Materials Map

Discover the materials research landscape. Find experts, partners, networks.

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The Materials Map is an open tool for improving networking and interdisciplinary exchange within materials research. It enables cross-database search for cooperation and network partners and discovering of the research landscape.

The dashboard provides detailed information about the selected scientist, e.g. publications. The dashboard can be filtered and shows the relationship to co-authors in different diagrams. In addition, a link is provided to find contact information.

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The Materials Map is still under development. In its current state, it is only based on one single data source and, thus, incomplete and contains duplicates. We are working on incorporating new open data sources like ORCID to improve the quality and the timeliness of our data. We will update Materials Map as soon as possible and kindly ask for your patience.

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in Cooperation with on an Cooperation-Score of 37%

Topics

Publications (3/3 displayed)

  • 2021A population-based study of head injury, cognitive function and pathological markers9citations
  • 2019Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy78citations
  • 2018Short Acquisition Time PET/MR Pharmacokinetic Modelling Using CNNs5citations

Places of action

Chart of shared publication
Ourselin, Sebastien
3 / 10 shared
Cardoso, M. Jorge
2 / 4 shared
Scott, Catherine J.
1 / 1 shared
Jiao, Jieqing
1 / 1 shared
Kläser, Kerstin
1 / 1 shared
Markiewicz, Pawel J.
1 / 1 shared
Melbourne, Andrew
1 / 1 shared
Hutton, Brian F.
1 / 1 shared
Chart of publication period
2021
2019
2018

Co-Authors (by relevance)

  • Ourselin, Sebastien
  • Cardoso, M. Jorge
  • Scott, Catherine J.
  • Jiao, Jieqing
  • Kläser, Kerstin
  • Markiewicz, Pawel J.
  • Melbourne, Andrew
  • Hutton, Brian F.
OrganizationsLocationPeople

article

A population-based study of head injury, cognitive function and pathological markers

  • Nicholas, Jennifer M.
  • Keshavan, Ashvini
  • Sudre, Carole
  • Parker, Thomas D.
  • Murray-Smith, Heidi
  • Fox, Nick C.
  • Zetterberg, Henrik
  • Schott, Jonathan M.
  • Buchanan, Sarah M.
  • Malone, Ian B.
  • Cardoso, Jorge
  • Prosser, Lloyd
  • James, Sarah Naomi
  • Lu, Kirsty
  • Lane, Christopher A.
  • Coath, William
  • Ourselin, Sebastien
  • Richards, Marcus
  • Wong, Andrew
  • Barnes, Josephine
  • Crutch, Sebastian J.
  • Keuss, Sarah E.
  • Cash, David M.
  • Heslegrave, Amanda
  • Thomas, David L.
  • Modat, Marc
Abstract

<p>Objective: To assess associations between head injury (HI) with loss of consciousness (LOC), ageing and markers of later-life cerebral pathology; and to explore whether those effects may help explain subtle cognitive deficits in dementia-free individuals. Methods: Participants (n = 502, age = 69–71) from the 1946 British Birth Cohort underwent cognitive testing (subtests of Preclinical Alzheimer Cognitive Composite), <sup>18</sup>F-florbetapir Aβ-PET and MR imaging. Measures include Aβ-PET status, brain, hippocampal and white matter hyperintensity (WMH) volumes, normal appearing white matter (NAWM) microstructure, Alzheimer’s disease (AD)-related cortical thickness, and serum neurofilament light chain (NFL). LOC HI metrics include HI occurring: (i) &gt;15 years prior to the scan (ii) anytime up to age 71. Results: Compared to those with no evidence of an LOC HI, only those reporting an LOC HI&gt;15 years prior (16%, n = 80) performed worse on cognitive tests at age 69–71, taking into account premorbid cognition, particularly on the digit-symbol substitution test (DSST). Smaller brain volume (BV) and adverse NAWM microstructural integrity explained 30% and 16% of the relationship between HI and DSST, respectively. We found no evidence that LOC HI was associated with Aβ load, hippocampal volume, WMH volume, AD-related cortical thickness or NFL (all p &gt; 0.01). Interpretation: Having a LOC HI aged 50’s and younger was linked with lower later-life cognitive function at age ~70 than expected. This may reflect a damaging but small impact of HI; explained in part by smaller BV and different microstructure pathways but not via pathology related to AD (amyloid, hippocampal volume, AD cortical thickness) or ongoing neurodegeneration (serum NFL).</p>

Topics
  • microstructure
  • composite
  • aging