Abstract
Abnormal accumulation of iron is observed in neurodegenerative disorders. In Parkinson’s disease, an excess of iron has been demonstrated in different structures of the basal ganglia and is suggested to be involved in the pathogenesis of the disease. Using the 6-hydroxydopamine (6-OHDA) rat model of Parkinson’s disease, the edematous effect of 6-OHDA and its relation with striatal iron accumulation was examined utilizing in vivo magnetic resonance imaging (MRI). The results revealed that in comparison with control animals, injection of 6-OHDA into the rat striatum provoked an edematous process, visible in T2-weighted images that was accompanied by an accumulation of iron clearly detectable in T2*-weighted images. Furthermore, Prussian blue staining to detect iron in sectioned brains confirmed the existence of accumulated iron in the areas of T2* hypointensities. The presence of ED1-positive microglia in the lesioned striatum overlapped with this accumulation of iron, indicating areas of toxicity and loss of dopamine nerve fibers. Correlation analyses demonstrated a direct relation between the hyperintensities caused by the edema and the hypointensities caused by the accumulation of iron.
Highlights
Brain iron accumulation is a normal consequence of ageing
Hypointensities in the striatum To study hypointensities caused by the injection of 6-OHDA, T2*-weighted images (WI) and T2-WI were performed in parallel to study the presence of hypointense areas (Fig. 4)
Albeit to a lesser extent than after 6-OHDA treatment, a hypointense signal was observed as early as at 2 days (Figs. 2 and 4A), which remained constant during the time points of the study (F(2,8) = 2.392 p = 0.153, one-way repeated measurements ANOVA)
Summary
Brain iron accumulation is a normal consequence of ageing. In neurodegenerative disorders this accumulation of iron seems to be augmented and has been proposed as a possible cause of neural death [1,2,3]. Ferrous iron can react with H2O2 via the Fenton reaction and lead to the formation of ferric iron (Fe+3) and a hydroxyl radical. Under non-pathological conditions cells have different mechanisms to protect themselves from the formation of these hazardous radicals. With age or in situations of abnormal iron accumulation, the availability of ferrous iron and formation of ROS is normally augmented [4,9]
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