期刊
ACTA NEUROPATHOLOGICA
卷 123, 期 1, 页码 31-37出版社
SPRINGER
DOI: 10.1007/s00401-011-0912-1
关键词
Alzheimer; Amyloid; Prion; Seeding; Senile plaques; Transgenic mouse
资金
- Competence Network on Degenerative Dementias [BMBF-01GI0705]
- BMBF
- NIH [RR-00165, P50AG025688]
- Alzheimer's Association [NIRG-10-173099]
- CART Foundation
- Alexander von Humboldt Foundation (Bonn, Germany)
- NATIONAL CENTER FOR RESEARCH RESOURCES [P51RR000165] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P50AG025688] Funding Source: NIH RePORTER
The deposition of the beta-amyloid (A beta) peptide in senile plaques and cerebral A beta-amyloid angiopathy can be seeded in beta-amyloid precursor protein (APP)-transgenic mice by the intracerebral infusion of brain extracts containing aggregated A beta. Previous studies of seeded beta-amyloid induction have used relatively short incubation periods to dissociate seeded beta-amyloid induction from endogenous beta-amyloid deposition of the host, thus precluding the analysis of the impact of age and extended incubation periods on the instigation and spread of A beta lesions in brain. In the present study using R1.40 APP-transgenic mice (which do not develop endogenous A beta deposition up to 15 months of age) we show that: (1) seeding at 9 months of age does not induce more A beta deposition than seeding at 3 months of age, provided that the incubation period (6 months) is the same; and (2) very long-term (12 months) incubation after a focal application of the seed results in the emergence of A beta deposits throughout the forebrain. These findings indicate that the presence of A beta seeds, and not the age of the host per se, is critical to the initiation of A beta aggregation in the brain, and that A beta deposition, actuated in one brain area, eventually spreads throughout the brain.
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