Thursday, November 14, 2019

Journals on Neurology - BJSTR Journal

Abstract

Alzheimer's disease (AD) is a #neurodegenerative process; manifests as episodic memory loss and working memory impairment [1]. Prefrontal cortex plays a key role in working memory which depends on modulating transmitters, dopamine and #gamma-aminobutyric acid (GABA) [2,3]. The #neurohypophysial hormone, oxytocin acts on lactation, parturition, modulating stress responses, pain perception, learning and different aspects of social behavior. Investigators suggest that oxytocin has potential therapeutic effects on depressive disorders because it induces hippocampal #neurogenesis- a process altered in depression [4]. In this regard #intranasal oxytocin administration found to be the most effective way to access to the central nervous system [5]. Dopamine concentrations in Alzheimer patients decreased (about 18-27%) in temporal and #hippocampal cortices [6]. In addition to dopamine, significant reduction in GABA level has been identified in AD [7]. A recent study suggested that administration of single #oxytocin dose has improved "executive component" of working memory (component contributing in information maintenance plus manipulation) in schizophrenic patients [8]. One of the oxytocin analogues induces #GABAergic transmission [9].

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