Alzheimer's disease (AD) is a neurodegenerative disorder characterized by aggregation of β-amyloid peptide (Aβ) into senile plaques and cerebrovascular amyloid. It remains unclear if amyloid is initiated by the accumulation of Aβ in the extracellular space or by intraneuronal Aβ generation. In February 24 advanced online Nature Neuroscience, Melanie Meyer-Luehmann and colleagues at the University of Basel, Switzerland, show that diffusion of soluble Aβ in the extracellular space is involved in the spread of Aβ pathology, and that extracellular amyloid formation can lead to neurodegeneration (Nature Neuroscience, DOI:10.1038/nn1022, February 24, 2003).

Meyer-Luehmann et al. used APP23 transgenic (Tg) mice that develop cerebral amyloid with aging. After transplanting wild-type (WT) and APP23 embryonic brain tissue into the brains of both Tg and WT mice, they observed that APP23 grafts into wild-type hosts did not develop amyloid deposits for up to 20 months following grafting. In contrast, both...

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