Alcobra Releases New Neuroimaging Data Supporting Pro-Cognitive Effects of MDX
TEL AVIV, Israel, Aug. 8, 2014 (GLOBE NEWSWIRE) -- Alcobra Ltd. (ADHD), an emerging pharmaceutical company focused on the development of new medications to help patients with cognitive disorders, including Attention Deficit Hyperactivity Disorder (ADHD) and Fragile X Syndrome, today released new imaging data on brain activity associated with MDX treatment.
Alcobra released topline results from a pharmacological MRI study designed to evaluate the regions of the brain that are modulated by MDX. The study evaluated brain response to a single administration of Metadoxine in rats. The experiment included 3 treatment arms: a placebo group, a low-dose group (corresponding approximately to the 700mg MDX dose in humans), and a high-dose group (corresponding approximately to the 1400mg MDX dose in humans). Neuronal activity was examined by evaluating Blood Oxygen Level Dependent (BOLD) MRI imaging, which measures brain oxygen levels that are related to changes in brain nerve cell activity. BOLD phMRI was employed to study 170 different areas of the brain following placebo or drug administration.
The results showed that Metadoxine produced a significant, dose-dependent decrease in BOLD signal in highly selective regions of the brain including the prefrontal cortex and showed a statistically significant increase in BOLD response in brain regions including the central nucleus of the amygdala and the lateral hypothalamus. In addition, none of the mesolimbic dopamine system brain regions (such as the nucleus accumbens), known to be involved in the reinforcing effects of scheduled drugs, were significantly affected by Metadoxine at any dose level, which is consistent with previously presented data.
"Metadoxine produced a specific and extensive effect in brain areas related to executive function, learning and memory, motivation, information integration and processing, attention and cognition," said Dr. Jonathan Rubin, Chief Medical Officer of Alcobra. "A functional decrease in these neuronal circuits mediated by MDX may help ADHD patients filter unnecessary sensory stimuli. These findings also confirm and extend previous data demonstrating a novel monoamine-independent mechanism of action of Metadoxine characterized by GABAergic inhibitory transmission modulation."
Dr. Jonathan Rubin will present the results during the company's second quarter financial results and operational update call and webcast on Monday, August 11.
