Effects of AZD7325 on cutaneous sensation
Research type
Research Study
Full title
A phase I single site, single dose, randomized, double-blind, placebo controlled, 3-way cross-over biomarker study investigating the effect of the GABA modulator AZD7325 on cutaneous sensation in healthy volunteers
IRAS ID
173579
Contact name
Martin Koltzenburg
Contact email
Eudract number
2015-000642-35
Duration of Study in the UK
0 years, 5 months, 30 days
Research summary
GABA (gamma-aminobutyric acid) is the main inhibitory neurotransmitter in the human brain. Recent studies found that healthy individuals who performed better in several psychophysical tests had higher concentrations of GABA in relevant brain areas. For example, participants who performed better in a vibrotactile task had higher concentration of GABA in their sensory areas of the cortex. This suggests that enhancement of GABA effects in the brain could improve performance in healthy individuals.
Benzodiazepines (diazepam/Valium) or sleeping tablets like zolpidem (Stilnoct) are drugs that enhance effects of GABA by binding to its receptors. They are used to treat various disorders of the central nervous system, however, they have undesirable side effects, like sedation, cognitive impairment, and addiction.
Many of these side effects are linked to particular types of GABA receptor subtypes (GABA Aα1, Aα5). Therefore, efforts are made to develop drugs that do not act on these subtypes, but maintain their beneficial properties by acting on other GABA receptors subtypes (Aα2, Aα3) .
AZD7325 is a drug that selectively acts on GABA Aα2 and Aα3 receptors. It has been tested in more than 700 people and so far proved to be generally well tolerated. In this study, we will investigate its effects on manual dexterity and skin sensation in healthy volunteers.
If AZD7325 proves to enhance performance in healthy volunteers, this would provide a rationale for the use of this medication in certain neurological disorders presenting with impaired sensation and motor control of the hand, e.g. peripheral neuropathies. Although neuropathies are caused by a damage to peripheral nerves and not by lack of GABA in the brain, we wish to test the hypothesis that a use of a non-sedating drug to enhace GABA effects in the brain could compensate for the peripheral deficit for which there currently is no symptomatic treatment.REC name
London - West London & GTAC Research Ethics Committee
REC reference
15/LO/0814
Date of REC Opinion
17 Jul 2015
REC opinion
Further Information Favourable Opinion