Agomelatine improves sleep in a patient with fatal familial insomnia.

A young patient with FFI was started on agomelatine 25 mg to medicate nocturnal insomnia. Under this treatment sleep efficiency was improved, slow wave sleep was high and awakenings during sleep period time were far less than before. Clinically the patient was less restless during nighttime.

Psychiatric co-morbidities in patients attending specialist obesity services in the UK.

BACKGROUND: The prevalence of obesity is rising, but little is known about its psychosocial correlates. AIM: To assess psychological co-morbidities and impairment of quality of life in obese individuals seeking treatment at two specialist centres in the UK. DESIGN: Retrospective analysis of anthropometric and questionnaire data collected at initial clinic visit. METHODS: Patients attending for a first visit between April 2004 and March 2005 completed questionnaires that included scales for measurement of anxiety and depression (Hospital Anxiety and Depression Scale), eating disorder-behaviour (Eating Disorder Inventory 2), assessment of body image (Body Image Assessment for Obesity) and quality of life (Impact of Weight on Quality of Life-Lite). We examined the relationships between variables measured on these scales and anthropometric data. RESULTS: Of 253 questionnaires evaluated, there were elevated scores for depression in 48%, and elevated scores for anxiety in 56%. Twenty-two percent demonstrated scores suggestive of a personality trait that overlaps with an eating disorder; an additional 11.5% had an elevated score for bulimia. About a third of individuals had significant impaired quality of life in the areas of examined. DISCUSSION: Psychological co-morbidities are common in obese individuals attending specialist weight-management clinics, and may merit consideration at (or before) commencement of a weight loss programme.

Microglial expression of prostaglandin EP3 receptor in excitotoxic lesions in the rat striatum.

Prostaglandins (PG) are produced by the enzymatic activity of cyclooxygenase (COX). PGs and COX have been implicated in the pathophysiology of excitotoxicity and neurodegeneration in the central nervous system (CNS). The PGE2 receptor EP3 is the most abundantly expressed PGE2 receptor subtype in the brain. So far, in the innate rat brain EP3 receptors have been found exclusively in neurons. The aim of this study was to investigate whether EP3 expression in the brain changes under neurodegenerative circumstances such as an acute excitotoxic lesion. Intrastriatal injection of quinolinic acid (QUIN) resulted in a loss of EP3-positive striatal neurons, while simultaneously small glial-shaped EP3-positive cells appeared. Five days after lesioning, 63% of the glial-shaped EP3-positive cells could be identified as ED-1 expressing microglial cells. This percentage increased to 82% after 10 days, suggesting that most of the EP3-positive ED-1-negative cells on day 5 may be microglia which did not yet express ED-1. ED-1-positive microglia also expressed COX-1. These experiments show for the first time that activated microglial cells in excitotoxic lesions express in vivo the PGE2 receptor EP3 and the PGE2 synthesizing enzyme COX-1. Activation of EP3 receptor downregulates cAMP formation and may counteract the upregulation of cAMP formation via EP2 receptors, which has been linked to the anti-inflammatory effects of PGs. This change in EP3-receptor expression in microglia might participate in acute or chronic microglial activation in a variety of brain diseases such as ischemia or Alzheimer's disease (AD). Investigation of the expression of different PGE2 receptor subtypes might promote a better understanding of the pathophysiology of these diseases as well as leading to a modulation of microglial activation by a more specific interference with selective EP receptors than can be achieved by inhibiting global PG synthesis by selective or non-selective COX inhibitors.