A new study shows that mice lacking tau develop parkinsonism because of intracellular iron accumulation that results in degeneration of dopamine neurons. Tau deficiency seems to impair ferroportin iron export by retention of the amyloid precursor protein, a neuronal ferroxidase partner, inside the endoplasmic reticulum (pages 291–295).
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Stankowski, J., Dawson, V. & Dawson, T. Ironing out tau's role in parkinsonism. Nat Med 18, 197–198 (2012). https://doi.org/10.1038/nm.2668
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DOI: https://doi.org/10.1038/nm.2668