David A. Hosford

TL;DR: Exploratory analyses suggested that APOE ɛ4 non-carriers exhibited cognitive and functional improvement in response to RSG, whereas apolipoprotein E (APOE) genotype carriers showed no improvement and some decline was noted.

TL;DR: The genomewide association analysis again identified the APOE linkage disequilibrium region as the strongest genetic risk factor for AD.

TL;DR: Electrographic features and anticonvulsant sensitivity similar to those of human absence seizures in lethargic mice and enhanced GABAB receptor-mediated synaptic responses may underlie absence seizures, andGABAB receptor antagonists hold promise as anticonVulsants for absence seizures.

TL;DR: Genome-wide screens to identify copy number variation in patients with a diverse spectrum of epilepsy syndromes and in neurologically-normal controls implicate 16p13.11 and possibly other large deletions as risk factors for a wide range of epilepsy disorders, and they appear to point toward haploinsufficiency as a contributor to the pathogenicity of deletions.

TL;DR: It is found that the occurrence of seizure-evoked synchronous action potentials during the seizure exhibited a perfect qualitative correlation with the presence of c-fos mRNA expression in the granule cells 30 min following the seizure (Fisher's exact test, p = 0.002).