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dc.contributor.author
Roher, Alex E.
dc.contributor.author
Esh, Chera L.
dc.contributor.author
Kokjohn, Tyler A.
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Castaño, Eduardo Miguel
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Van Vickle, Gregory D.
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Kalback, Walter M.
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Patton, R. Lyle
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Luehrs, Dean C.
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Daugs, Ian D.
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Kuo, Yu-Min
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Emmerling, Mark R.
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Soares, Holly
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Quinn, Joseph F.
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Kaye, Jeffrey
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Connor, Donald J.
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Silverberg, Nina B.
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Adler, Charles H.
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Seward, James D.
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Beach, Thomas G.
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Sabbagh, Marwan N.
dc.date.available
2017-07-21T19:37:03Z
dc.date.issued
2009-01
dc.identifier.citation
Roher, Alex E.; Esh, Chera L.; Kokjohn, Tyler A.; Castaño, Eduardo Miguel; Van Vickle, Gregory D.; et al.; Amyloid beta peptides in human plasma and tissues and their significance for Alzheimer's disease; Elsevier Science Inc; Alzheimers & Dementia; 5; 1; 1-2009; 18-29
dc.identifier.issn
1552-5260
dc.identifier.uri
http://hdl.handle.net/11336/21114
dc.description.abstract
BACKGROUND: We evaluated the amounts of amyloid beta (Abeta)) peptides in the central nervous system (CNS) and in reservoirs outside the CNS and their potential impact on Abeta plasma levels and Alzheimer's disease (AD) pathology. METHODS: Amyloid beta levels were measured in (1) the plasma of AD and nondemented (ND) controls in a longitudinal study, (2) the plasma of a cohort of AD patients receiving a cholinesterase inhibitor, and (3) the skeletal muscle, liver, aorta, platelets, leptomeningeal arteries, and in gray and white matter of AD and ND control subjects. RESULTS: Plasma Abeta levels fluctuated over time and among individuals, suggesting continuous contributions from brain and peripheral tissues and associations with reactive circulating proteins. Arteries with atherosclerosis had larger amounts of Abeta40 than disease-free vessels. Inactivated platelets contained more Abeta peptides than activated ones. Substantially more Abeta was present in liver samples from ND patients. Overall, AD brain and skeletal muscle contained increased levels of Abeta. CONCLUSIONS: Efforts to use plasma levels of Abeta peptides as AD biomarkers or disease-staging scales have failed. Peripheral tissues might contribute to both the circulating amyloid pool and AD pathology within the brain and its vasculature. The wide spread of plasma Abeta values is also due in part to the ability of Abeta to bind to a variety of plasma and membrane proteins. Sources outside the CNS must be accounted for because pharmacologic interventions to reduce cerebral amyloid are assessed by monitoring Abeta plasma levels. Furthermore, the long-range impact of Abeta immunotherapy on peripheral Abeta sources should also be considered.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Science Inc
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Plasma Abeta
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Alzheimer'S Disease
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Peripheral Abeta
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Atherosclerotic Vascular Disease
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Neurociencias
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Amyloid beta peptides in human plasma and tissues and their significance for Alzheimer's disease
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2017-07-18T14:50:54Z
dc.identifier.eissn
1552-5279
dc.journal.volume
5
dc.journal.number
1
dc.journal.pagination
18-29
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Orlando
dc.description.fil
Fil: Roher, Alex E.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Esh, Chera L.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Kokjohn, Tyler A.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Castaño, Eduardo Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
dc.description.fil
Fil: Van Vickle, Gregory D.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Kalback, Walter M.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Patton, R. Lyle. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Luehrs, Dean C.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Daugs, Ian D.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Kuo, Yu-Min. National Cheng Kung University; República de China
dc.description.fil
Fil: Emmerling, Mark R.. Pfizer Global Research and Development; Estados Unidos
dc.description.fil
Fil: Soares, Holly. Pfizer Global Research and Development; Estados Unidos
dc.description.fil
Fil: Quinn, Joseph F.. University Of Oregon; Estados Unidos
dc.description.fil
Fil: Kaye, Jeffrey. University Of Oregon; Estados Unidos
dc.description.fil
Fil: Connor, Donald J.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Silverberg, Nina B.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Adler, Charles H.. Mayo Clinic; Estados Unidos
dc.description.fil
Fil: Seward, James D.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Beach, Thomas G.. Sun Health Research Institute; Estados Unidos
dc.description.fil
Fil: Sabbagh, Marwan N.. Sun Health Research Institute; Estados Unidos
dc.journal.title
Alzheimers & Dementia
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S1552526008028963
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1016/j.jalz.2008.10.004
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