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Sökning: WFRF:(Englund Elisabet)

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1.
  • Brunnström, Hans, et al. (författare)
  • Correlations of CSF tau and amyloid levels with Alzheimer pathology in neuropathologically verified dementia with Lewy bodies.
  • 2013
  • Ingår i: International Journal of Geriatric Psychiatry. - : Wiley. - 1099-1166 .- 0885-6230. ; 28:7, s. 738-744
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The presence of concomitant Alzheimer pathology has been linked to earlier death in cases with dementia with Lewy bodies (DLB). Recently, elevated cerebrospinal fluid (CSF) tau protein levels have been reported to be associated with shorter survival in clinically diagnosed DLB. Correlations between CSF biomarkers and neuropathological findings in DLB are missing. The aim of this study was to investigate correlations between CSF biomarker levels and histopathological findings, with a focus on concomitant Alzheimer pathology, in neuropathologically verified DLB cases. METHODS: The extent of neurofibrillary pathology (Braak stage), neuritic plaques (CERAD stage), Alzheimer pathology (PPAD9 stage) and cerebral amyloid angiopathy was assessed in 16 cases with DLB in whom total tau (T-tau), hyperphosphorylated tau and amyloid beta 1-42 (Aβ42) protein levels in CSF had been analyzed in vivo. Demographic and clinical data were collected. RESULTS: Both Braak and PPAD9 stages were inversely correlated with Aβ42 levels, whereas CERAD stage showed no significant correlations. Cerebral amyloid angiopathy correlated positively with T-tau and T-tau/Aβ42 ratio, and inversely with Aβ42 levels, but the group showed a very heterogeneous extent of cerebral amyloid angiopathy. CONCLUSIONS: The burden of concomitant Alzheimer pathology correlates with CSF Aβ42 but not with T-tau levels in cases with neuropathologically defined DLB. Copyright © 2012 John Wiley & Sons, Ltd.
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2.
  • Londos, Elisabet, et al. (författare)
  • Extreme sleep pattern in Lewy body dementia : A hypothalamic matter?
  • 2019
  • Ingår i: BMJ Case Reports. - : BMJ. - 1757-790X. ; 12:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Excessive sleep during the night and for >2 hours during the day is part of the fluctuating wakefulness criterion of dementia with Lewy bodies (DLB). The phenomenon â € sleep days' is not uncommon in nursing homes. Here, we describe a woman who, for months, slept for 3 days and nights in a row and thereafter was awake for 3 days and nights. Electroencephalogram (EEG) showed slow background activity and increased delta activity. No epileptiform activity was detected. Polysomnography showed a severely disturbed, markedly fragmented sleep pattern. On her death, neuropathology revealed degeneration and loss of neurons along with α-synuclein-containing Lewy body inclusions and neurites in the substantia nigra, locus coeruleus, hypothalamus, and neocortex, thus fulfilling the criteria of DLB, cortical type. We propose that the hypothalamic degeneration contributed significantly to the clinical profile in this case. We suggest that patients with sleep days should be investigated for other DLB signs.
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4.
  • Adler, Aleksandra, 1983- (författare)
  • Cognitive load in dialogue interpreting : Experience and directionality
  • 2023
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • This dissertation investigates the effect of experience and language direction on cognitive load in dialogue interpreting. The general objective of the study is to contribute to a better understanding of cognitive processes involved in dialogue interpreting. The present inquiry employs a multi- and mixed- method design and seeks to investigate disfluency measures as indicators of cognitive load in dialogue interpreting. Furthermore, the study aims to explore whether blink-based measures are sensitive to changes in cognitive load of dialogue interpreters. The present study is positioned within cognitive translation and interpreting studies (CTIS) and employs cognitive translatology as a framework, encompassing both cognitive and psycholinguistic approaches to translation and interpreting. Chen’s multidimensional theoretical construct of cognitive load in interpreting is explored in the study and remodeled to fit the context of dialogue interpreting and the assumptions of cognitive translatology. The data were collected from 17 dialogue interpreters during simulated interpreted encounters that recreated a situation commonly arising in a public service context in Sweden. The 10 inexperienced and 7 experienced interpreters all had Swedish as their working language, and the other working languages were French, Polish, and Spanish. Following the revised cognitive load model, the analyses of cognitive load focus on interpreter characteristics (interpreting experience) and on task and environmental characteristics (directionality). The results of analyses show that, in line with previous research, both interpreting experience and directionality modulate cognitive load of dialogue interpreters. Specifically, interpreting experience is demonstrated to attenuate cognitive load. In terms of directionality, interpreting into L2 is shown to be more cognitively demanding than interpreting into L1. Moreover, blink rate and blink rate variability (BRV) are explored as possible indicators of cognitive load. The analyses of blink measures suggest that no meaningful relationship can be found between blink measures and cognitive load.Finally, the complementary analyses of disfluency types in the utterances of the Polish interpreters (n=4) point to multifunctionality of disfluency in dialogue interpreting and to the multiple origins of cognitive load in interpreting dialogues. The analysis is performed from the perspective of the functional-cognitive view of disfluency proposed in the dissertation, whereby three disfluency context categories are identified and applied (cognitive-monitoring, cognitive-pragmatic, and cognitive-processing). Lexical access and rendition planning are identified as recurrent causes of cognitive load in dialogue interpreting. The study also makes theoretical and methodological contributions, primarily by revising the theoretical model of cognitive load in interpreting, which allows for operationalization of cognitive load with additional measures, in both experimental and naturalistic settings. Practical implications are a contribution to the understanding of the challenges interpreting into L2, and the impact of interpreters’ experience on interpreting. Overall, the study contributes to the emerging cognitive profile of dialogue interpreters.
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5.
  • Ahlenius, Henrik, et al. (författare)
  • Adaptor Protein LNK Is a Negative Regulator of Brain Neural Stem Cell Proliferation after Stroke.
  • 2012
  • Ingår i: The Journal of Neuroscience : the official journal of the Society for Neuroscience. - 1529-2401. ; 32:15, s. 5151-5164
  • Tidskriftsartikel (refereegranskat)abstract
    • Ischemic stroke causes transient increase of neural stem and progenitor cell (NSPC) proliferation in the subventricular zone (SVZ), and migration of newly formed neuroblasts toward the damaged area where they mature to striatal neurons. The molecular mechanisms regulating this plastic response, probably involved in structural reorganization and functional recovery, are poorly understood. The adaptor protein LNK suppresses hematopoietic stem cell self-renewal, but its presence and role in the brain are poorly understood. Here we demonstrate that LNK is expressed in NSPCs in the adult mouse and human SVZ. Lnk(-/-) mice exhibited increased NSPC proliferation after stroke, but not in intact brain or following status epilepticus. Deletion of Lnk caused increased NSPC proliferation while overexpression decreased mitotic activity of these cells in vitro. We found that Lnk expression after stroke increased in SVZ through the transcription factors STAT1/3. LNK attenuated insulin-like growth factor 1 signaling by inhibition of AKT phosphorylation, resulting in reduced NSPC proliferation. Our findings identify LNK as a stroke-specific, endogenous negative regulator of NSPC proliferation, and suggest that LNK signaling is a novel mechanism influencing plastic responses in postischemic brain.
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6.
  • Alafuzoff, Irina, et al. (författare)
  • The need to unify neuropathological assessments of vascular alterations in the ageing brain : Multicentre survey by the BrainNet Europe consortium
  • 2012
  • Ingår i: Experimental Gerontology. - : Elsevier BV. - 0531-5565 .- 1873-6815. ; 47:11, s. 825-833
  • Tidskriftsartikel (refereegranskat)abstract
    • Here, we summarise the results after carrying out a large survey regarding the assessment of vascular alterations, both vessel changes and vascular lesions in an inter-laboratory setting. In total, 32 neuropathologists from 22 centres, most being members of BrainNet Europe (BNE), participated by filling out a questionnaire with emphasis on assessment of common vascular alterations seen in the brains of aged subjects. A certain level of harmonisation has been reached among BNE members regarding sectioning of the brain, harvesting of brain tissue for histology and staining used when compared to the survey carried out in 2006 by Pantoni and colleagues. The most significant variability was seen regarding the assessment of severity and of clinical significance of vascular alterations. Two strategies have recently been recommended regarding the assessment of vascular alterations in aged and demented subjects. The National Institute on Aging - Alzheimer's Association (NIA-AA) recommends the assessment of hippocampal sclerosis, vascular brain injury and microvascular lesions in 12 regions. Although this strategy will be easy to follow, the recommendations do not inform how the load of observed alterations should be assessed and when the observed lesions are of significance. Deramecourt and his colleagues recommend an assessment and semiquantitative grading of various pathologies in 4 brain regions. This strategy yielded a total score of 0 to 20 as an estimate of pathology load. It is, however, not clear which score is considered to be of clinical significance. Furthermore, in several BNE trials the semiquantitative assessment has yielded poor agreement rates; an observation that might negatively influence the strategy proposed by Deramecourt and his colleagues. In line with NIA-AA, a dichotomised approach of easily recognisable lesions in a standardised set of brain regions harvested for neuropathological assessment and applying reproducible sampling and staining strategies is recommended by BNE. However, a simple strategy regarding assessment of load of alteration is urgently needed to yield reproducible, and at the same time, comparable results between centres.
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7.
  • Allard, Per, et al. (författare)
  • Caudate nucleus dopamine D-2 receptors in vascular dementia
  • 2002
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 14:1, s. 22-25
  • Tidskriftsartikel (refereegranskat)abstract
    • Caudate nucleus dopamine (DA) D-2 receptors were studied in patients with vascular dementia (VaD) and in a control group using [H-3]raclopride as a radioligand. There was no significant difference in the number of DA D-2 receptors in the VaD group as compared with controls. The binding affinity was significantly lower in the VaD group. When the VaD group was subdivided into subjects with or without neuroleptic treatment, there were no differences in the numbers of receptors as compared with controls, and the significant differences in binding affinity remained for both VaD subgroups. The present results are. discussed with reference to the previous finding of a reduced density of caudate nucleus DA uptake sites in the same VaD group and to results from studies on DA D-2 receptors in Alzheimer's disease and Parkinson's disease. Copyright (C) 2002 S. Karger AG, Basel.
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8.
  • Andersson, Elin Möller, et al. (författare)
  • Clinicopathological concordance in cognitive disease diagnostics
  • 2020
  • Ingår i: Clinical Neuropathology. - 0722-5091. ; 39:3, s. 99-104
  • Tidskriftsartikel (refereegranskat)abstract
    • Neurocognitive disorder encompasses many separate diagnoses, such as frontotemporal dementia (FTD), Alzheimer's disease (AD), Lewy body dementia (LBD), vascular dementia (VaD), and mixed dementia (MD). Because of the many variations between and within each subtype, it may be a challenge to clinically diagnose each condition. In a previous study on 176 dementia patients in a university hospital cohort between the years 1996 and 2006, a full diagnostic concordance of 49% was demonstrated between clinical diagnoses and pathological morphology [1]. The aims of this study were to do a follow-up on diagnostic concordance from the subsequent 10 years (2007 - 2016) and to compare the results with the previous study from 2009. In all cases of neuropathologically diagnosed dementia disorders (n = 324), the clinical records were searched for information on the clinical diagnosis of dementia, including on subtype. All individuals who had been diagnosed by a specialist were selected (n = 210). In this study, a full concordance between clinical diagnoses and neuropathological morphology was found in 61% of individuals, with marked variations between subgroups, including the lowest (31%) in the group of VaD. Vigilance in clinicopathological concordance is important for quality maintenance as well as the improvement of skills in diagnostic work. In light of the previous study, VaD one decade later remains elusive. The unmasking of this complicated and multifaceted disorder may be beneficial to the overall diagnostic accuracy in cognitive disease investigations.
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9.
  • Andin, Ulla, et al. (författare)
  • Alzheimer's disease (AD) with and without white matter pathology-clinical identification of concurrent cardiovascular disorders.
  • 2007
  • Ingår i: Archives of Gerontology and Geriatrics. - : Elsevier BV. - 1872-6976 .- 0167-4943. ; 44, s. 277-286
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinical vascular features, either as manifest vascular disease or as cardiovascular risk factors were compared in AD with and without neuropathological white matter disease (WMD). The aim of the study was to investigate whether the presence of WMD and the severity of either AD pathology or WMD were associated with different cardiovascular profiles. A total of 44 AD cases were retrospectively studied. All the cases were neuropathologically diagnosed as AD with WMD (n = 22) and as AD without WMD (n = 22), respectively. The patients' medical records were studied with regard to their medical history and to somatic and neurological findings including arrhythmia, congestive heart failure, angina, myocardial infarctions, signs of TIA/stroke, diabetes mellitus, and blood pressure abnormalities, such as hypertension and orthostatic hypotension. In AD-WMD, hypertension, orthostatic hypotension as well as dizziness/unsteadiness were significantly more common than in AD without WMD. Cardiovascular symptoms were more frequent in AD-WMD than in the other group, though the difference did not reach statistical significance. Hypothetically, abnormal and unstable blood pressure levels underlie recurrent cerebral hypoperfusion, which may in turn leave room for the development of WMD. Furthermore, dizziness/unsteadiness may be a symptom reflecting the presence of WMD. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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10.
  • Arvidsson, Ida, et al. (författare)
  • Early terminal complement blockade and C6 deficiency are protective in enterohemorrhagic Escherichia coli-infected mice
  • 2016
  • Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 197:4, s. 1276-1286
  • Tidskriftsartikel (refereegranskat)abstract
    • Complement activation occurs during enterohemorrhagic Escherichia coli (EHEC) infection and may exacerbate renal manifestations. In this study, we show glomerular C5b-9 deposits in the renal biopsy of a child with EHEC-associated hemolytic uremic syndrome. The role of the terminal complement complex, and its blockade as a therapeutic modality, was investigated in a mouse model of E. coli O157:H7 infection. BALB/c mice were treated with monoclonal anti-C5 i.p. on day 3 or 6 after intragastric inoculation and monitored for clinical signs of disease and weight loss for 14 d. All infected untreated mice (15 of 15) or those treated with an irrelevant Ab (8 of 8) developed severe illness. In contrast, only few infected mice treated with anti-C5 on day 3 developed symptoms (three of eight, p < 0.01 compared with mice treated with the irrelevant Ab on day 3) whereas most mice treated with anti-C5 on day 6 developed symptoms (six of eight). C6-deficient C57BL/6 mice were also inoculated with E. coli O157:H7 and only 1 of 14 developed disease, whereas 10 of 16 wild-type mice developed weight loss and severe disease (p < 0.01). Complement activation via the terminal pathway is thus involved in the development of disease in murine EHEC infection. Early blockade of the terminal complement pathway, before the development of symptoms, was largely protective, whereas late blockade was not. Likewise, lack of C6, and thereby deficient terminal complement complex, was protective in murine E. coli O157:H7 infection.
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