Background: The basal ganglia contain the highest levels of iron in the bra
in, and postmortem studies indicate a disruption of iron metabolism in the
basal ganglia of patients with Alzheimer disease (AD). Iron can catalyze fr
ee radical reactions and may contribute to oxidative damage observed in AD
brains. Treatments aimed at reducing oxidative damage have offered novel wa
ys to delay the rate of progression and could possibly defer the onset of A
D. Brain iron levels were quantified in vivo using a new magnetic resonance
imaging method.
Methods: Thirty-one patients with AD and 68 control subjects participated i
n this study. A magnetic resonance imaging method was employed that quantif
ies the iron content of ferritin molecules (ferritin iron) with specificity
through the combined use of high and low field-strength magnetic resonance
imaging instruments. Three basal ganglia structures (caudate, putamen, and
globus pallidus) and one comparison region (frontal lobe white matter) wer
e evaluated.
Results: Basal ganglia ferritin iron levels were significantly increased in
the caudate (P = .007; effect size, 0.69) and putamen (P = .008; effect si
ze, 0.67) of AD subjects, with a trend toward an increase in the globus pal
lidus (P = .13). The increased basal ganglia ferritin iron levels were not
a generalized phenomenon; white matter ferritin iron levels were unchanged
in patients with AD (P = .50).
Conclusions: The data replicate and extend prior results and suggest that b
asal ganglia ferritin iron levels are increased in AD. Prospective studies
are needed to evaluate whether premorbid iron levels are increased in indiv
iduals who develop AD.