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toxic brain ferrous ions
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Study of the localization of iron, ferritin, and hemosiderin in
Alzheimer's disease hippocampus by analytical microscopy at the
subcellular level.
Quintana C, Bellefqih S, Laval JY, Guerquin-Kern JL, Wu TD, Avila J,
Ferrer I, Arranz R, Patiño C
J Struct Biol. 2006 Jan ; 153(1): 42-54

Previous studies of the structure of core nanocrystals of ferritin (Ft)
in the brains of patients with Alzheimer's disease (AD) have shown
differences in the mineral compound in comparison with physiological
Ft. Both Ft cores have a polyphasic composition but whereas the major
phase in physiological Ft is hexagonal ferric iron oxide
(ferrihydrite), the major phases in brain AD Ft are two cubic mixed
ferric-ferrous iron oxides (magnetite and wüstite). One of these
(wüstite) is similar to what is detected in hemosiderin (Hm) cores in
primary hemochromatosis (Quintana, C., Cowley, J.M, Marhic, C., 2004.
Electron nanodiffraction and high resolution electron microscopy
studies of the structure and composition of physiological and
pathological ferritin. J. Struct. Biol. 147, 166-178). We have studied,
herein, the distribution of iron, Ft, and Hm in sections of AD
hippocampus using analytical microscopy. Iron present in Ft cores was
directly mapped in a nanoSIMS microscope and the iron distribution has
been correlated with the constituent elements N, P, and S. Ft and Hm
cores were visualized at an ultrastructural level in an analytical
transmission electron microscope. In senile plaques, Ft was observed in
the coronal region associated with a non-beta-amyloid component and in
the periphery of plaques, together with Hm, in sulfur-rich dense bodies
of dystrophic neurites. Hm was also found in lysosomes and siderosomes
of glial cells. Ft was observed in the cytoplasm and nucleus of
oligodendrocytes. Ft was particularly abundant in myelinated axons in
association with oligodendrocyte processes. These findings provide new
arguments to support the hypothesis of a dysfunction of Ft (with
eventual degradation to Hm) in AD resulting in an increase of toxic
brain ferrous ions that may contribute to the production of free
radicals that induce both cellular oxidative stress and aged-related
myelin breakdown associated with cognitive decline and AD (Bartzokis,
G., 2004. Age-related myelin breakdown: a developmental model of
cognitive decline and Alzheimer's disease. Neurobiol. Aging 25, 5-18).

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