Depression in Parkinson's disease

The prevalence of major and minor depression in Parkinson’s disease is around 30–40% but, unfortunately, depression remains frequently underrecognized and often undertreated. However, recognition and appropriate treatment of depression in patients with Parkinson’s disease is essential for improving the cross-sectional picture and longitudinal course. This review focuses on the epidemiology, pathophysiology and different treatment modalities of depression in Parkinson’s disease. | A major és minor depresszió prevalenciája Parkinson-kórban szenvedôk között körülbelül 30-40%, ugyanakkor a depresszió ebben a betegcsoportban aluldiagnosztizált és alulkezelt kórkép. A depresszió diagnózisának és az adekvát kezelésének elmaradása nemcsak a depressziós tünetek perzisztálásához, de csökkent életminôséghez, az alapbetegség súlyosabb tüneti képéhez és kedvezôtlenebb prognózisához is vezetnek. Összefoglaló tanulmányunkban a Parkinson-kórban megjelenô depresszió epidemiológiai, patofiziológiai és terápiás vonatkozásait tárgyaljuk

Antidepresszivumok, stresszorok es a szerotonin 1A receptor.

5-HT1A receptor is a receptor of surprises. Buspirone, an anxiolytic drug with a then yet unidentified mechanism of action had been marketed for years when it was discovered that it is a 5-HT1A partial agonist. Several more years had to pass before it was accepted that this receptor plays the key role in the action mechanism of buspirone. This was followed by further surprises. It was discovered that in spite of its anxiolytic effect buspirone activates the hypothalamic-pituitary-adrenal (HPA) stress axis, furthermore, it increases peripheral noradrenaline and adrenaline concentration via a central mechanism. Thus activation of this receptor leads to ACTH/corticosterone and catecholamine release and also increases beta-endorphine, oxytocin and prolactin secretion while decreasing body temperature, increasing food uptake, eliciting characteristic behavioural responses in rodents and also playing a role in the development of certain types of epilepsy. Human genetic studies revealed the role of 5-HT1A receptors in cognitive processes playing a role in the development of depression such as impulsiveness or response to environmental stress. This exceptionally wide spectrum of effects is attributable to the presence of 5-HT1A receptors in serotonergic as well as other, for example glutamatergic, cholinergic, dopaminergic and noradrenergic neurons. The majority of the effects of 5-HT1A receptors is manifested via the mediation of Gi proteins through the hyperpolarisation or inhibition of the neuron carrying the receptor. 5-HT1A receptors on serotonergic neurons can be found in the somatodendritic area and play a significant role in delaying the effects of antidepressants which is an obvious disadvantage. Therefore the newest serotonergic antidepressants including vilazodone and vortioxetine have been designed to possess 5-HT1A receptor partial agonist properties. In the present paper we focus primarily on the role of 5-HT1A receptors in stress and antidepressant response

A new clinical evidence-based gene-environment interaction model of depression.

In our current understanding of mood disorders, the role of genes is diverse including the mediation of the effects of provoking and protective factors. Different or partially overlapping gene sets play a major role in the development of personality traits including also affective temperaments, in the mediation of the effects of environmental factors, and in the interaction of these elements in the development of depression. Certain genes are associated with personality traits and temperaments including e.g., neuroticism, impulsivity, openness, rumination and extroversion. Environmental factors consist of external (early and provoking life events, seasonal changes, social support etc.) and internal factors (hormones, biological rhythm generators, comorbid disorders etc). Some of these environmental factors, such as early life events and some prenatal events directly influence the development of personality traits and temperaments. In the NEWMOOD cohort polymorphisms of the genes of the serotonin transporter, 5-HT1A, 5-HT1B and 5-HT2A and endocannabinoid CB1 receptors, tryptophan hydroxylase, CREB1, BDNF and GIRK provide evidence for the involvement of these genes in the development of depression. Based on their role in this process they could be assigned to different gene sets. The role of certain genes, such as promoter polymorphisms of the serotonin transporter (5-HTTLPR) and CB1 receptor has been shown in more than one of the above factors. Furthermore, gene-gene interactions of these promoters associated with anxiety suggest the application of these polymorphisms in personalized medicine. In this review we introduce a new model including environmental factors, genes, trait and temperament markers based on human genetic studies

30 év az öngyilkosság ellen: Munkacsoportunk depresszió- és szuicidprevenciós kutatásainak összefoglalása – 1985–2015

In this paper we gather and discuss the results of our workgroup on depression and suicide prevention published between 1985 and 2015. We hope that this summary will focus the interest of the scientific community on suicidology and turn the attention of decision-makers on the fact that despite of its marked decrease in the past three decades, the suicide rate in Hungary is still the second highest in the EU. So, based on expert opinion, joint action is needed in order to achieve a further decrease of suicide rate in Hungary. © 2015, Hungarian Association of Psychopharmacology. All rights reserved