IN TWO MOUSE MODELS OF ALZHEIMER’S
DISEASE COPPER DIDN’T INCREASE TOXICITY
In two mouse models of
Alzheimer’s disease, in contrast with previous in vitro results,
researchers found that copper could contrast beta-amyloid toxicity.
In the first paper Bayer
et al. (Dietary Cu stabilizes brain superoxide dismutase1 activity and reduces
amyloid Aβ production in APP23 transgenic mice, Proc. Natl Acad. Sci.
USA 100, 14187-14192, 2003) demonstrated that in APP23
transgenic mice dietary copper restores the activity of superoxide dismutase 1
(SOD1), which was reduced by the overexpression of the amyloid precursor
protein (APP), and also lower levels of β-amyloid in the brain.
In the second mouse model
Phinney et al. (In vivo reduction of amyloid-β by a
mutant copper transporter, Proc. Natl Acad. Sci. USA 100, 14193-14198,
2003)
found that in the homozygous variant for a mutant copper transporter that
causes accumulation of copper in the cytoplasm, levels of β-amyloid and
deposition of amyloid plaques are reduced.