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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