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4. Discussion The key result of this study indicates that accumulation of iron in different brain regions is not homogenous among patients with PD and that certain phase thresholds within these brain regions may be useful as to differentiate PD from controls. 4.1. MS-275 solubility dmso Role of the Iron in Neurodegeneration Although older studies have questioned the role of iron in neurodegenerative disorders such as PD the advent of improved imaging techniques in vivo and of autopsy tissue preparations argues in favor of a role for iron in neurodegeneration [2�C5]. Based on the role of iron in the Fenton reaction and generating detrimental free radicals, the role of iron in PD has already been discussed in several review articles [3, 7, 10]. Brain iron metabolism results in oxygen free-radical-induced oxidative stress. Two oxygen free-radical species have been identified to damage biological systems which are superoxide and hydroxyl free radical. Fe3+. Fe2+ plays an essential Quinapyramine role in the formation of hydroxyl free radical from H2O2 and superoxide. Consequences of free radical generation include a series of reactions ending in lipid peroxidation of cell membranes, followed by membrane fluidity, and ultimately in cell death [7, 10]. In PD, the melanized nigrostriatal dopamine neurons of SN, where iron is increased, degenerate selectively. Here we showed a trend for increasing iron accumulation in SN among PD patients compared to control subjects. 4.2. Brain Iron as Biomarker in PD A reliable biological marker to help clinicians confirm the diagnosis of PD and measure the progression of the disease is currently an unmet need. The diagnosis GDC-0449 in vivo of PD is based on neurologically observable clinical signs and symptoms, with a definitive diagnosis provided solely at autopsy. Ideally, a reliable biomarker should be able to identify individuals at risk before the onset of motor symptoms in PD and accurately diagnose individuals at the threshold of clinical PD. Such a biomarker should also be able to monitor PD progression throughout its course and objectively measure and evaluate responses to therapeutic interventions. To have the above features, the potential biomarker should be related to the mechanisms of the disease and its pathophysiology. Pathological studies from autopsies of patients with PD have provided evidence of increased brain iron accumulation in PD and raised the possibility of its use as a biomarker [2�C7]. Whether or not the role of iron is primary in the pathophysiology of the disease or its accumulation is secondary to the cell loss is still debatable. But it seems there is strong evidence to support its positive correlation with the disease state. For this reason, recent multiple neuroimaging techniques have been applied to measure brain iron levels in vivo [13�C25]. Similar to previous studies, we utilized SWI and used quantitative phase (radians) as a surrogate measure of brain iron levels.
