Person: Schachter, Steven
Loading...
Email Address
AA Acceptance Date
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
Schachter
First Name
Steven
Name
Schachter, Steven
2 results
Search Results
Now showing 1 - 2 of 2
Publication Natural Products in Epilepsy—the Present Situation and Perspectives for the Future(MDPI, 2010) Ekstein, Dana; Schachter, StevenMore efficacious and better tolerated treatments for epilepsy are clearly needed. Complementary and alternative medicine (CAM) has a long history of use in certain parts of the world and has gained increasing interest over the last decades in Western countries. In countries with a Western-based type of medical system, people with epilepsy (PWE) take natural products or engage in other forms of CAM mainly to enhance general health, but also to prevent seizures or to alleviate symptoms of comorbidities or side effects of antiepileptic medications. In other countries, well developed medical systems, such as traditional Chinese Medicine and Ayurveda, are often the basis for treating PWE. Based on anecdotal reports of efficacy in PWE, natural products from these and other traditions are increasingly being studied in animal models of epilepsy, and candidates for further clinical development have been identified. It is likely, therefore, that natural products will be further evaluated for safety, tolerability and efficacy in PWE with drug-resistant seizures.Publication Huperzine A Provides Robust and Sustained Protection against Induced Seizures in Scn1a Mutant Mice(Frontiers Media S.A., 2016) Wong, Jennifer C.; Dutton, Stacey B. B.; Collins, Stephen D.; Schachter, Steven; Escayg, AndrewDe novo loss-of-function mutations in the voltage-gated sodium channel (VGSC) SCN1A (encoding Nav1.1) are the main cause of Dravet syndrome (DS), a catastrophic early-life encephalopathy associated with prolonged and recurrent early-life febrile seizures (FSs), refractory afebrile epilepsy, cognitive and behavioral deficits, and a 15–20% mortality rate. SCN1A mutations also lead to genetic epilepsy with febrile seizures plus (GEFS+), which is an inherited disorder characterized by early-life FSs and the development of a range of adult epilepsy subtypes. Current antiepileptic drugs often fail to protect against the severe seizures and behavioral and cognitive deficits found in patients with SCN1A mutations. To address the need for more efficacious treatments for SCN1A-derived epilepsies, we evaluated the therapeutic potential of Huperzine A, a naturally occurring reversible acetylcholinesterase inhibitor. In CF1 mice, Hup A (0.56 or 1 mg/kg) was found to confer protection against 6 Hz-, pentylenetetrazole (PTZ)-, and maximal electroshock (MES)-induced seizures. Robust protection against 6 Hz-, MES-, and hyperthermia-induced seizures was also achieved following Hup A administration in mouse models of DS (Scn1a+/−) and GEFS+ (Scn1aRH/+). Furthermore, Hup A-mediated seizure protection was sustained during 3 weeks of daily injections in Scn1aRH/+ mutants. Finally, we determined that muscarinic and GABAA receptors play a role in Hup A-mediated seizure protection. These findings indicate that Hup A might provide a novel therapeutic strategy for increasing seizure resistance in DS and GEFS+, and more broadly, in other forms of refractory epilepsy.