423 results about "Neuroprotective factors" patented technology

Novobiocin analogues useful as Hsp90 inhibitors in the treatment of cancer, neuroprotection, and autoimmune disorders.

Devices, systems and methods are disclosed for treating or preventing a stroke and / or a transient ischemic attack in a patient. The methods comprise transmitting impulses of energy non-invasively to selected nerve fibers, particularly those in a vagus nerve. Vagus nerve stimulation is used to modulate the release of GABA, norepinephrine, and / or serotonin, thereby providing neuroprotection to the patient; to modulate the activity of resting state neuronal networks, particularly the sensory-motor network or resting state networks containing the insula; and to avert a stroke or transient ischemic attack that has been forecasted.

Compositions and methods are provided for inhibiting neuronal cell death and the loss of neuronal contacts resulting from acute and chronic neurological disorders, including neurodegenerative and neuroinflammatory diseases. The subject compositions and methods utilize RDP-58 compositions capable of providing a direct neuroprotective effect on neuronal cells in conjunction with the inhibition of autoimmune and inflammatory processes.

Nitrate esters and methods for mitigating neurodegeneration, affecting neuroprotection, affecting cognition enhancement, and / or preventing or mitigating tissue and / or cellular damage in a subject are described. Neurological or cognitive conditions, or damage mediated by free radicals are treated by administering to a subject an effective amount of a therapeutic compound comprising a nitrate ester, or a pharmaceutically acceptable salt thereof.

Disclosed herein is a method for protecting dopaminergic neurons of a mammal against death resulting from Parkinson's disease. The method comprises administering a neuroprotective amount of the tripeptide Gly-Pro-Glu.

Methods and apparatus for temperature modification of selected body regions including an induced state of local hypothermia of the brain region for neuroprotection. A heat exchange catheter is provided with heat transfer fins projecting or extending outward from the catheter which may be inserted into selected blood vessels or body regions to transfer heat with blood or fluid in the selected blood vessels or body regions. Another aspect of the invention further provides methods and apparatus for controlling the internal body temperature of a patient. By selectively heating or cooling a portion of the catheter lying within a blood vessel, heat may be transferred to or from blood flowing within the vessel to increase or decrease whole body temperature or the temperature of a target region. Feed back from temperature sensors located within the patient's body allow for control of the heat transfer from the catheter to automatically control the temperature of the patient or of the target region within the patient. The apparatus may include a blood channeling sleeve that directs body fluid over a heat exchanger where the body fluid's temperature is altered, and then is discharged out the distal end of the sleeve to a desired location, for example, cooled blood to the brain for neuroprotection. The catheter may be used alone or in conjunction with other heat exchangers to cool one region of a patient's body while heating another.

A unique DHA product, 10, 17S-docosatriene (“Neuroprotectin D1” or “NPD1”), was found to provide surprisingly effective neuroprotection when administered right after an experimental stroke. Moreover, both nerve cells and retinal pigment epithelial (RPE) cells were found to synthesize 10,17S-docosatriene (NPD1) from DHA. NPD1 also potently counteracted H2O2 / TNFα oxidative stress-mediated cell apoptotic damage. Under the same oxidative-stress conditions, NPD1 up-regulated the anti-apoptotic Bcl-2 proteins, Bcl-2 and Bcl-xL, and decreased expression of the pro-apoptotic proteins, Bad and Bax. Moreover, in RPE cells NPD1 inhibited oxidative stress-induced caspase-3 activation, IL-1β-stimulated human COX-2 promoter expression, and apoptosis due to N-retinylidene-N-retinylethanolamine (A2E). Overall, NPD1 protected both nerve and retinal pigment epithelial cells from cellular apoptosis and damage due to oxidative stress. NPD1 concentration in the brain of Alzheimer's patients was found to be significantly decreased from that of controls. In cultured human brain cells, NPD1 synthesis was up-regulated by neuroprotective soluble β amyloid, and NPD1 was found to inhibit secretion of toxic β amyloid peptides.

Methods for treating neurodegeneration and / or myelination in patients are disclosed comprising treating the patient with a progestin compound which exerts binding to progesterone receptors and elicits progesterone-receptor-induced biological responses without interacting with the androgen receptor and without inducing androgen or glucocorticoid biological responses at a dosage sufficient to prevent or reduce neurodegeneration. The progestin compound preferably comprises 16-methylene-17α-acetoxy-19-norpregn-4-ene-3,20-dione, and the methods include combining the progestin compound with an estrogen compound to provide both contraception and treatment for myelin repair and neurodegeneration.

Compounds and methods for mitigating neurodegeneration, effecting neuroprotection and / or effecting cognition enhancement in a subject are described. Neurological or cognitive conditions are treated by administering to a subject an effective amount of a therapeutic compound comprising a nitrate ester, or a pharmaceutically acceptable salt or ester thereof.

Cycic di-GMP, or a cyclic dinucleotide analogue thereof that has the same effect as cyclic di-GMP, stimulates or enhances immune or inflammatory response in a patient or enhances the immune response to a vaccine by serving as an adjuvant. Cyclic di-GMP, or a cyclic dinucleotide analogue thereof, also has neuroprotective properties for use as a neuroprotective agent to inhibit, treat, or ameliorate the effects of injuries, diseases, disorders or conditions that result in neurodegeneration.

The subject invention provides methods for reducing or inhibiting progression of the level of fatigue in a multiple sclerosis human patient, for improving or inhibiting deterioration of the functional status of a multiple sclerosis human patient, and for improving or inhibiting deterioration of the general health of a multiple sclerosis human patient, comprising orally administering to the human patient laquinimod or a pharmaceutically acceptable salt thereof. The subject invention also provides a method for providing neuroprotection to a human subject, the method comprising orally administering to the human subject laquinimod or a pharmaceutically acceptable salt thereof.

Methods and pharmaceutical compositions for preconditioning and / or providing neuroprotection to the animal central nervous system against the effects of ischemia, trauma, metal poisoning and neurodegeneration, including the associated cognitive, behavioral and physical impairments. In one embodiment, the method is accomplished by stimulating and stabilizing hypoxia-inducible factor-1α (HIF-1α). HIF-1α is known to provide a neuroprotective benefit under ischemic conditions. Patients at risk for certain diseases or disorders that are associated with risk for cerebral ischemia may benefit, e.g., those at risk for Alzheimer's disease, Parkinson's disease, Wilson's disease or stroke or those patients having head or spinal cord injury. Patients undergoing certain medical procedures that may result in ischemia may also benefit. Initially, the possibility of ischemia or neurodegeneration is recognized. Intranasal therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and / or copper such as iron chelators, copper chelators, and antioxidants. A particular example of such therapeutic agents is the iron chelator deferoxamine (DFO). Intranasal administration of DFO is known to stimulate and / or stabilize HIF-1α and provides an efficient and safe method for pre-conditioning the brain to protect against cerebral ischemia. Moreover, DFO is shown to decrease weight loss in subjects when administered pre and / or post stroke.

Provided are methods for protecting against or reducing neurotoxicity of exposure to a neurotoxic agent, comprising administering an electrokinetically altered aqueous fluid as provided herein in an amount sufficient to provide for neuroprotection against the neurotoxic agent, preferably where protecting against or reducing loss of motor coordination in the subject exposed to the neurotoxin is afforded. In certain aspects, protecting or reducing neurotoxin-mediated neuronal apoptosis is afforded, and / or activating or inducing at least one of PI-3 kinase and Akt phosphorylation in neurons is afforded. Preferably, administering the fluid comprises administering the fluid prior to exposure to the neurotoxic agent. Additionally provided are methods for preserving or improving motor coordination in a subject having a neurodegenerative condition or disease, comprising administering an electrokinetically altered aqueous fluid as provided herein in an amount sufficient to provide for preserving or improving motor coordination in the subject.

Cycic di-GMP, or a cyclic dinucleotide analogue thereof that has the same effect as cyclic di-GMP, stimulates or enhances immune or inflammatory response in a patient or enhances the immune response to a vaccine by serving as an adjuvant. Cyclic di-GMP, or a cyclic dinucleotide analogue thereof, also has neuroprotective properties for use as a neuroprotective agent to inhibit, treat, or ameliorate the effects of injuries, diseases,

The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and / or signaling of lysyl oxidase (LOX) or a lysyl oxidase-like protease (LOXL).

The invention reveals that endogenous cholesterol metabolic product cholestane-3 beta, 5 alpha, 6 beta-triol (YC-5) has protection function for neuronal damage caused by cerebral ischemia, ischemia ofspinal cord, epileptic seizure and convulsion and relates to an application of YC-5 in preparation of neuronal protection medicine. The YC-5 can be prepared from cholesterol through two steps. The primitive cell culture in vitro and spinal cord ischemia animal model proves that YC-5 has protection function for neuronal damage caused by cerebral ischemia, ischemia of spinal cord, epileptic seizureand convulsion. YC-5 in effective dose has no toxic and side reactions. YC-5 is an effective neural protectant which aims to multiple molecular mechanism and cures cerebral ischemia damage, spinal cord ischemia damage, epileptic seizure and convulsion.

The present invention relates to methods of suppressing neuronal death, such as is observed with ischemia-related diseases and disorders, including neuronal and cardiac conditions arizing from a sudden loss of oxygen and / or energy loss, and degenerative diseases, such as Alzheimer's disease to name just one. The methods involve the use of inhibitors that act primarily in a simultaneous manner on the cyclin-dependent kinases, CDK4 and CDK6.

The present invention provides compositions and methods for enhancing the neuroprotective effect of umbilical cord blood cells. More particularly, the present invention provides methods of treating neurodegenerative disorders by administering umbilical cord blood cells and a substance capable of permeabilizing the blood brain barrier. In one embodiment, the blood brain barrier permeabilizer is mannitol. In another embodiment, the blood brain barrier permeabilizer is Cereport.

The use of red or near infrared light upon neurons of the lumbar plexus that are in distress due to retraction-induced ischemia. The surgeon may protect nerves made ischemic in the surgery by:a) making an incision in a patient,b) inserting an access device into the patient through the incision to at least partially create a path to a spine of the patient, andc) irradiating nervous tissue adjacent the path with an amount of NIR or red light effective to provide neuroprotection.

Methods and pharmaceutical compositions for preconditioning and / or providing neuroprotection to the animal central nervous system against the effects of neurological disorders involving ischemia, trauma, metal poisoning and neurodegeneration, including the associated cognitive, behavioral and physical impairments. In one embodiment, the method is accomplished by stimulating and / or stabilizing hypoxia-inducible factor-1α (HIF-1α). HIF-1α is known to provide a neuroprotective benefit under ischemic conditions. In another embodiment, the method is accomplished by differentially reducing, inhibiting or preventing the increased expression of selected genes caused by neurological disorders. Patients at risk for certain diseases or disorders that are associated with risk for cerebral ischemia may benefit, e.g., those at risk for Alzheimer's disease, Parkinson's disease, Wilson's disease, Huntington's disease, thalassemia or stroke, or those patients having head or spinal cord injury. Patients undergoing certain medical procedures that may result in ischemia may also benefit. Initially, the possibility of ischemia or neurodegeneration is recognized. Intranasal therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and / or copper such as iron chelators, copper chelators, and antioxidants. Particular examples of such therapeutic agents are the iron chelators deferoxamine (DFO) and deferasirox. Intranasal administration of DFO is known to stimulate and / or stabilize HIF-1α and provides an efficient and safe method for pre-conditioning the brain to protect against cerebral ischemia.

The present disclosure relates to nutritional compositions comprising a neurologic component, wherein, the neurologic component may promote brain and nervous system development and further provide neurological protection and repair. The neurologic component may include phosphatidylethanolamine, sphingomyelin, cytidine diphosphate-choline, ceramide, uridine, at least one ganglioside, and mixtures thereof. The disclosure further relates to methods of promoting brain and nervous system health by providing said nutritional compositions to target subjects, which includes pediatric subjects.

The present invention relates to the compound of formula which is 4-hydroxy-4-methyl-piperidine-1-carboxylic acid(4-methoxy-7-morpholin-4-yl-benzothiazol-2-yl)-amide, and to pharmaceutically acceptable acid addition salts thereof. It has been found that the compound is useful for the treatment or prevention of Alzheimer's disease, Parkinson's disease, Huntington's disease, neuroprotection, schizophrenia, anxiety, pain, respiration deficits, depression, ADHD (attention deficit hyper-activity disorder), drug addiction to amphetamines, cocaine, opioids, ethanol, nicotine, or cannabinoids, or for the treatment of asthma, allergic responses, hypoxia, ischemia, seizure, substance abuse, or for use as muscle relaxants, antipsychotics, antiepileptics, anticonvulsants and cardioprotective agents.

The invention is directed to methods of preventing, delaying, or reducing motor neuron damage in an individual by administering to the individual a composition containing an extract of gingko biloba. The methods can be used to treat an individual having or at risk of having a condition characterized by motor neuron damage, e.g., amyotrophic lateral sclerosis. The invention also includes methods of preventing or reducing weight loss in an individual by administering to the individual a composition containing an extract of gingko biloba.

The present invention belongs to the field of medicine, and particularly relates to a novel curcumin pharmaceutical preparation, which comprises a solid dispersion, a micellar preparation, SMEDDS and a nanometer emulsion. According to the present invention, by increasing the solubility and the bioavailability of curcumin, the curcumin pharmaceutical preparation can effectively utilize the pharmacological effects of anti-oxidation, anti-inflammation, anti-cancer, apoptosis induction, antiangiogenesis, neuroprotection, anti-microorganism, liver and kidney protection, vascular formation inhibition, myocardial infarction prevention, blood glucose lowering, anti-rheumatism and the like of the curcumin.

The present invention provides a method of providing acute neuroprotection by inducing the erythropoietin (EPO) signaling pathway in neuronal cells close to or subsequent to the time of excitatory insult; and inducing an insulin-like growth factor (IGF) signaling pathway in the neuronal cells close to or subsequent to the time of excitatory insult, thereby producing a synergistic acute neuroprotective effect in the neuronal cells. The invention also provides a method of preventing or reducing the severity of a neurologic condition in a subject by administering to the subject EPO or an active fragment or analog thereof at a dose of at most 2000 U / kg; and administering to the subject an IGF or an active fragment or analog thereof, thereby providing neuroprotection and preventing or reducing the severity of the neurologic condition. Such a method can be used to prevent or reduce the severity of, for example, Alzheimer's disease, Parkinson's disease, Huntington's disease, epilepsy, amyotrophic lateral sclerosis, multiple sclerosis, a movement disorder, HIV-associated dementia, HIV-associated neuropathy, neuropathic pain, migraine, glaucoma, drug addiction, drug withdrawal, drug dependency, depression or anxiety.

This invention relates to compositions and methods for lowering intraocular pressure and treatment and / or prevention of glaucoma and ocular hypertension. The invention provides insulin, isoforms of insulin, analoges of insulin, fragments of insulin peptide and other products of protein / gene engineered modifications of insulin for the lowering of intraocular pressure. The invention also provides insulin, isoforms of insulin, analoges of insulin, fragments of insulin and other products of protein / gene engineered modifications of insulin for increasing the success of glaucoma surgical procedures. The invention further provides insulin, isoforms of insulin, analoges of insulin, fragments of insulin and other products of protein / gene engineered modifications of insulin for neuroprotection of retinal ganglion cells.

Novel iron chelators exhibiting neuroprotective and good transport properties are useful in iron chelation therapy for treatment of a disease, disorder or condition associated with iron overload and oxidative stress, eg. a neurodegenerative or cerebrovascular disease or disorder, a neoplastic disease, hemochromatosis, thalassemia, a cardiovascular disease, diabetes, a inflammatory disorder, anthracycline cardiotoxicity, a viral infection, a protozoal infection, a yeast infection, retarding ageing, and prevention and / or treatment of skin ageing and skin protection against sunlight and / or UV light. The iron chelator function is provided by a 8-hydroxyquinoline, a hydroxypyridinone or a hydroxamate moiety, the neuroprotective function is imparted to the compound e.g. by a neuroprotective peptide, and a combined antiapoptotic and neuroprotective function by a propargyl group.