Functionalization of stable fluorescent nanodiamonds towards reliable detection of biomarkers for Alzheimer's disease
Author
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Morales Zavala, Francisco
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Casanova Morales, Nathalie
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Gonzalez, Raúl B.
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Chandia Cristi, América
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Estrada, Lisbell D.
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Alvizu, Ignacio
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Waselowski, Víctor
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Guzmán, Fanny
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Guerrero, Simón
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Oyarzún Olave, Marisol
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Rebolledo, Cristian
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Rodríguez, Enrique
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Armijo, Julien
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Bhuyan, Heman
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Favre, Mario
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Alvarez, Alejandra R.
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Kogan Bocian, Marcelo
Author
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Maze, Jerónimo R.
Admission date
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2018-12-26T22:58:19Z
Available date
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2018-12-26T22:58:19Z
Publication date
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2018
Cita de ítem
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J Nanobiotechnol (2018) 16:60
es_ES
Identifier
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10.1186/s12951-018-0385-7
Identifier
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https://repositorio.uchile.cl/handle/2250/159218
Abstract
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Background: Stable and non-toxic fluorescent markers are gaining attention in molecular diagnostics as powerful tools for enabling long and reliable biological studies. Such markers should not only have a long half-life under several assay conditions showing no photo bleaching or blinking but also, they must allow for their conjugation or functionalization as a crucial step for numerous applications such as cellular tracking, biomarker detection and drug delivery.
Results: We report the functionalization of stable fluorescent markers based on nanodiamonds (NDs) with a bifunctional peptide. This peptide is made of a cell penetrating peptide and a six amino acids long beta-sheet breaker peptide that is able to recognize amyloid beta (A beta) aggregates, a biomarker for the Alzheimer disease. Our results indicate that functionalized NDs (fNDs) are not cytotoxic and can be internalized by the cells. The fNDs allow ultrasensitive detection (at picomolar concentrations of NDs) of in vitro amyloid fibrils and amyloid aggregates in AD mice brains.
Conclusions: The fluorescence of functionalized NDs is more stable than that of fluorescent markers commonly used tostain A beta aggregates such as Thioflavin T. These results pave the way for performing ultrasensitive and reliable detection of A beta aggregates involved in the pathogenesis of the Alzheimer disease.
es_ES
Patrocinador
dc.description.sponsorship
Conicyt-PIA program
ACT1108
Beca Doctorado Nacional
21120617
Fondap
15130011
Fondecyt
1130425
3150587
1161065
Conicyt-Fondecyt program
1141185
1180673
AFOSR
FA9550-15-1-0113
FA9550-16-1-0384
CONICYT-PFB-12/2007