@Article{Lehallier2019,
  author       = {Benoit Lehallier and David Gate and Nicholas Schaum and Tibor Nanasi and Song Eun Lee and Hanadie Yousef and Patricia Moran Losada and Daniela Berdnik and Andreas Keller and Joe Verghese and Sanish Sathyan and Claudio Franceschi and Sofiya Milman and Nir Barzilai and Tony Wyss-Coray},
  title        = {Undulating changes in human plasma proteome profiles across the lifespan},
  journal      = {Nature Medicine},
  year         = {2019},
  volume       = {25},
  issue        = {12},
  pages        = {1843-1850},
  abstract     = {Aging is a predominant risk factor for several chronic diseases that limit healthspan1. Mechanisms of aging are thus increasingly recognized as potential therapeutic targets. Blood from young mice reverses aspects of aging and disease across multiple tissues2-10, which supports a hypothesis that age-related molecular changes in blood could provide new insights into age-related disease biology. We measured 2,925 plasma proteins from 4,263 young adults to nonagenarians (18-95 years old) and developed a new bioinformatics approach that uncovered marked non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh and eighth decades of life reflected distinct biological pathways and revealed differential associations with the genome and proteome of age-related diseases and phenotypic traits. This new approach to the study of aging led to the identification of unexpected signatures and pathways that might offer potential targets for age-related diseases.},
  doi          = {10.1038/s41591-019-0673-2},
  pii          = {10.1038/s41591-019-0673-2},
}

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E.","Yousef, H.","Losada, P. M.","Berdnik, D.","Keller, A.","Verghese, J.","Sathyan, S.","Franceschi, C.","Milman, S.","Barzilai, N.","Wyss-Coray, T."],"bibdata":{"bibtype":"article","type":"article","author":[{"firstnames":["Benoit"],"propositions":[],"lastnames":["Lehallier"],"suffixes":[]},{"firstnames":["David"],"propositions":[],"lastnames":["Gate"],"suffixes":[]},{"firstnames":["Nicholas"],"propositions":[],"lastnames":["Schaum"],"suffixes":[]},{"firstnames":["Tibor"],"propositions":[],"lastnames":["Nanasi"],"suffixes":[]},{"firstnames":["Song","Eun"],"propositions":[],"lastnames":["Lee"],"suffixes":[]},{"firstnames":["Hanadie"],"propositions":[],"lastnames":["Yousef"],"suffixes":[]},{"firstnames":["Patricia","Moran"],"propositions":[],"lastnames":["Losada"],"suffixes":[]},{"firstnames":["Daniela"],"propositions":[],"lastnames":["Berdnik"],"suffixes":[]},{"firstnames":["Andreas"],"propositions":[],"lastnames":["Keller"],"suffixes":[]},{"firstnames":["Joe"],"propositions":[],"lastnames":["Verghese"],"suffixes":[]},{"firstnames":["Sanish"],"propositions":[],"lastnames":["Sathyan"],"suffixes":[]},{"firstnames":["Claudio"],"propositions":[],"lastnames":["Franceschi"],"suffixes":[]},{"firstnames":["Sofiya"],"propositions":[],"lastnames":["Milman"],"suffixes":[]},{"firstnames":["Nir"],"propositions":[],"lastnames":["Barzilai"],"suffixes":[]},{"firstnames":["Tony"],"propositions":[],"lastnames":["Wyss-Coray"],"suffixes":[]}],"title":"Undulating changes in human plasma proteome profiles across the lifespan","journal":"Nature Medicine","year":"2019","volume":"25","issue":"12","pages":"1843-1850","abstract":"Aging is a predominant risk factor for several chronic diseases that limit healthspan1. Mechanisms of aging are thus increasingly recognized as potential therapeutic targets. Blood from young mice reverses aspects of aging and disease across multiple tissues2-10, which supports a hypothesis that age-related molecular changes in blood could provide new insights into age-related disease biology. We measured 2,925 plasma proteins from 4,263 young adults to nonagenarians (18-95 years old) and developed a new bioinformatics approach that uncovered marked non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh and eighth decades of life reflected distinct biological pathways and revealed differential associations with the genome and proteome of age-related diseases and phenotypic traits. This new approach to the study of aging led to the identification of unexpected signatures and pathways that might offer potential targets for age-related diseases.","doi":"10.1038/s41591-019-0673-2","pii":"10.1038/s41591-019-0673-2","bibtex":"@Article{Lehallier2019,\n author = {Benoit Lehallier and David Gate and Nicholas Schaum and Tibor Nanasi and Song Eun Lee and Hanadie Yousef and Patricia Moran Losada and Daniela Berdnik and Andreas Keller and Joe Verghese and Sanish Sathyan and Claudio Franceschi and Sofiya Milman and Nir Barzilai and Tony Wyss-Coray},\n title = {Undulating changes in human plasma proteome profiles across the lifespan},\n journal = {Nature Medicine},\n year = {2019},\n volume = {25},\n issue = {12},\n pages = {1843-1850},\n abstract = {Aging is a predominant risk factor for several chronic diseases that limit healthspan1. Mechanisms of aging are thus increasingly recognized as potential therapeutic targets. Blood from young mice reverses aspects of aging and disease across multiple tissues2-10, which supports a hypothesis that age-related molecular changes in blood could provide new insights into age-related disease biology. We measured 2,925 plasma proteins from 4,263 young adults to nonagenarians (18-95 years old) and developed a new bioinformatics approach that uncovered marked non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh and eighth decades of life reflected distinct biological pathways and revealed differential associations with the genome and proteome of age-related diseases and phenotypic traits. This new approach to the study of aging led to the identification of unexpected signatures and pathways that might offer potential targets for age-related diseases.},\n doi = {10.1038/s41591-019-0673-2},\n pii = {10.1038/s41591-019-0673-2},\n}\n\n","author_short":["Lehallier, B.","Gate, D.","Schaum, N.","Nanasi, T.","Lee, S. E.","Yousef, H.","Losada, P. 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