PURPOSE: To test the hypothesis that the T2 shortening observed on MR images of the brain in patients with Parkinson and Huntington diseases is due to tissue iron deposition. METHODS: Tissue iron and ferritin assays were performed on postmortem putamen and globus pallidus samples from subjects with Huntington and Parkinson disease. The assays were correlated with T2 measurements. Normal samples were included as controls. RESULTS: There were significant differences in T2 values, and iron and ferritin concentrations among the putamen samples. Compared with normal controls, subjects with Huntington disease had approximately a threefold increase in iron and a sixfold increase in ferritin concentrations; however, they also had the longest T2 values. Parkinson disease putamens had milder elevations of iron concentrations above that of controls (33%) and demonstrated slightly shorter T2 values. The globus pallidus samples demonstrated a similar trend in their T2s, iron, and ferritin levels, but there was a larger overlap in the T2 values. CONCLUSIONS: Our results indicate that tissue iron and ferritin concentrations are elevated in the brains of subjects with both Parkinson and Huntington disease but the elevated concentrations do not correlate with T2 shortening. Although iron and ferritin can shorten T2, we conclude that other factors must play a significant role in determining the T2 relaxation time and that iron or ferritin are not dominant in this regard.
PURPOSE: To test the hypothesis that the T2 shortening observed on MR images of the brain in patients with Parkinson and Huntington diseases is due to tissue iron deposition. METHODS: Tissue iron and ferritin assays were performed on postmortem putamen and globus pallidus samples from subjects with Huntington and Parkinson disease. The assays were correlated with T2 measurements. Normal samples were included as controls. RESULTS: There were significant differences in T2 values, and iron and ferritin concentrations among the putamen samples. Compared with normal controls, subjects with Huntington disease had approximately a threefold increase in iron and a sixfold increase in ferritin concentrations; however, they also had the longest T2 values. Parkinson disease putamens had milder elevations of iron concentrations above that of controls (33%) and demonstrated slightly shorter T2 values. The globus pallidus samples demonstrated a similar trend in their T2s, iron, and ferritin levels, but there was a larger overlap in the T2 values. CONCLUSIONS: Our results indicate that tissue iron and ferritin concentrations are elevated in the brains of subjects with both Parkinson and Huntington disease but the elevated concentrations do not correlate with T2 shortening. Although iron and ferritin can shorten T2, we conclude that other factors must play a significant role in determining the T2 relaxation time and that iron or ferritin are not dominant in this regard.
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