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Persistence of Aβ seeds in APP null mouse brain
Lan Ye1,2,3, Sarah K Fritschi1,2, Juliane Schelle1,2,3
1Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Nature Neuroscience
|September 10, 2015
Summary
Amyloid-beta (Aβ) seeds persist in the brain for months, even in the absence of amyloid precursor protein (APP). These seeds regain their ability to cause cerebral beta-amyloidosis when APP is present.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Cerebral beta-amyloidosis is a hallmark of Alzheimer's disease, characterized by the accumulation of amyloid-beta (Aβ) plaques in the brain.
- Amyloid precursor protein (APP) is central to Aβ production, and its presence is generally considered necessary for Aβ seeding and propagation.
Purpose of the Study:
- To investigate the persistence and infectivity of Aβ seeds in the absence of host APP.
- To determine if Aβ seeds can retain pathogenic potential over time in a non-permissive environment.
Main Methods:
- Inoculation of Aβ seeds into APP transgenic mice and App(-/-) (APP null) mice.
- Extraction of brain material from inoculated APP null mice after a 6-month period.
- Secondary transmission of these brain extracts to naive APP transgenic mice to assess Aβ seeding activity.
Main Results:
- Aβ seeds failed to induce cerebral beta-amyloidosis in APP null mice upon initial inoculation.
- Brain extracts from APP null mice, inoculated 6 months prior with Aβ seeds, successfully induced beta-amyloidosis in APP transgenic hosts.
- This demonstrates that Aβ seeds can persist in the brain for extended periods without host APP.
Conclusions:
- Aβ seeds possess inherent stability and can persist in the brain for at least 6 months, independent of host APP.
- The presence of host APP is crucial for the reactivation and propagation of dormant Aβ seeds, leading to pathogenic cerebral beta-amyloidosis.
