ABSTRACT: Label-free proteomics of human brain FFPE archival tissue. Comparison of proteome composition between epilepsy and controls across 3 brain regions.
Project description:Ion channel splice array data from temporal cortex brain tissue samples collected from control subjects (no mesial temporal lobe epilepsy). Keywords: disease associated splicing changes Temporal cortex samples from control subjects were compared to temporal neocortex of patients with mesial temporal lobe epilepsy
Project description:The ketogenic diet has long been used to treat epilepsy, but its mechanism is not yet clearly understood. To explore the potential mechanism, the changes in gene expression induced by the ketogenic diet in the rat kainic acid (KA) epilepsy model were analyzed. Two-condition experiment, Normal diet-fed rat brain vs. Ketogenic diet-fed rat brain. Duplicate per array
Project description:Direct comparison of FACS sorted EGFP positive brain macrophages vs pooled Total Brain extract Keywords: Direct pairwise comparison
Project description:Epilepsy frequently develops as a result of brain insult, for example brain injury or stroke. Currently there are no tools allowing us to predict which trauma patients will eventually develop epilepsy. There is evidence that microRNAs levels are altered in the blood, making them attractive candidates for peripheral biomarkers of epilepsy. We analyzed miRNA levels in blood samples using Affymetrix microarrays 4.1 and performed comparative analysis of samples. We performed 3 comparisons: i) control animals vs. Status epilepticus animals, ii) animals which developed first spontaneous seizure around 7 days post stimulation (EARLY), or later after 21days post stimulation (LATE), iii) animals that had high or low number of seizures as determined by seizures number (EARLY vs. LATE).
Project description:Epilepsy frequently develops as a result of brain insult, for example brain injury or stroke. Currently there are no tools allowing us to predict which trauma patients will eventually develop epilepsy. There is evidence that microRNAs levels are altered in the blood, making them attractive candidates for peripheral biomarkers of epilepsy. We analyzed miRNA levels in blood samples using Affymetrix microarrays 4.1 and performed comparative analysis of samples. We performed 3 comparisons: i) control animals vs. Status epilepticus animals, ii) animals which developed first spontaneous seizure around 7 days post stimulation (EARLY), or later after 21days post stimulation (LATE), iii) animals that had high or low number of seizures as determined by seizures number (EARLY vs. LATE).
Project description:Epilepsy frequently develops as a result of brain insult, for example brain injury or stroke. Currently there are no tools allowing us to predict which trauma patients will eventually develop epilepsy. There is evidence that microRNAs levels are altered in the blood, making them attractive candidates for peripheral biomarkers of epilepsy. We analyzed miRNA levels in blood samples using Affymetrix microarrays 4.1 and performed comparative analysis of samples. We performed 3 comparisons: i) control animals vs. Status epilepticus animals, ii) animals which developed first spontaneous seizure around 7 days post stimulation (EARLY), or later after 21days post stimulation (LATE), iii) animals that had high or low number of seizures as determined by seizures number (EARLY vs. LATE).
Project description:The diagnosis of epilepsy is complex and challenging and would benefit from the availability of molecular biomarkers, ideally measurable in a biofluid such as blood. Experimental and human epilepsy are associated with altered brain and blood levels of various microRNAs (miRNAs). Evidence is lacking, however, as to whether any of the circulating pool of miRNAs originates from the brain. To explore the link between circulating miRNAs and the pathophysiology of epilepsy, we first sequenced Ago2-bound miRNAs in plasma samples collected from mice subject to status epilepticus (SE) induced by intraamygdala microinjection of kainic acid. This identified time-dependent changes in plasma levels of miRNAs with known neuronal and microglial-cell origins. To explore whether the circulating miRNAs had originated from the brain, we generated mice expressing FLAG-Ago2 in neurons or microglia using tamoxifen-inducible Thy1 or Cx3cr1 promoters, respectively. FLAG immunoprecipitates from the plasma of these mice after seizures contained miRNAs, including let-7i-5p and miR-19b-3p. Taken together, these studies confirm that a portion of the circulating pool of miRNAs in experimental epilepsy originates from the brain, increasing support for miRNAs as mechanistic biomarkers of epilepsy.