<<snip>>
We hypothesize that locally increased concentrations of iron induce
accumulation of exogenous and endogenous Abeta in SMCs, triggering
beta-amyloid angiopathy.
<<snip>>

Neurobiol Aging. 2005 Jun 30; [Epub ahead of print] Related Articles,
Links

Induction of vascular amyloidosis-beta by oxidative stress depends on
APOE genotype.

Mazur-Kolecka B,{*filter*}son D, Frackowiak J.

New York State Institute for Basic Research in Developmental
Disabilities, Department of Developmental Neurobiology, 1050 Forest
Hill Road, Staten Island, NY 10314, USA.

The reduced antioxidant defense in apolipoprotein E
varepsilon4/varepsilon4 carriers may contribute to beta-amyloidosis.
Previously we found that Fe(2+)-induced oxidative stress caused greater
protein oxidation in varepsilon4/varepsilon4 than in
varepsilon3/varepsilon3 human brain vascular smooth muscle cells.
Moreover, Fe(2+) induced lysosomal accumulation of endogenous Abeta and
APOE in cultured cells, and Abeta deposition in vascular tunica media
in organotypic cultures of brain vessels. Here we demonstrated that
Fe(2+) enhanced an uptake of exogenous Abeta 1-40 and its deposition
together with APOE in lysosomes in myocytes. Abeta deposits were
associated with lipid-peroxidation and protein ubiquitination, and were
more abundant and stable in varepsilon4/varepsilon4 than in
varepsilon3/varepsilon3 cells. In organotypic cultures of brain vessels
Fe(2+) induced deposition of non-fibrillar and fibrillar Abeta 1-40 in
vascular tunica media. We hypothesize that locally increased
concentrations of iron induce accumulation of exogenous and endogenous
Abeta in SMCs, triggering beta-amyloid angiopathy. The greater
susceptibility of varepsilon4 carriers to Fe(2+) ions may result in an
increased risk of beta-amyloidosis.

PMID: 15993987 [PubMed - as supplied by publisher]

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