278 results about "Neuronal damage" patented technology

The present invention relates to novel neurosteroid derivatives with anti-apoptotic, neuroprotective and neurogenic properties that act on the nervous system as well as methods for making the same and their applications in the treatment and/or prevention or amelioration of neurodegenerative diseases related to neuronal apoptosis or neuronal injury, or conditions related to or resulting from apoptosis, including but not limited to Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis and amyotrophic lateral sclerosis (ALS), retinal degeneration and detachment, peripheral neuropathy caused by genetic abnormalities, diabetes, polio, herpes, AIDS and chemotherapy, brain trauma, or ischemia and stroke. The active compounds are represented by Formula (I): wherein R¹, R², R³, R⁴, R⁵, R⁶, R⁷, A, B, X, Y and Z are defined in the description of the invention. The present invention also includes compositions which comprise one or more of the compounds of Formula (I).

Compositions and methods are provided for prophylactic or therapeutic treatment of a mammal for hearing or balance impairments involving neuronal damage, loss, or degeneration, by administration of a therapeutically effective amount of a redox-active therapeutic. Also provided are improved compositions and methods for treatments requiring administration of a pharmaceutical having an ototoxic side-effect in combination with a therapeutically effective amount of a redox-active therapeutic to treat the ototoxicity.

Processes and materials are provided for the detection, diagnosis, or determination of the severity of a neurological injury or condition, including traumatic brain injury, multiple-organ injury, stroke, Alzeimer's disease, Pakinson disease and Chronic Traumatic Encephalopathy (CTE). The processes and materials include biomarkers detected or measured in a biological sample such as whole blood, serum, plasma, or CSF. Such biomarkers include Tau and GFAP proteins, their proteolytic breakdown products, brain specific or enriched micro-RNA, and brain specific or enriched protein directed autoantibodies. The processes and materials are operable to detect the presence of absence of acute, subacute or chronic brain injuries and predict outcome for the brain injury.

The present invention relates to the use of exosome-preparations derived from neonatal or adult tissue-derived mesenchymal stem-cells (MSCs) for the prevention or for therapy of inflammatory conditions, such as, for example, pre- and postnatally acquired damages of the brain (i.e. neuronal damages) or in complications following stem cell transplantation (“graft vs host-disease”, GvHD).

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 provides composition comprising one or more glycosaminoglycan mimetics and uses thereof. The subject glycosaminoglycan mimetics are particularly useful for treatment of neuronal injuries including without limitation spinal cord injuries.

The invention provides compositions, kits, and methods for treatment of neuronal injury. In one embodiment, the composition comprises a biomembrane sealing agent, such as PEG, and a bioactive agent, such as a magnesium compound. The biomembrane sealing agent and/or the bioactive agent an intravenous administration, an intramuscular administration, an intrathecal administration, a subcutaneous administration, an epidural administration, a parenteral administration, a direct application onto or adjacent to a site of the pathological condition, and any combinations thereof. Alternatively, the biomembrane sealing agent and/or the bioactive agent may be delivered from a pump or an implant.

The present invention relates to novel non-sedating barbituric acid derivatives, pharmaceutical compositions containing them and methods of neuroprotection in cases of cerebral ischemia, head trauma and other acute neurologic injuries, and prevention of resulting neuronal damage. The invention also relates to the use of non-sedating barbituric acid derivatives given in a manner and dosage effective to produce blood levels and brain levels of these drugs and/or their active metabolites sufficient to provide a therapeutic effect.

Provided is a composition for treating nerve damage-related diseases. The composition includes a human umbilical cord blood-derived mesenchymal stem cell as an active ingredient. The mesenchymal stem cell isolated and incubated from the human umbilical cord blood migrates to an injured area to be differentiated into a nerve cell or a neuroglial cell at the time of in vivo transplantation. Thus, the mesenchymal stem cell and a composition including the same can be effectively used in cell replacement therapy and gene therapy for treating diseases caused by nerve damage including a stroke, Parkinson's disease, Alzheimer's disease, Pick's disease, Huntington's disease, amyotrophic lateral sclerosis, traumatic central nervous system disease and a spinal cord injury.

A method of inhibiting excitotoxicity by indirectly activating α4β2 nicotinic acetylcholine receptors (nAChRs) which indirectly activate synaptic AMPA and NMDA receptors is disclosed. Inhibitors of α7 nACHRs, such as macrocyclic diterpenoids, more specifically cembranoids or methyllycaconitine (MLA), indirectly activate α4β2 nAChRs and can be used to treat neurodegenerative diseases, including, but not limited to, Alzheimer's Disease, Parkinson Disease, AIDS related dementia and the delayed effects of stroke. They can also be used to treat diseases associated with neuronal impairment, including, but not limited to glaucoma caused by optical nerve damage, delayed effects of epilepsy; and multiple sclerosis.

A device for topical cooling of the nervous system via cooling of cerebrospinal fluid, or CSF, using a solid thermally conductive material. The solid thermally conductive material is coupled to a heat exchange apparatus. The thermally conductive material may be coupled to any catheter that is used in existing clinical standard of care for acute neuronal injuries, such as catheters used to monitor and relieve intracranial pressure. The thermally conductive material is a biocompatible and solid material, for instance, metals such as steel, tungsten and titanium, and non-metallic materials such as thermal diamond paste.

The present invention provides minimally invasive methods of detecting, diagnosing, and assessing neuronal damage associated with traumatic brain injury (TBI) or chronic traumatic encephalopathy (CTE). Specific species of microRNAs (miRNA), small, noncoding RNA molecules that play gene regulatory functions, are correlated with cellular damage and oxidative stress following TBI or CTE, allowing for rapid, minimally-invasive diagnosis and assessment of brain injury. The early identification and longitudinal assessment of neuronal damage in subjects suffering from or at risk of suffering from a TBI (e.g., football players, boxers, military personnel, fall victims) will improve clinical outcomes by guiding critical medical and behavioral decision making.

In a method and an apparatus for measuring degree of neuronal impairment in brain cortex, scalp potentials or magnetic fields of a subject are measured by mounting a plurality of sensors on a head of the subject, the measured scalp potentials or magnetic fields are converted into numerical data to obtain a dipolarity at each sampling, mean values of squared errors, within a fixed time interval, between a scalp potential or a magnetic field by an equivalent dipole at a dipolarity peak emergence time and the measured scalp potentials or magnetic fields, or variances of the squared errors from the mean values are obtained for the sensors, and a contour concerning a distribution of the mean values or the variances on a scalp or a brain surface corresponding thereto is mapped as an output. Alternatively, the squares of potentials sensed by the sensors are averaged for several seconds, and variances of these mean values are obtained for numerous reference persons. The mean value and the standard deviation of the variances for a group of the reference persons are obtained, so that the variance of an individual subject is ranked depending on which area of the standard deviation of the group of the reference persons the variance is located. By allocating the values to a brain surface corresponding to the sensors, maps are prepared. By these maps, a local impairment degree of a neuronal function is indicated.

The invention is generally directed to treatment of neuronal injury. In particular, the invention is directed to reducing axonal retraction (“dieback”) that occurs as a result of the interaction of activated macrophages with dystrophic axons that are produced during nervous system acute or chronic injury. The invention is also directed to promoting axonal growth/regeneration. The invention is specifically directed to using stem cells or their secreted cellular factors, such as would be produced in conditioned cell culture medium, to ameliorate or prevent axonal dieback and/or promote growth/regeneration of axons.

A method is provided for the prevention and treatment of selective progressive degeneration within the central nervous system caused by hydroxyl-free or ferryl-free radicals formed by Fenton-type catalyzed reactions between diffusible hydrogen peroxide and localized bivalent iron. The invention embodies unique pharmacologic composition for antioxidant protection by oral supplementation with hypoxanthine conjointly with either sodium L-ascorbate or L-ascorbic acid. The hypoxanthine is provided for its sodium-dependent intestinal absorption and transport for the systemic production of higher antioxidant and iron-chelating uric acid levels. Ascorbate is provided as potent antioxidant to raise body ascorbic acid levels concurrently and to protect against possible deleterious effect from nucleobase or other molecular injury induced by oxidized uric acid as urate anion free radical caused in the antioxidant action of the uric acid. It is contemplated that such oral supplementation conjointly with hypoxanthine and L-ascorbate will support better health and will mitigate the progressive oxidative neuronal damage in Alzheimer's disease, amnestic mild cognitive impairment, Down syndrome, amyotrophic lateral sclerosis, and Parkinson's disease.

This invention provides a method for treating a subject either during or soon after a seizure, in order to reduce the extent of neuronal damage in the subject resulting from the seizure comprising administering to the subject, either during or soon after the seizure, a therapeutically effective amount of an inhibitor of receptor for advanced glycation endproducts (RAGE), so as to thereby reduce the extent of neuronal damage in the subject. This invention further provides a method for inhibiting neuronal damage which would otherwise result from a seizure in a subject predisposed to having a seizure, comprising administering to the subject a prophylactically effective amount of an inhibitor of receptor for advanced glycation endproducts (RAGE), so as to inhibit neuronal damage which would otherwise result from a seizure in the event the subject were to suffer a seizure.

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.

Compositions and methods for treating patients with pre-existing neuronal damage are disclosed. The compositions and methods use an adeno-associated virus (AAV)-based gene delivery system to deliver glial cell line-derived neurotrophic factor (GDNF) to patients with neurodegenerative disorders such as Parkinson's disease .