Ironing out tau's role in parkinsonism

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 e...

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Bibliographic Details
Published in	Nature medicine Vol. 18; no. 2; pp. 197 - 198
Main Authors	Stankowski, Jeannette N, Dawson, Valina L, Dawson, Ted M
Format	Journal Article
Language	English
Published	New York Nature Publishing Group US 01.02.2012 Nature Publishing Group
Subjects	631/378/1689/364 631/45/612/1228 692/420 692/699/375/365/1718 Amyloid beta-Protein Precursor - metabolism Animals Biomedical and Life Sciences Biomedicine Cancer Research Care and treatment Dementia - etiology Development and progression Humans Infectious Diseases Iron Iron - metabolism Male Metabolic Diseases Molecular Medicine Neurons Neurosciences news-and-views Parkinson's disease Parkinsonian Disorders - etiology Parkinsonism Physiological aspects Proteins Rodents tau Proteins - deficiency United States
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ISSN	1078-8956 1546-170X 1546-170X
DOI	10.1038/nm.2668

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Summary:	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 ).
Bibliography:	SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-News-1 ObjectType-Commentary-2 content type line 23
ISSN:	1078-8956 1546-170X 1546-170X
DOI:	10.1038/nm.2668