期刊
BIOCHEMISTRY
卷 53, 期 36, 页码 5804-5809出版社
AMER CHEMICAL SOC
DOI: 10.1021/bi501050g
关键词
-
资金
- NIH/NINDS [R01NS076619]
- NIH/NIA [P50 AG16573]
The propagation of Tau pathology in Alzheimers disease (AD) is thought to proceed through templated conversion of Tau protein into fibrils and cell-to-cell transfer of elongation-competent seeds. To investigate the efficiency of Tau conversion, we adapted the protein misfolding cyclic amplification assay used for the conversion of prions. Utilizing heparin as a cofactor and employing repetitive cycles of shearing and growth, synthetic Tau fibrils and Tau fibrils in AD brain extract are progressively amplified. Concurrently, self-nucleation is suppressed. The results highlight breakage-induced replication of Tau fibrils as a potential facilitator of disease spread.
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