Gad Informative Speech
Good morning everyone. My name is Arnaud Pierre and today, the topic of my presentation is going to be on generalised anxiety disorder (aka GAD). So GAD is a persistent and common disorder where the patient has unfocused worry and anxiety which is not associated with stressful situations. According to recent studies, GAD has a lifetime prevalence rate of 4-7% and therefore, being able to understand the mechanisms triggering GAD is essential. Let us begin with some important definitions. γ-Aminobutyric acid, also known as GABA is the chief inhibitory neurotransmitter in the mammalian central nervous system. It plays the principal role in reducing neuronal excitability throughout the nervous system. GABA-A receptors are one form of GABA receptors
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Evidence from animal and human studies suggests that alteration of function of the GABA neuronal system plays a significant role in the pathophysiology of GAD. Benzodiazepine receptors (BDZ-Rs) and GABAAreceptors are part of the same macromolecular complex. Clinical studies have shown that benzodiazepines are effective in treating patients with GAD.42 Patients with GAD have been shown to have low levels of peripheral benzodiazepine receptors (pBR) and low levels of pBR messenger ribonucleic acid in lymphocytes.43 These levels increased to normal after 2 months of treatment with a diazepam-related compound, and remained normal up to 1 month after discontinuing treatment. In this study, the level of pBR was also correlated with the amount of clinical improvement. These results suggest that the lower expression of pBR is a state-related biological abnormality in patients with GAD that can be remediated with appropriate treatment. However, the mechanism by which the levels of pBRs are normalized is still unknown and one must always be careful when extrapolating from studies of the pBRs to the function of the central
Evidence from animal and human studies suggests that alteration of function of the GABA neuronal system plays a significant role in the pathophysiology of GAD. Benzodiazepine receptors (BDZ-Rs) and GABAAreceptors are part of the same macromolecular complex. Clinical studies have shown that benzodiazepines are effective in treating patients with GAD.42 Patients with GAD have been shown to have low levels of peripheral benzodiazepine receptors (pBR) and low levels of pBR messenger ribonucleic acid in lymphocytes.43 These levels increased to normal after 2 months of treatment with a diazepam-related compound, and remained normal up to 1 month after discontinuing treatment. In this study, the level of pBR was also correlated with the amount of clinical improvement. These results suggest that the lower expression of pBR is a state-related biological abnormality in patients with GAD that can be remediated with appropriate treatment. However, the mechanism by which the levels of pBRs are normalized is still unknown and one must always be careful when extrapolating from studies of the pBRs to the function of the central