Abstract
β-Amyloid plaques and neurofibrillary tangles (NFTs) are the defining neuropathological hallmarks of Alzheimer's disease, but their pathophysiological relation is unclear. Injection of β-amyloid Aβ 42 fibrils into the brains of P301L mutant tau transgenic mice caused fivefold increases in the numbers of NFTs in cell bodies within the amygdala from where neurons project to the injection sites. Gallyas silver impregnation identified NFTs that contained tau phosphorylated at serine 212/threonine 214 and serine 422. NFTs were composed of twisted filaments and occurred in 6-month-old mice as early as 18 days after Aβ 42 injections. Our data support the hypothesis that Aβ 42 fibrils can accelerate NFT formation in vivo.
Keywords
FibrilGenetically modified mouseChemistrySerineIn vivoTransgeneThreonineNeurofibrillary tanglePathophysiologyPathologyTau proteinAmyloid (mycology)PhosphorylationCell biologyAlzheimer's diseaseMolecular biologyNeuroscienceSenile plaquesBiologyBiochemistryDiseaseMedicineGene
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Publication Info
- Year
- 2001
- Type
- article
- Volume
- 293
- Issue
- 5534
- Pages
- 1491-1495
- Citations
- 1499
- Access
- Closed
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Cite This
Jürgen Götz,
F. Chen,
Jo Van Dorpe
et al.
(2001).
Formation of Neurofibrillary Tangles in P301L Tau Transgenic Mice Induced by Aβ42 Fibrils.
Science
, 293
(5534)
, 1491-1495.
https://doi.org/10.1126/science.1062097
Identifiers
- DOI
- 10.1126/science.1062097