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Higher iron levels in males may contribute to higher risk for younger\u2010onset PD and recent studies have linked the presence of the hemochromatosis gene with a younger age at onset of AD. We examined whether age at onset of PD and AD was associated with increased brain ferritin iron. Ferritin iron can be measured with specificity <jats:italic>in vivo<\/jats:italic> with MRI utilizing the field\u2010dependent relaxation rate increase (FDRI) method. FDRI was assessed in three basal ganglia regions (caudate, putamen, and globus pallidus) and frontal lobe white matter for younger\u2010 and older\u2010onset male PD and AD patients and healthy controls. Significant increases in basal ganglia FDRI levels were observed in the younger\u2010onset groups of both diseases compared to their respective control groups, but were absent in the older\u2010onset patients. The results support the suggestion that elevated ferritin iron and its associated toxicity is a risk factor for age at onset of neurodegenerative diseases such as AD and PD. Clinical phenomena such as gender\u2010associated risk of developing neurodegenerative diseases and the age at onset of such diseases may be associated with brain iron levels. <jats:italic>In vivo<\/jats:italic> MRI can measure and track brain ferritin iron levels and provides an opportunity to design therapeutic interventions that target high\u2010risk populations early in the course of illness, possibly even before symptoms appear.<\/jats:p>","DOI":"10.1196\/annals.1306.019","type":"journal-article","created":{"date-parts":[[2004,4,23]],"date-time":"2004-04-23T03:27:51Z","timestamp":1082690871000},"page":"224-236","source":"Crossref","is-referenced-by-count":155,"title":["Brain Ferritin Iron as a Risk Factor for Age at Onset in Neurodegenerative Diseases"],"prefix":"10.1111","volume":"1012","author":[{"given":"GEORGE","family":"BARTZOKIS","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"TODD A.","family":"TISHLER","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"IL\u2010SEON","family":"SHIN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PO H.","family":"LU","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JEFFREY L.","family":"CUMMINGS","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,1,25]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.58.5.461"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2003.03.001"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2003.08.001"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199606)17:2<83::AID-GLIA1>3.0.CO;2-7"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0165-3806(96)00020-X"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2001.0352"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2002.0610"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4439(00)00040-5"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/68.3.683"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/0006-3223(94)90047-7"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0730-725X(96)00234-2"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.57.1.47"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1958.tb12607.x"},{"key":"e_1_2_6_15_2","unstructured":"Klintworth G.K. 1973. 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