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  • Ashton, Nicholas J.Gothenburg University,Göteborgs universitet,University of Gothenburg,South London and Maudsley NHS Foundation Trust,King's College London,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry (author)

Increased plasma neurofilament light chain concentration correlates with severity of post-mortem neurofibrillary tangle pathology and neurodegeneration

  • Article/chapterEnglish2019

Publisher, publication year, extent ...

  • 2019-01-09
  • Springer Science and Business Media LLC,2019

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:3c3d6060-d275-47e2-b028-8ed12429066d
  • https://lup.lub.lu.se/record/3c3d6060-d275-47e2-b028-8ed12429066dURI
  • https://doi.org/10.1186/s40478-018-0649-3DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:140010000URI
  • https://gup.ub.gu.se/publication/276809URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Alzheimer's disease (AD) is pathologically characterized by the accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles and widespread neuronal loss in the brain. In recent years, blood biomarkers have emerged as a realistic prospect to highlight accumulating pathology for secondary prevention trials. Neurofilament light chain (NfL), a marker of axonal degeneration, is robustly elevated in the blood of many neurological and neurodegenerative conditions, including AD. A strong relationship with cerebrospinal fluid (CSF) NfL suggests that these biomarker modalities reflect the same pathological process. Yet, the connection between blood NfL and brain tissue pathology has not been directly compared. In this study, longitudinal plasma NfL from cognitively healthy controls (n = 12) and AD participants (n = 57) were quantified by the Simoa platform. On reaching post-mortem, neuropathological assessment was performed on all participants, with additional frozen and paraffin-embedded tissue acquired from 26 participants for further biochemical (Aβ1-42, Aβ1-40, tau) and histological (NfL) evaluation. Plasma NfL concentrations were significantly increased in AD and correlated with cognitive decline, independent of age. Retrospective stratification based on Braak staging revealed that baseline plasma NfL concentrations were associated with higher neurofibrillary tangle pathology at post-mortem. Longitudinal increases in plasma NfL were observed in all Braak groupings; a significant negative association, however, was found between plasma NfL at time point 1 and both its rate of change and annual percentage increase. Immunohistochemical evaluation of NfL in the medial temporal gyrus (MTG) demonstrated an inverse relationship between Braak stages and NfL staining. Importantly, a significant negative correlation was found between the plasma NfL measurement closest to death and the level of NfL staining in the MTG at post-mortem. For the first time, we demonstrate that plasma NfL associates with the severity of neurofibrillary tangle pathology and neurodegeneration in the post-mortem brain.

Subject headings and genre

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  • Leuzy, AntoineGothenburg University,Göteborgs universitet,University of Gothenburg,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xleuan (author)
  • Lim, Yau MunSouth London and Maudsley NHS Foundation Trust,King's College London (author)
  • Troakes, ClaireKing's College London,South London and Maudsley NHS Foundation Trust (author)
  • Hortobágyi, TiborUniversity of Debrecen,King's College London (author)
  • Höglund, Kina,1976Gothenburg University,Göteborgs universitet,University of Gothenburg,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xgukri (author)
  • Aarsland, DagKarolinska Institutet (author)
  • Lovestone, SimonWarneford Hospital,University of Oxford (author)
  • Schöll, MichaelGothenburg University,Göteborgs universitet,University of Gothenburg,Lund University,Lunds universitet,Klinisk minnesforskning,Forskargrupper vid Lunds universitet,Clinical Memory Research,Lund University Research Groups,University College London,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xschom (author)
  • Blennow, KajGothenburg University,Göteborgs universitet,University of Gothenburg,Sahlgrenska University Hospital,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xbleka (author)
  • Zetterberg, HenrikGothenburg University,Göteborgs universitet,University of Gothenburg,Sahlgrenska University Hospital,University College London,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xzethe (author)
  • Hye, AbdulKing's College London,South London and Maudsley NHS Foundation Trust (author)
  • University of GothenburgSouth London and Maudsley NHS Foundation Trust (creator_code:org_t)

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  • In:Acta Neuropathologica Communications: Springer Science and Business Media LLC7:12051-5960

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