Abstract
This paper delves deeply into the subject of Parkinson's disease, a progressive neurodegenerative disorder, explaining that advances have been made in identifying the genes and environmental factors that may predispose an individual to developing Parkinson's, as well as in developing pharmaceuticals to alleviate some of the physical symptoms of the condition. The paper points out that, regardless, much debate remains over the molecular mechanisms that malfunction and lead to dopaminergic neuron death, the hallmark pathology of Parkinson's. The paper contains various figures of illustration, and concludes that impairment of calcium signaling might lead to protein aggregation as well, and combined with oxidative damage from other sources, might be a key to the selectivity of dopaminergic cell death in Parkinson's disease.

Outline:
Introduction to Parkinson's Disease
Mitochondrial Function, Malfunction, and Parkinson's Disease
Mitochondria and Parkinson's Disease Genetics: PINK1 and Parkin
Why Dopaminergic Cells?
Proposal for Further Study

From the Paper
"Although mitochondrial damage has been strongly implicated as a pathway common to idiopathic and familial Parkinson's disease, the question remains as to why dopaminergic neurons are exclusively destroyed. This is especially puzzling considering that mitochondria are universally present in every cell, and both PINK1 and parkin are expressed throughout the brain. One proposed explanation as to why dopaminergic neurons are selectively killed focuses on dopamine metabolism. Within dopaminergic neurons and astrocytes, cytosolic dopamine is hydrolyzed by MAO (monoamine oxidase) into DOPAC (3,4-dihydroxyphenylacetic acid). This process results in the production of free radicals, toxic quinonic compounds and melanin [6]. In addition, dopaminergic neurons are very energy-demanding and may produce more reactive oxygen species by-products of electron transport than other cell types. Placing a population of neurons that is already experiencing stress from natural metabolic processes under even more oxidative stress via mitochondrial damage may be the key as to why dopaminergic neurons are selectively destroyed in Parkinson's disease."

Tags:genetic, pink1, dopaminergic, parkin

Abstract
This paper provides a review of three articles related to the use of fluvoxamine or controlled-release fluvoxamine and the use of a placebo for generalized social anxiety disorder (GASD) and for obsessive-compulsive disorder (OCD). A third article is a literature review that details the efficacy of placebos for dopaminergic disorders and emphasizes the strong biochemical basis for the use of placebos. The first two articles are compared in a formal comparison and then both are contrasted against the third.

From the Paper
"In order to gain the most knowledge one can from reading published research one must assess the work beyond the normal article critique in order to glean the greatest benefits and applicable knowledge. Primarily when working in the field, often one has to compare the relative merits of the published work in relation to other published work on the same topic. This paper presents a classic comparison between two articles and then contrasts both with a third. Each deal with the use of a placebo either studying the efficacy of fluvoxamine compared to a placebo or reporting on the physiological/neurological basis for the efficacy seen in studies where placebos are used."

Tags:social, anxiety, dopaminergic, obsessive-compulsive

Abstract
This paper provides a review of three articles related to the use of fluvoxamine or controlled-release fluvoxamine and the use of a placebo for generalized social anxiety disorder (GASD) and for obsessive-compulsive disorder (OCD). A third article is a literature review that details the efficacy of placebos for dopaminergic disorders and emphasizes the strong biochemical basis for the use of placebos. The first two articles are compared in a formal comparison and then both are contrasted against the third.

Tags:placebo, comparison

Abstract
This paper describes and defines the prevalence and severity of Parkinson's disease and discusses the history, development and focus of the Magnet Hospital Recognition Program of Excellence. The paper also examines the findings of a 'gaps' analysis using the standards from the Magnet Hospital Program of Excellence as compared to the standards of the Department of Veterans Affairs Hospitals regarding the care of patients with Parkinson's.

From the Paper
"In the past decades, Parkinson's disease has emerged as a significant concern in healthcare, affecting policy makers, government and healthcare administrators alike. It is a serious health problem in the United States, affecting about 1.5 million Americans who are diagnosed with the disease (Department of Veterans Affairs, 2001). Research indicates approximately 50,000 new cases are diagnosed each year, and while treatments exist, there is no cure for this debilitating disease (Department of Veterans Affairs, 2001). Parkinson's disease is a progressive degenerative disorder of the central nervous system, with physical symptoms of tremor, rigidity and bradykinesia (Mitchell et. al., 1996)."

Tags:tremor, bradykinesia, dopaminergic, neurons

Abstract
The paper looks at the anatomical origins of the neurotransmitters dopamine, serotonin and noradrenaline and their associated pathways, as well as the basic anatomy of the limbic system and its associated structures. The essay then goes on to explain that our brain is structured such that certain environmental stimuli can cause us to have positive or negative reinforcing experiences based on how our neurochemicals react in response to the situation. The reward pathways in our brain help to determine much of our everyday behavior, whether it may be the urge to eat, the drive to have sex or the addiction associated with mind-altering drugs. As such, we must receive appropriate stimulation and positive reward in order to function as individuals and be happy, or we are at risk of a reward deficiency resulting in negative emotions such as sadness or depression. There is also a discussion of how addictive behavior can be due to positive reward systems which have a very strong influence on the way we act.

From the Paper
"Happiness and sadness are two primary human emotions, and whilst more often than not caused as a result of external stimuli, they are largely determined by neurobiological processes that occur in the brain namely that of biogenic amine reward pathways. We have to stimulate these pathways adequately every day if we are to function well mentally, physically and emotionally. The experience of emotion is integral to who we are as humans. Darwin (1872 in Ekman, 1973) defined emotion as essential to the welfare of group-living species. Without emotion, we would be unable to be attracted to one another, reproduce, or interact socially, amongst other things. Emotions also have distinct motivational properties (Izard, 1971) and understandably, the reward system and its close association with pleasure plays a large part in determining our actions. "Pleasure is unquestionably a key factor in controlling the motivated behaviors of humans." (Kandel et. al., 2000 p.1007) Emotions are known to lead to specific behavioral patterns that determine the way in which we live our lives and influence the experience of consequent emotions, for example, happiness or sadness."

Tags:addiction, antidepressants, dopaminergic, hippocampus