11 results about "Epileptogenesis" patented technology

This disclosure relates to materials and method of using MEK inhibitors, such as the MAP2K inhibitor CI-1040 to treat a subject having an existing epileptic disorder or prevent epilepsy in a subject without an existing epileptic disorder following a brain injury alone or in combination with a second anti-epileptic drug such as an mTOR inhibitor.

The invention provides application of OPC-like cell detection in prediction of glioblastoma with epilepsy. Specifically, the invention provides an application of a detection reagent of OPC-like cell markers PDGFRA and EGFRvIII in prediction of epilepsy of people with glioblastoma. The invention has an application prospect in the field of diagnosis and treatment of diseases of glioblastoma with epilepsy.

To provide therapeutic approaches for treating epileptogenesis associated with a brain insult, e.g., traumatic brain injury (TBI), stroke, or brain infection.SOLUTION: Provided are liquid pharmaceutical compositions including topiramate or a pharmaceutically acceptable salt thereof, meglumine, and a pharmaceutically acceptable excipient, the liquid pharmaceutical compositions optionally further including, e.g., levetiracetam or brivaracetam and / or atorvastatin or a pharmaceutically acceptable salt thereof (e.g., atorvastatin sodium).SELECTED DRAWING: Figure 1

The subject matter of the present invention is the use of 2-Pentadecyl-2-oxazoline (also known as PEA-OXA) in association with butyric acid, in acidic or salified form, in the treatment of epilepsy and associated psychiatric comorbidities (such as social isolation). In particular, the present invention relates to PEA-OXA for use, in humans and animals, in the prevention and treatment of epileptogenesis and comorbidities associated with epilepsy, such as limited social interaction, wherein PEA-OXA is administered in association or in combination with butyric acid or a salt thereof, wherein said administration is separate, joint, or simultaneous.

The invention relates to the technical field of biological medicine, and discloses an application of biomarkers in preparation of a product for predicting epilepsy, the biomarkers are CXCL17 and GPR35, and a detection result is related to the combined expression level of CXCL17 and GPR35 in a biological sample. The invention further discloses a kit for assisting in predicting epilepsy occurrence and monitoring the drug treatment effect. The invention provides a product capable of applying the combined expression level of CXCL17 and GPR35 for the first time, the product can carry out rapid, objective, high-sensitivity and high-specificity prediction in the early stage of epilepsy occurrence, and after definite diagnosis of epilepsy, by monitoring the compensatory increase of CXCL17 and GPR35 in the chronic stage, the epilepsy can be quickly and objectively predicted in a high-sensitivity and high-specificity manner. The invention discloses an important role in an epilepsy nerve protection mechanism as a protective molecule.

A system and method to facilitate the analysis of long-term scalp EEG recordings and the investigation of underlying epileptogenicity. Pathological high frequency oscillations are identified and extracted from the EEG recordings and electrophysiological source imaging is used to reconstruct cortical activity, which can be used as an aid in surgical resection for the treatment of epilepsy.

The invention provides application of KCND2 detection in prediction of glioblastoma with epilepsy. Specifically, the invention provides application of KCND2 and a detection reagent thereof in predicting epilepsy of people with glioblastoma. The invention further provides a mouse model constructed by using the xenotransplantation KCND2 overexpressed patient-derived primary GBM tumor cells, and the mouse model can be used for further researching a mechanism of GBM with epilepsy and screening therapeutic drugs. The invention has an application prospect in the field of diagnosis and treatment of diseases of glioblastoma with epilepsy.

Provided herein are alpha? nicotinic receptor specific activators as anti-epileptogenic agents effective against epilepsy or epileptogenesis and associated comorbidities in a subject after a traumatic brain injury. Provided herein are methods for treating epilepsy in a subject, preventing seizures in a subject at risk for the same and preventing epileptogenesis in a traumatic brain injured subject and associated comorbidities. a7-nAChR activators are administered to the subject alone or in combination with established anti-epileptic or anti- epileptogenic drugs.

Provided herein are alpha? nicotinic receptor specific activators as anti-epileptogenic agents effective against epilepsy or epileptogenesis and associated comorbidities in a subject after a traumatic brain injury. Provided herein are methods for treating epilepsy in a subject, preventing seizures in a subject at risk for the same and preventing epileptogenesis in a traumatic brain injured subject and associated comorbidities. a7-nAChR activators are administered to the subject alone or in combination with established anti-epileptic or anti- epileptogenic drugs.

The invention provides an application of targeted KCND2 in prevention or treatment of glioblastoma with epilepsy. Specifically, the invention provides an application of a KCND2 inhibitor in preventing and / or treating epilepsy of a patient with glioblastoma. The invention also provides a pharmaceutical composition containing the KCND2 inhibitor and a method for preventing and / or treating epilepsy of a patient with glioblastoma by using the pharmaceutical composition. The invention has an application prospect in the field of treatment of diseases of glioblastoma with epilepsy.

The present invention is related to use of marimastat or a pharmaceutically acceptable salt, solvate or polymorph thereof in preventing or treating epileptogenesis in a subject that suffered a brain insult. Said brain insult is a stroke, traumatic brain injury, or a result of status epilepticus, evoked by structural or metabolic reasons. Marimastat or a pharmaceutically acceptable salt thereof is administered preferably within the first 24 hours after induction of epileptogenesis.