Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation
The Arctic mutation within the amyloid-β (Aβ) peptide causes Alzheimer disease. In vitro,
Arctic-mutant Aβ forms (proto) fibrils more effectively than wild-type Aβ. We generated
transgenic mouse lines expressing Arctic-mutant human amyloid precursor proteins (hAPP).
Amyloid plaques formed faster and were more extensive in Arctic mice than in hAPP mice
expressing wild-type Aβ, even though Arctic mice had lower Aβ1-42/1-40 ratios. Thus, the
Arctic mutation is highly amyloidogenic in vivo.
Arctic-mutant Aβ forms (proto) fibrils more effectively than wild-type Aβ. We generated
transgenic mouse lines expressing Arctic-mutant human amyloid precursor proteins (hAPP).
Amyloid plaques formed faster and were more extensive in Arctic mice than in hAPP mice
expressing wild-type Aβ, even though Arctic mice had lower Aβ1-42/1-40 ratios. Thus, the
Arctic mutation is highly amyloidogenic in vivo.
Abstract
The Arctic mutation within the amyloid-β (Aβ) peptide causes Alzheimer disease. In vitro, Arctic-mutant Aβ forms (proto)fibrils more effectively than wild-type Aβ. We generated transgenic mouse lines expressing Arctic-mutant human amyloid precursor proteins (hAPP). Amyloid plaques formed faster and were more extensive in Arctic mice than in hAPP mice expressing wild-type Aβ, even though Arctic mice had lower Aβ1-42/1-40 ratios. Thus, the Arctic mutation is highly amyloidogenic in vivo.
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