Present perception of the cause of Parkinson’s disease -- PD indicates a role for genetic as well as environmental influences. Similar to a multiplicity of possible causes of nigral cell deterioration in PD is the occurrence of oxidative stress. Analysis performed postmortem reveals high levels of iron, subdued complex I activity, and a decline in glutathione -- GSH levels. The decline in GSH levels might be a specific vital constituent of the chain of events ultimately resulting in cellular death as it happens in the presymptomatic phase of PD and might directly stimulate nigral cell denegeration or make the neurons vulnerable to the actions of toxins. Proof is available indicating that oxidative pressure might initiate in glial cells instead of neurons, and changes in glial functions might be an important trigger to the pathological process that takes place in PD. Oxidative degeneration happens inside the brain, as revealed by higher levels of lipid perooxidation and DNA damage in the substantia nigra. Higher protein oxidation is also imminent, but this happens in a lot of parts of the brain and increases the presence of a higher extensive pathologic processes happening in PD to which the substantia nigra is especially susceptible. The lack of ability of the substantia nigra to deal with the damaged or mutant for instance alphs-synnuclein proteins might lead to their aggravation and deposition and to the formation of Lewy bodies. (Jenner; Olanow, S74)
The symptoms of PD are described by gradual loss of neurons related with Lewy bodies in lot of subcortical nuclei resulting in multiple biochemical and pathophysiological modifications of medical importance. Loss of neurons resulting in striatal dopamine deficiency is associated with period as well as severity of the disease. (Jellinger, 23)
Depressive symptoms ranging from mild to moderate within the elderly are often considered by the clinicians or family members as a natural outcome of aging. Considerable proof nevertheless point out that such type of symptoms have vital personal and public health outcomes. Dysthymic disorder, minor depression, and associated conditions are believed to impact roughly 15% of the elders living in communities and almost 70% of the people residing in long-term care environment contributing to large scale functional damage and morbidity. (Ellison; Verma, 57)
The effect of the power of placebos has for a greater period been identified for enhancing a lot of medical conditions like PD. Less is understood, nevertheless regarding the system causing the placebo effect. Through the potential of endogenous dopamine to compete for craclopride binding as gauged by positron emission tomography, in vivo proof has been given for large scale release of endogenous dopamine in the striatum of PD patients in response to the placebo. Results show that the placebo effect in PD is strong and is mediated by means of activation of the degenerated nigrostriantal dopamine system. (Fuente-Fernández; Ruth; Sossi; Schulzer; Calne; Stoessl, 1165)
James Parkinson is credited with the description of PD more than 180 years back which bears his name and 30 years back Levodopa which continues to be the most fruitful therapy, was launched. The disease is a neurodegeneratibe disorder, the cause of which is still unknown affects more than a million people in
Diagnosis of PD is done by confirmation of the presence of Lewy bodies and cell loss in the substantia nigra and pathological changes of the striatonigral degeneration, major neurofibrillary tangles and nigral cell loss compatible with post-encepthalitic parkinsonian syndrome, and degeneration of the Lewy bodies and straitonigral denegeration. Pathological examination of the brain reveals Lewy bodies with cell loss in the nigra, which is a different pathological diagnosis, or normal basal ganglia. (Gibb; Lees, 30)
Present accepted clinical standards for the diagnosis of PD give sensitivity for identifying parkinsoniasm, but normally display poor specificity for detecting brainstem Lewy body disease. Biochemical markers which can be used to dependably diagnose both clinical and prechemical PD have since been searched but without success. It is presently understood that some PD kindred have a mutation of the alpha-syneclein gene, however this cannot be utilized as a way of discriminating standardized from non-standard PD, showing typical patterns of loss of depaminergic function. (Brooks, S8)
Brooks, D. J. (1998, Sep) “The early diagnosis of Parkinson’s disease.” Ann Neurology, vol.
44, no. 3 Suppl 1, pp: S8-S10.
Ellison, James M;
Fuente-Fernández, Raúl de la; Ruth, Thomas J; Sossi, Vesna; Schulzer, Michael; Calne,
Donald B; Stoessl, A. Jon. (2001, 10 Aug) “Expectation and Dopamine Release: Mechanism of the Placebo Effect in Parkinson’s disease.” Science, vol. 293, no. 5532, pp. 1164 – 1166.
Gibb, W. R; Lees, A. J. (1989, Jan-Feb) “The significance of the Lewy body in the diagnosis
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