compound butyrolactone-I. The invention discloses application of the marine fungi aspergillus terreus butyrolactone compound butyrolactone-I as shown in a formula (I) to preparation of medicaments for resisting to peripheral and neurogenic inflammation and resisting to neurodegenerative diseases. The formula is shown in the description. The invention finds that besides a DPPH free radical, butyrolactone-I can also well remove an ABTS free radical and an OH free radical; the marinefungi aspergillus terreus butyrolactone compound butyrolactone-I has better oxidation resistance and inflammation resistance and has better neuroprotection activity; therefore, the marine fungi aspergillus terreus butyrolactone compound butyrolactone-I has a wide application prospect in the aspect of preparing the medicaments for resisting to peripheral and neurogenic inflammation and resisting toneurodegenerative diseases. Meanwhile, by the preparation method of the butyrolactone-I, which is provided by the invention, the butyrolactone-I can be successfully prepared; the method is simple andeasy to realize large-scale production; culture conditions can also be optimized by addition of an inducer, so that yield of the butyrolactone-I is greatly improved.

The invention relates to application of sodium alginate oligose and a derivative to treatment of inflammations. The sodium alginate oligose and the derivative of the sodium alginate oligose are particularly mannuronic acid oligose or mannuronic acid oligose with a carboxyl at a 1-position of a reducing end and the derivative or a pharmaceutically acceptable salt, formed by connecting a beta-D-mannuronic acid through a 1,4-glucosidic bond. The inflammations are particularly a vascular inflammation, a neuroinflammation, a nervous centralis inflammation, arthritis, Crohn's disease, ulcerative colitis, inflammatory diabetic ulcer, psoriasis, atopic dermatitis and eczema.

The present invention provides methods of preventing and treating neural inflammatory or demyelinating disease, such as multiple sclerosis, via an inhibition of the activity or expression of phospholipase A₂. The invention further relates to methods of identifying phospholipase A₂ inhibitors and their use thereof for the prevention and/or treatment of neural inflammatory or demyelinating disease. An observed increase in the amount of phospholipase A₂ in neural lesions in the EAE animal model system indicates that elevated phospholipase A₂ activity or levels correlate with neural inflammatory or demyelinating disease. Therefore, in a further aspect the invention provides methods for the diagnosis and prognostication of neural inflammatory or demyelinating disease, such as multiple sclerosis.

The invention relates to the fields of pharmaceutical chemistry and pharmaceutical therapeutics, and more particularly to an optically active ring-opening butylphthalide-telmisartan heterocomplex or a pharmaceutically acceptable salt or ester thereof, preparation methods thereof, pharmaceutical compositions containing the compounds, and pharmaceutical application of the pharmaceutical compositions, particularly application in prevention and treatment of neuroinflammation-related diseases, including ischemic stroke, alzheimer's disease, brain trauma, Parkinson's disease, multiple sclerosis and depression.

Furanone derivatives and the pharmaceutically acceptable salts thereof have cytoprotective activity and protective activity for neuroinflammation, and neurodegenerative disorders; they are useful in the treatment of stroke, cerebral ischemia, myocardial infarction, myocardial ischemia, chronic heart failure, inflammation and other oxidative stress-related conditions, as well as Alzheimer's disease and senile dementia; they are also useful in the manufacture of pharmaceutical formulations for the treatment of such conditions.

The invention provides a compound. The compound and pharmaceutically acceptable salt, various isotopes, various crystal forms or various isomers have the structure shown as a formula (I): A-L-B (I), wherein A is a non-steroidal anti-inflammatory drug compound monomer, B is a hydrogen sulfide releaser or an antioxidant compound, and L is a group or a functional group which connects A and B. The invention further provides an application of the compound as a medicine for inhibiting neuroinflammation as well as a combined application of the compound and other drugs as medicines for inhibiting neuroinflammation. By applying the concept of double prodrugs, the non-steroidal anti-inflammatory drug and the hydrogen sulfide releaser or the antioxidant compound are covalently connected together to form a multiple-target point compound which can effectively inhibit inflammatory response of the microglial cell induced by lipopolysaccharide, so that the compound can be used for treating or preventing various neurodegenerative diseases.

The invention discloses novel coumarin compounds and pharmaceutically acceptable salts thereof, the preparation method of the compounds, pharmaceutical compositions containing the compounds, and application of the compounds to preparation of medicaments for prevention or treatment of cerebral diseases, especially prevention or treatment of diseases related to neuron damage and neuroinflammation, and prevention or treatment of Parkinson's disease, dementia, cerebral ischemia, depression and cerebral apoplexy.

The present invention encompasses isolated antibodies, or antigen-binding portions thereof, that specifically bind mature human IL-1 Beta. These antibodies, or antigen-binding portions thereof, generally exhibit high binding affinities (low k_ooff values), reduced deamidation compared to the native antibody, and can be used to treat various diseases such as rheumatoid arthritis, osteoarthritis, or neuroinflammation.

Methods of treating a subject having a condition characterized by at least one of neurodegeneration and neuroinflammation are provided. Methods of reducing astrogliosis in a subject having a condition characterized by increased astrogliosis are also provided. Methods of providing neuroprotection to a subject in need thereof are also provided.