The Administrative Prevalence of Multiple Sclerosis in Greece on the Basis of a Nationwide Prescription Database.

Objective: To estimate current prevalence of multiple sclerosis (MS) in Greece using administrative data from the nationwide medicine prescription database. Methods: Prescription records of a 24-month period (June 2017-May 2019) were analyzed in order to identify cases of MS. Sex, age, and place of residence were recorded for each identified case. Prevalence of MS was calculated based on the updated records of the Greek population according to Hellenic Statistical Authority. Results: The 2-year cumulative period prevalence of MS was estimated to 197.8 per 100,000 (95% CI 197.6-198.0). In total, 21,218 patients (65.8% female) were identified. During this period, the prevalence of MS was 138.7 per 100,000 (95% CI 138.4-139.0) in men and 253.6 per 100,000 (95% CI 253.3-254.1) in women. Prevalence was higher in the 45-49 age group in both sexes. Analysis of the place of residence revealed higher prevalence in the Attica region and Western Greece while lower prevalence was observed in Northern Greece. No north-south latitude gradient was detected. Point prevalence on 1 January 2019 was calculated to 188.9 per 100,000 (95% CI 188.7-189.1). Regarding treatment, 73.1% of the identified cases received at least once a Disease Modifying Drug. Conclusions: According to this national-level study conducted in Greece, estimated prevalence of MS was found to be similar to those of other European countries. Heterogeneity of MS prevalence across the country was observed and needs further investigation.

Glucokinase Activators for Type 2 Diabetes: Challenges and Future Developments.

Increased hepatic glucose output, the primary liver dysregulation associated with Type 2 diabetes mellitus (T2DM), is not directly or effectively targeted by the currently available classes of glucose-lowering medications except metformin. This unmet need might be addressed through activation of a specific enzyme-member of the hexokinase family, namely glucokinase (GK). GK serves as a "glucose-sensor" or "glucose receptor" in pancreatic cells, eliciting glucose-stimulated insulin secretion, and as glucose "gate-keeper" in hepatocytes, promoting hepatic glucose uptake and glycogen synthesis and storage. GK activation by small molecules present an alternative approach to restore/improve glycaemic control in patients with T2DM. GK activators (GKAs) may increase insulin secretion from the pancreas and promote glycogen synthesis in the liver, and hence reduce hepatic glucose output. Despite several setbacks in their development, interest in the GKA class has been renewed, particularly since the introduction of a novel, dual-acting full GKA, dorzagliatin, and a novel hepatoselective molecule, TTP399. In this article we provide an overview of the role, efficacy, safety and future developments of GKAs in the management of T2DM.

Nandrolone abuse decreases anxiety and impairs memory in rats via central androgenic receptors.

Anabolic androgenic steroids (AASs) affect areas of the central nervous system, which are involved in emotional and cognitive responses such as sexuality, anxiety, and memory. In the present study we imitated the abuse of AASs by administering high doses of the AAS nandrolone decanoate (ND) to rats. Thereafter rats were exposed to an elevated plus-maze and an olfactory social memory test to evaluate their anxiety-like and cognitive behaviour. To reveal whether these emotional and cognitive changes evoked by ND were caused via direct activation of androgenic receptors (ARs) in the brain, the AR antagonist flutamide (FL) was administered intracerebroventricularly (i.c.v.). Male rats were randomly divided in four groups, one group received 15 mg/kg ND subcutaneously, once daily for 6 wk (ND group). In the second group, in addition to ND, a daily dose of 5 microg FL was injected i.c.v. also for 6 wk (ND+FL group). The third group of rats received only FL and in the control group the vehicle was injected. The ND group clearly spent more time investigating the open arms in the maze test and recognizing the juvenile during the olfactory social memory test in comparison to the control group. In the ND+FL group rats showed similar emotional behaviour and cognitive ability to that of the control group. Injection of FL alone did not affect either anxiety or memory. These results indicate that repeated, high-dose administration of ND decreases anxiety and impairs memory in rats via direct activation of central ARs.

Neuroprotection by lamotrigine in a rat model of neonatal hypoxic-ischaemic encephalopathy.

Hypoxic-ischaemic (HI) encephalopathy is a severe complication of perinatal asphyxia and remains a frequent cause of a variety of brain disorders with long-term effects on the patients' life. The associated brain damage is strongly related to the toxic action of excitatory amino acids, especially glutamate and aspartate. Lamotrigine is an anti-epileptic drug that blocks the voltage-gated sodium channels of the presynaptic neuron and inhibits the release of glutamate. In the present study a well-established model of perinatal asphyxia in 7-d-old rats was used to investigate the effect of lamotrigine on HI-induced damage to different hippocampal brain structures, since disruption of this brain area is thought to play a key role in schizophrenia and epilepsy. Therefore, a combination of ischaemia, induced by unilateral occlusion of the left common carotid artery, followed by exposure to a 1-h period of hypoxia, was carried out in neonatal 7-d-old rats. Immediately after the insult, lamotrigine was given i.p. The histological outcome in the hippocampus was conducted and the tissue levels of glutamate, aspartate, GABA, and glutamine in the same area were determined. A remarkable reduction of HI-evoked damaged neurons in most of the investigated hippocampal regions was noted after lamotrigine administration. Furthermore, lamotrigine decreased the asphyxia-induced hippocampal tissue levels of glutamate and aspartate. Immediately after perinatal asphyxia GABA levels were enhanced, while levels of glutamine were decreased. Lamotrigine administration did not affect either GABA or glutamine levels. These results suggest a neuroprotective effect of lamotrigine in this particular animal model of neonatal HI encephalopathy.