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Sökning: WFRF:(Beach Thomas G)

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21.
  • Nilsson-Lindström, Margareta, et al. (författare)
  • Utbildningsfältets professionalisering
  • 2019
  • Ingår i: Det professionella landskapets framväxt. - 9789144122052 ; , s. 147-208
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
    • Kapitlet behandlar det svenska utbildningsfältets professionalisering från kyrkligt förankrade kunskapsideal till skolundervisningens förvetenskapligande. Utbildningsfältet är avgränsat i förhållande till den högre utbildningens fält och omfattar utbildningar på grundskole- och gymnasienivå. I Bourdieus mening är fältet ett system av specialiserade institutioner och agenter (kyrka, stat, akademi, lärarförbund etc.) som utifrån olika intressen och positioner konkurrerar om erkännande och makt att definiera skolutbildningens syften och innehåll. Fältets framväxt och förändring följer olika faser från formering, konsolidering och konstituering till professionalisering. Den historiska exposén visar hur kampen mellan etablerade och konkurrerande kunskapsideal och utbildningspolitiska intressen utmynnade i att existerande strukturer utmanades och förändrades. Nya skolformer och lärarkategorier växte fram och etablerades. Den senaste fasen, fältets professionalisering, inleddes med välfärdsstatens strävan att modernisera och demokratisera skolundervisningen genom inrättandet av ett enhetligt skolsystem, en ny lärarprofession samt förvetenskapligande av lärarutbildningen och läraryrkets kunskapsbas.
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22.
  • Thal, Dietmar Rudolf, et al. (författare)
  • [(18)F]flutemetamol amyloid positron emission tomography in preclinical and symptomatic Alzheimer's disease : Specific detection of advanced phases of amyloid-β pathology.
  • 2015
  • Ingår i: Alzheimer's & Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 11:8, s. 975-85
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Amyloid positron emission tomography (PET) has become an important tool to identify amyloid-β (Aβ) pathology in Alzheimer's disease (AD) patients. Here, we determined the diagnostic value of the amyloid PET tracer [(18)F]flutemetamol in relation to Aβ pathology at autopsy.METHODS: [(18)F]flutemetamol PET was carried out in a cohort of 68 patients included in a [(18)F]flutemetamol amyloid PET imaging end-of-life study (GE067-007). At autopsy, AD pathology was determined and Aβ plaque pathology was classified into phases of its regional distribution (0-5).RESULTS: [(18)F]flutemetamol PET was universally positive in cases with advanced stage postmortem Aβ pathology (Aβ phases 4 and 5). Negative amyloid PET was universally observed in nondemented or non-AD dementia cases with initial Aβ phases 1 and 2, whereas 33.3% of the phase 3 cases were positive.CONCLUSIONS: [(18)F]flutemetamol amyloid PET detects primarily advanced stages of Aβ pathology in preclinical and symptomatic AD cases.
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23.
  • Wennström, Malin, et al. (författare)
  • Cellular localization of p-tau217 in brain and its association with p-tau217 plasma levels
  • 2022
  • Ingår i: Acta Neuropathologica Communications. - : Springer Science and Business Media LLC. - 2051-5960. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent studies highlight phosphorylated tau (p-tau) at threonine tau 217 (p-tau217) as a new promising plasma biomarker for pathological changes implicated in Alzheimer’s disease (AD), but the specific brain pathological events related to the alteration in p-tau217 plasma levels are still largely unknown. Using immunostaining techniques of postmortem AD brain tissue, we show that p-tau217 is found in neurofibrillary tangles (NFTs) and neuropil threads that are also positive for p-tau181, 202, 202/205, 231, and 369/404. The p-tau217, but not the other five p-tau variants, was also prominently seen in vesicles structure positive for markers of granulovacuolar degeneration bodies and multi-vesicular bodies. Further, individuals with a high likelihood of AD showed significantly higher p-tau217 area fraction in 4 different brain areas (entorhinal cortex, inferior temporal gyrus, and superior frontal gyrus) compared to those with Primary age related tauopathy or other non-AD tauopathies. The p-tau217 area fraction correlated strongly with total amyloid-beta (Aβ) and NFT brain load when the whole group was analyzed. Finally, the mean p-tau217 area fraction correlated significantly with p-tau217 concentrations in antemortem collected plasma specifically in individuals with amyloid plaques and not in those without amyloid plaques. These studies highlight differences in cellular localization of different p-tau variants and suggest that plasma levels of p-tau217 reflect an accumulation of p-tau217 in presence of Aβ plaque load.
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24.
  • Wennström, Malin, et al. (författare)
  • The Relationship between p-tau217, p-tau231, and p-tau205 in the Human Brain Is Affected by the Cellular Environment and Alzheimer’s Disease Pathology
  • 2024
  • Ingår i: Cells. - 2073-4409. ; 13:4
  • Tidskriftsartikel (refereegranskat)abstract
    • The levels of p-tau217 and p-tau231 in cerebrospinal fluid (CSF) are associated with early amyloid beta (Aß) changes in the brain, while the CSF levels of p-tau205 are foremost related to tau pathology in the later stages of the disease. To investigate if the three p-tau variants are found to the same degree in different tau structures and if their co-localization is affected by the diagnosis and presence of Aß plaques, we immunostained sections of the entorhinal cortex (EC) and inferior temporal gyrus (ITG) from non-demented controls (NC), patients with Alzheimer’s disease (AD), and primary age-related tauopathy (PART) against p-tau217, p-tau231, and p-tau205 together with Methoxi-X04. An analysis using confocal microscopy showed that the co-localization variable, the Pearson correlation coefficient (PCC), was significantly higher between p-tau231 and p-tau205 in neurofibrillary tangles compared to neuropil threads and dystrophic neurites in plaques. The PCC value between all three p-tau variants in the neuropil threads was significantly lower in the ECs of patients with AD compared to the NC and in the ITGs of patients with AD, with a high Aß load compared to PART. The lowered value was associated with proportionally higher amounts of non-colocalized p-tau231 and p-tau217 compared to p-tau205, and the PCC values were negatively correlated with Aß and the tangle loads in patients with AD, but positively correlated with tangles in PART. These results suggest that the proportion of and co-localization between p-tau217, p-tau231, and p-tau205 are dependent on cellular localization and are altered in response to AD pathology in a spatial–temporal manner.
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