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  • 1. Kyriacou, Andreas
    et al.
    Johansson, Sverker
    Högskolan för lärande och kommunikation, Högskolan i Jönköping, HLK, Ämnesforskning.
    Why language evolution research might help in identifying biologically plausible linguistic processing primitives2006Inngår i: The Science of Aphasia VII, 7-12 Sept 2006, Sardinia, 2006Konferansepaper (Annet (populærvitenskap, debatt, mm))
  • 2. McLaughlin, David
    et al.
    Karlsson, Fredrik
    a Division of Biomedical Sciences, The University of Edinburgh, Hugh Robson Building, George Square, Edinburgh.
    Tian, Natasha
    Pratt, Thomas
    Bullock, Simon L.
    Wilson, Valerie A.
    Price, David J.
    Mason, John O.
    Specific modification of heparan sulphate is required for normal cerebral cortical development2003Inngår i: Mechanisms of Development, ISSN 0925-4773, E-ISSN 1872-6356, Vol. 120, nr 12, s. 1481-1488Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Proteoglycans are cell surface and extracellular matrix molecules to which long, unbranched glycosaminoglycan side chains are attached. Heparan sulphate, a type of glycosaminoglycan chain, has been proposed as a co-factor necessary for signalling by a range of growth factors. Here we provide evidence that loss of 2-O-sulphation in heparan sulphate leads to a significant reduction in cell proliferation in the developing cerebral cortex. The gene encoding heparan sulphate 2-sulphotransferase (Hs2st) is expressed in embryonic cortex and histological analysis of mice homozygous for a null mutation in Hs2st indicated a reduction in the thickness of the embryonic cerebral cortex. Using 5′-bromodeoxyuridine (BrdU) incorporation assays we found a reduction of approximately 40% in labelling indices of cortical precursor cells at E12. Comparison of the fates of cortical cells born on E13 and E15 in Hs2st−/− mutant and wildtype littermate embryos revealed no differences in the pattern of cell migration. Our findings suggest a critical role for 2-O-sulphation of heparan sulphate proteoglycan (HSPG) in regulating cell proliferation during development of the cerebral cortex, perhaps through the modulation of cellular responses to growth factor signalling.

  • 3. Samrani, George
    et al.
    Marklund, Petter
    Engström, Lisa
    Broman, Daniel
    Högskolan Dalarna, Akademin Utbildning, hälsa och samhälle. Högskolan i Skövde.
    Persson, Jonas
    Behavioral facilitation and increased brain responses from a high interference working memory context.2018Inngår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, nr 1, artikkel-id 15308Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Many real-life situations require flexible behavior in changing environments. Evidence suggests that anticipation of conflict or task difficulty results in behavioral and neural allocation of task-relevant resources. Here we used a high- and low-interference version of an item-recognition task to examine the neurobehavioral underpinnings of context-sensitive adjustment in working memory (WM). We hypothesized that task environments that included high-interference trials would require participants to allocate neurocognitive resources to adjust to the more demanding task context. The results of two independent behavioral experiments showed enhanced WM performance in the high-interference context, which indicated that a high-interference context improves performance on non-interference trials. A third behavioral experiment showed that when WM load was increased, this effect was no longer significant. Neuroimaging results further showed greater engagement of inferior frontal gyrus, striatum, parietal cortex, hippocampus, and midbrain in participants performing the task in the high- than in the low-interference context. This effect could arise from an active or dormant mode of anticipation that seems to engage fronto-striatal and midbrain regions to flexibly adjust resources to task demands. Our results extend the model of conflict adaptation beyond trial-to-trial adjustments by showing that a high interference context affects both behavioral and biological aspects of cognition.

  • 4.
    Santillo, Alexander Frizell
    et al.
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Skoglund, Lena
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Lindau, Maria
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Eeg-Olofsson, Karin Edebol
    Uppsala Univ, Dept Neurosci Clin Neurophysiol, Uppsala 75185, Sweden.
    Tovi, Metin
    Karolinska Univ Hosp, Dept Diagnost Radiol, Stockholm, Sweden.
    Engler, Henry
    Uppsala Univ, Dept Med Sci Clin Physiol, Uppsala 75185, Sweden.
    Brundin, Rose-Marie
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Ingvast, Sofie
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Lannfelt, Lars
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Glaser, Anna
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Kilander, Lena
    Uppsala Univ, Dept Publ Hlth Geriatr, Uppsala 75185, Sweden.
    Frontotemporal Dementia-amyotrophic Lateral Sclerosis Complex is Simulated by Neurodegeneration With Brain Iron Accumulation2009Inngår i: Alzheimer Disease and Associated Disorders, ISSN 0893-0341, E-ISSN 1546-4156, Vol. 23, nr 3, s. 298-300Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We describe a case of late onset neurodegeneration with brain iron accumulation (NBIA) presenting as frontotemporal dementia (FTD) with amyotrophic lateral sclerosis (ALS). A male patient presented at age 66 with change of personality: disinhibition, emotional blunting, and socially inappropriate behavior, coupled with dysarthria, dystonia, and corticospinal tract involvement. Magnetic resonance imaging showed general cortical atrophy, iron deposits in the globus pallidus, and the “eye of the tiger” sign. Neuropsychologic performance was globally reduced, especially executive functions. Fluorodeoxyglucose positron emission tomography showed hypometabolism predominantly in frontal and temporal areas. Repeated neurophysiologic examinations showed signs of chronic denervation. The patient was diagnosed with NBIA but fulfilled consensus criteria for FTD and had a clinical picture of ALS, without neurophysiologic confirmation. Our finding introduces NBIA as a possible cause of FTD and as a differential diagnosis of the FTD-ALS complex.

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