The present invention relates to the use of the editing profile of PDE8A pre-mRNA as a specific bio marker of ADARs activities in evolved primate, particularly in Human tissues. The present invention also relates to an in vitro method for predicting in Human an alteration of the mechanism of the ADARs catalysed pre-mRNA editing of target genes, by analysing the PDE8A pre-mRNA editing profile in a peripheral tissue sample containing cells expressing said PDE8A pre-mRNA, such as blood sample. The present invention is also directed to an in vitro method for the screening of potential therapeutic compound and to predict and assess therapeutic efficacy and/or efficiency or to diagnose potential severe brain or peripheral drug side effects implementing said PDE8A pre-mRNA editing profile as specific biomarker. The present invention is further directed to a method for determining the PDE8A pre-mRNA editing profile in Human, particularly by capillary electrophoresis single-strand conformation polymorphism (CE-SSCP) method after amplification by a nested PCR. Finally the invention relates to particular nucleic acid primers implemented in said nested PCR and kit comprising such sets of primers and human cells capable of expressing PDE8A and ADARs.

The present invention relates to methods of detecting a neural injury biomarker in a biological sample. The method includes subjecting a biological sample to an assay according to the present invention that produces a measurable signal and detecting the measurable signal. The presence or absence of the measurable signal indicates the presence or absence of the biomarker in the sample. The present invention also relates to methods of determining the state of a subject's neural injury. The present invention also relates to systems and devices useful in carrying out the methods of the present invention.

Epileptic seizures are difficult to diagnose and are often difficult to distinguish from several conditions with similar presentations, and therefore, diagnosis of seizures is often a long, expensive, and unreliable process. This invention provides biomarkers for identifying seizures and epilepsy, assays for measuring and assessing biomarker concentration, predictive models based on biomarkers and computational systems for detecting, assessing and diagnosing phasic and tonic changes associated with seizures and epilepsy in all clinical and healthcare settings. Diagnostic and treatment methods, systems, kits, and predictive models provided herein, provide quantitative and/or qualitative assessment in order to allow patients to proceed immediately to diagnostic and/or treatment protocols, and assess therapeutic treatment effectiveness.

The present discloses relates to a composition, a kit or a method using an eIF4E inhibitor for diagnosis or treatment of a condition associated with increased activity of eIF4E.

Epileptic seizures are difficult to diagnose and are often difficult to distinguish from several conditions with similar presentations, and therefore, diagnosis of seizures is often a long, expensive, and unreliable process. This invention provides biomarkers for identifying seizures and epilepsy, assays for measuring and assessing biomarker concentration, predictive models based on biomarkers and computer systems for detecting, assessing and diagnosing phasic and tonic changes associated with seizures and epilepsy in all clinical and healthcare settings. Diagnostic methods, kits and predictive models provided herein provide quantitative and/or qualitative assessment in order to allow patients to proceed immediately to diagnostic and/or treatment protocols, and assess therapeutic treatment effectiveness.

A diagnostically useful carrier includes a peptide including the amino acid sequence set forth in SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 4 or a variant thereof. A kit, a composition, a detection method, use for detecting a neurological disease, a human autoantibody specifically binding to Drebrin and a therapeutic compound or combination for use in the treatment of a neurological use are also useful.

An area-specific tissue analysis (ASTA) method and system are disclosed for the precision harvesting and processing of tissue from acute brain slices (referred to herein as “brain chads”), e.g., for the purposes of cell and molecular biology/analysis. The exemplary ASTA system and method can sample tissue from hard-to-reach regions of the brain that has been cut acutely, e.g., into 100 to 500 microns-thick sections, for cell biological analysis.

Methods for determining the presence or amount of oxopiperidine in a biological sample using mass spectrometry. These methods may be used to efficiently and non-invasively diagnose pyridoxine dependent epilepsy (PDE) due to deficient a-aminoadipic-δ-semialdehyde (α-AASA) dehydrogenase activity due to mutations in ALDH7A1, resulting in the accumulation of Δ.sup.1-P6C, P6CH, and 6-Oxo-PIP in biological samples.

A method for determining the severity of a mammalian dive response (MDR) triggered during a patient's seizure that includes the following steps: (1) collecting an ictal specimen, the ictal specimen being a saliva or any other secretion from the mouth of the patient when the patient is in a peri-ictal period; (2) analyzing the ictal specimen to measure a level of a specimen marker, the specimen marker being a cellular or non-cellular biological component; and (3) determining the severity of the MDR or other autonomic reflex based on the level of the specimen marker.

Provided are a knockout mouse, a method for screening a substance for suppressing mesial temporal lobe epilepsy, and a method for selecting a technique for suppressing mesial temporal lobe epilepsy. A knockout mouse 30 or more days of age that has lost the function of the Girdin gene in at least the nervous tissues and exhibits the phenotypes of (1), (2), and (3) below. (1) hippocampal sclerosis should be present, (2) extrahippocampal brain damage should be limited, and (3) spontaneous epilepsy that can be said to be of hippocampal origin should be present.