Contribution to the study of experimentally-simulated toxic and metabolic encephalopathies

This current PhD Thesis (by published work / retrospective) in Neuroscience focuses on performed studies of three crucial brain enzyme activities under seven categories of experimentally- simulated toxic and metabolic encephalopathies. The studied enzymes were: (a) acetylcholinesterase (AChE, EC 3.1.1.7), (b) sodium-potassium adenosine triphosphatase (Na+,K+- ATPase, EC 3.6.3.9, formerly EC 3.6.1.3), and (c) magnesium adenosine triphosphatase (Mg2+- ATPase, EC 3.6.3.2, formerly EC 3.6.1.3). The studied experimentally-simulated toxic and metabolic encephalopathies were: (a) thyroid-hormone-related brain dysfunctions (as a result of hyper- or hypothyroidism), (b) thioacetamide-induced fulminant hepatic encephalopathy, (c) streptozotocin-induced diabetic encephalopathy, (d) experimentally-simulated Wernicke’s encephalopathy (arising from chronic ethanol consumption, dietary thiaminedeprivation and pyrithiamine-administration), (e) manganese-induced neurotoxicity, (f) lanthanum- induced neurotoxicity, and (g) nickel-induced neurotoxicity. Enzymatic activities were determined spectrophotometrically on albino Wistar rat brain homogenates. Assessments of brain homogenates’ antioxidant status, in vivo antioxidant administrations, in vitro experiments, brain homogenates’ enzymatic activity determinations, as well as pure enzyme activity determinations (under various conditions), were performed (wherever required) in order to elucidate the nature of some of the observed in vivo findings, to evaluate the potential limitations of the experimental-simulation techniques and / or to study the potential use of known antioxidants as neuroprotective agents. All experiments were performed at the Medical School of the National and Kapodistrian University of Athens. The current PhD Thesis condenses and presents the significance of the aforementioned contribution to the study of experimentally-simulated toxic and metabolic encephalopathies, based on published work

Serotoninergic impairment and aggressive behavior in Alzheimer's disease.

The overall goal of all therapeutic interventions in Alzheimer's disease (AD) is to: (a) optimize the impaired functions and (b) restore an affordable quality of life for both the patient and his surroundings. AD has been characterized by a significant serotoninergic impairment. It is well known that impaired serotoninergic function is related to aggressive behavior. We, herein, review the past and recent evidence that seems to link the serotoninergic system with aggressive manifestations in AD patients. Managing the aggressive behavior of these patients might be of significant medical, social and economical importance. However, there is still a long way to go until we verify the exact pathophysiological mechanism(s) involved in the induction of aggression in AD patients. The current data underlines a complex relationship between the observed serotoninergic impairment in AD patients and the (a) cholinergic system, (b) the endocrine (hormonal) state, (c) the nutritional habits, (d) the genetic background and (e) the caregiving environment

Serotoninergic impairment and aggressive behavior in Alzheimer's disease.

The overall goal of all therapeutic interventions in Alzheimer's disease (AD) is to: (a) optimize the impaired functions and (b) restore an affordable quality of life for both the patient and his surroundings. AD has been characterized by a significant serotoninergic impairment. It is well known that impaired serotoninergic function is related to aggressive behavior. We, herein, review the past and recent evidence that seems to link the serotoninergic system with aggressive manifestations in AD patients. Managing the aggressive behavior of these patients might be of significant medical, social and economical importance. However, there is still a long way to go until we verify the exact pathophysiological mechanism(s) involved in the induction of aggression in AD patients. The current data underlines a complex relationship between the observed serotoninergic impairment in AD patients and the (a) cholinergic system, (b) the endocrine (hormonal) state, (c) the nutritional habits, (d) the genetic background and (e) the caregiving environment