Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease

Alzheimer's disease (AD) is a neurodegenerative process characterized by the accumulation of extracellular deposits of amyloid β-peptide (Aβ), which induces neuronal death. Monomeric Aβ is not toxic but tends to aggregate into β-sheets that are neurotoxic. Therefore to prevent or delay AD o...

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Autores: Picón-Pagès, Pol, Bonet Martínez, Jaume, 1982-, García-García, Javier, 1982-, Garcia-Buendia, Joan, Gutierrez, Daniela, Valle, Javier, Gómez-Casuso, Carmen E.S., Sidelkivska, Valeriya, Alvarez, Alejandra, Perálvarez Marín, Alex, Suades, Albert, Fernàndez Busquets, Xavier, Andreu Martínez, David, Vicente García, Rubén, 1978-, Oliva Miguel, Baldomero, Muñoz López, Francisco José, 1964-
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2019
País:España
Institución:Universitat Pompeu Fabra
Repositorio:Repositorio Digital de la UPF
OAI Identifier:oai:repositori.upf.edu:10230/42277
Acceso en línea:http://hdl.handle.net/10230/42277
http://dx.doi.org/10.1016/j.csbj.2019.06.017
Access Level:acceso abierto
Palabra clave:Alzheimer&apos
s disease
Amyloid
Albumin
β-Sheet
Docking
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spelling Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's diseasePicón-Pagès, PolBonet Martínez, Jaume, 1982-García-García, Javier, 1982-Garcia-Buendia, JoanGutierrez, DanielaValle, JavierGómez-Casuso, Carmen E.S.Sidelkivska, ValeriyaAlvarez, AlejandraPerálvarez Marín, AlexSuades, AlbertFernàndez Busquets, XavierAndreu Martínez, DavidVicente García, Rubén, 1978-Oliva Miguel, BaldomeroMuñoz López, Francisco José, 1964-Alzheimer&aposs diseaseAmyloidAlbuminβ-SheetDockingAlzheimer's disease (AD) is a neurodegenerative process characterized by the accumulation of extracellular deposits of amyloid β-peptide (Aβ), which induces neuronal death. Monomeric Aβ is not toxic but tends to aggregate into β-sheets that are neurotoxic. Therefore to prevent or delay AD onset and progression one of the main therapeutic approaches would be to impair Aβ assembly into oligomers and fibrils and to promote disaggregation of the preformed aggregate. Albumin is the most abundant protein in the cerebrospinal fluid and it was reported to bind Aβ impeding its aggregation. In a previous work we identified a 35-residue sequence of clusterin, a well-known protein that binds Aβ, that is highly similar to the C-terminus (CTerm) of albumin. In this work, the docking experiments show that the average binding free energy of the CTerm-Aβ1-42 simulations was significantly lower than that of the clusterin-Aβ1-42 binding, highlighting the possibility that the CTerm retains albumin's binding properties. To validate this observation, we performed in vitro structural analysis of soluble and aggregated 1 μM Aβ1-42 incubated with 5 μM CTerm, equimolar to the albumin concentration in the CSF. Reversed-phase chromatography and electron microscopy analysis demonstrated a reduction of Aβ1-42 aggregates when the CTerm was present. Furthermore, we treated a human neuroblastoma cell line with soluble and aggregated Aβ1-42 incubated with CTerm obtaining a significant protection against Aβ-induced neurotoxicity. These in silico and in vitro data suggest that the albumin CTerm is able to impair Aβ aggregation and to promote disassemble of Aβ aggregates protecting neurons.This work was supported by the Spanish Ministry of Economy and Business through grant Plan Estatal SAF2017-83372-R & SAF2014-52228-R (FEDER funds/UE) to FJM and RV; BIO2017-85329-R to BO; AGL2014-52395-C2 and AGL2017- 84097-C2-2-R to D.A.; MDM-2014-0370 through the “María de Maeztu” Programme for Units of Excellence in R&D to “Departament de Ciències Experimentals i de la Salut”; the Chilean Government through Fondecyt 11611065 and AFB170005 to AA, and REDES 180084 to AA and FJM; ISGlobal and IBEC are members of the CERCA Programme, Generalitat de Catalunya.Elsevier201920192019info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/42277http://dx.doi.org/10.1016/j.csbj.2019.06.017reponame:Repositorio Digital de la UPFinstname:Universitat Pompeu FabraInglésComputational and Structural Biotechnology Journal. 2019;17:963-71info:eu-repo/grantAgreement/ES/2PE/SAF2017-83372-Rinfo:eu-repo/grantAgreement/ES/1PE/SAF2014-52228-Rinfo:eu-repo/grantAgreement/ES/1PE/BIO2017-85329-Rinfo:eu-repo/grantAgreement/ES/1PE/AGL2014-52395-C2info:eu-repo/grantAgreement/ES/2PE/AGL2017-84097-C2-2-R© 2019 Published by Elsevier B.V. on behalf of Research Network of Computational and Structural Biotechnology. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)http://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:repositori.upf.edu:10230/422772026-06-12T07:21:37Z
dc.title.none.fl_str_mv Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
title Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
spellingShingle Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
Picón-Pagès, Pol
Alzheimer&apos
s disease
Amyloid
Albumin
β-Sheet
Docking
title_short Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
title_full Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
title_fullStr Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
title_full_unstemmed Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
title_sort Human albumin impairs amyloid β-peptide fibrillation through its C-terminus: from docking modeling to protection against neurotoxicity in alzheimer's disease
dc.creator.none.fl_str_mv Picón-Pagès, Pol
Bonet Martínez, Jaume, 1982-
García-García, Javier, 1982-
Garcia-Buendia, Joan
Gutierrez, Daniela
Valle, Javier
Gómez-Casuso, Carmen E.S.
Sidelkivska, Valeriya
Alvarez, Alejandra
Perálvarez Marín, Alex
Suades, Albert
Fernàndez Busquets, Xavier
Andreu Martínez, David
Vicente García, Rubén, 1978-
Oliva Miguel, Baldomero
Muñoz López, Francisco José, 1964-
author Picón-Pagès, Pol
author_facet Picón-Pagès, Pol
Bonet Martínez, Jaume, 1982-
García-García, Javier, 1982-
Garcia-Buendia, Joan
Gutierrez, Daniela
Valle, Javier
Gómez-Casuso, Carmen E.S.
Sidelkivska, Valeriya
Alvarez, Alejandra
Perálvarez Marín, Alex
Suades, Albert
Fernàndez Busquets, Xavier
Andreu Martínez, David
Vicente García, Rubén, 1978-
Oliva Miguel, Baldomero
Muñoz López, Francisco José, 1964-
author_role author
author2 Bonet Martínez, Jaume, 1982-
García-García, Javier, 1982-
Garcia-Buendia, Joan
Gutierrez, Daniela
Valle, Javier
Gómez-Casuso, Carmen E.S.
Sidelkivska, Valeriya
Alvarez, Alejandra
Perálvarez Marín, Alex
Suades, Albert
Fernàndez Busquets, Xavier
Andreu Martínez, David
Vicente García, Rubén, 1978-
Oliva Miguel, Baldomero
Muñoz López, Francisco José, 1964-
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Alzheimer&apos
s disease
Amyloid
Albumin
β-Sheet
Docking
topic Alzheimer&apos
s disease
Amyloid
Albumin
β-Sheet
Docking
description Alzheimer's disease (AD) is a neurodegenerative process characterized by the accumulation of extracellular deposits of amyloid β-peptide (Aβ), which induces neuronal death. Monomeric Aβ is not toxic but tends to aggregate into β-sheets that are neurotoxic. Therefore to prevent or delay AD onset and progression one of the main therapeutic approaches would be to impair Aβ assembly into oligomers and fibrils and to promote disaggregation of the preformed aggregate. Albumin is the most abundant protein in the cerebrospinal fluid and it was reported to bind Aβ impeding its aggregation. In a previous work we identified a 35-residue sequence of clusterin, a well-known protein that binds Aβ, that is highly similar to the C-terminus (CTerm) of albumin. In this work, the docking experiments show that the average binding free energy of the CTerm-Aβ1-42 simulations was significantly lower than that of the clusterin-Aβ1-42 binding, highlighting the possibility that the CTerm retains albumin's binding properties. To validate this observation, we performed in vitro structural analysis of soluble and aggregated 1 μM Aβ1-42 incubated with 5 μM CTerm, equimolar to the albumin concentration in the CSF. Reversed-phase chromatography and electron microscopy analysis demonstrated a reduction of Aβ1-42 aggregates when the CTerm was present. Furthermore, we treated a human neuroblastoma cell line with soluble and aggregated Aβ1-42 incubated with CTerm obtaining a significant protection against Aβ-induced neurotoxicity. These in silico and in vitro data suggest that the albumin CTerm is able to impair Aβ aggregation and to promote disassemble of Aβ aggregates protecting neurons.
publishDate 2019
dc.date.none.fl_str_mv 2019
2019
2019
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10230/42277
http://dx.doi.org/10.1016/j.csbj.2019.06.017
url http://hdl.handle.net/10230/42277
http://dx.doi.org/10.1016/j.csbj.2019.06.017
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Computational and Structural Biotechnology Journal. 2019;17:963-71
info:eu-repo/grantAgreement/ES/2PE/SAF2017-83372-R
info:eu-repo/grantAgreement/ES/1PE/SAF2014-52228-R
info:eu-repo/grantAgreement/ES/1PE/BIO2017-85329-R
info:eu-repo/grantAgreement/ES/1PE/AGL2014-52395-C2
info:eu-repo/grantAgreement/ES/2PE/AGL2017-84097-C2-2-R
dc.rights.none.fl_str_mv http://creativecommons.org/licenses/by-nc-nd/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:Repositorio Digital de la UPF
instname:Universitat Pompeu Fabra
instname_str Universitat Pompeu Fabra
reponame_str Repositorio Digital de la UPF
collection Repositorio Digital de la UPF
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repository.mail.fl_str_mv
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