Research News

In previous posts we have profiled fenfluramine as a recent promising add-on therapy for Dravet syndrome, which not only reduces seizures but also improves executive functioning (behavior, emotions, and cognition). Fenfluramine\’s known pharmacological profile is to bind at 5-HT receptors and enhance the release of serotonin. It is thought that this mechanism is probably insufficient […]

Glucagon-like peptide-1 (GLP-1) is a hormone that is secreted from intestinal cells after food ingestion, stimulates insulin secretion, and helps regulate blood sugar levels. It also binds to receptors in the brain and promotes satiety, thereby reducing food intake. For these reasons, GLP-1 analogs have become popular as second-line drugs to treat type 2 diabetes

Dravet Syndrome is caused by loss-of-function mutations affecting the NaV1.1 sodium channel.  In a July 2019 research summary, we pointed out that gain-of-function mutations in another sodium channel, called NaV1.6, can lead to severe epileptic conditions – suggesting that NaV1.1 and NaV1.6 exist in a balance that maintains proper nerve conduction.   This raised the possibility

This study explored EEG characteristics over the life cycle of Dravet mice; that is, through the febrile, worsening, and stabilization stages. One common way to analyze EEG spectra is to compute the “power spectral density” (PSD) profile. The authors found that normal EEG patterns were observed at the febrile stage, however a marked reduction in

Dravet syndrome is caused by a mutation in the SCN1A gene, which codes for the NaV1.1 sodium channel a subunit. As described in previous summaries, gene therapy is becoming a very promising approach for fixing genetic disorders, with the use of adeno-associated virus (\”AAV\”) as the preferred delivery system – but the coding region of