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  • Brunnström, Hans, et al. (författare)
  • History of depression prior to Alzheimer's disease and vascular dementia verified post-mortem.
  • 2013
  • Ingår i: Archives of Gerontology and Geriatrics. - : Elsevier. - 1872-6976. ; 56:1, s. 80-84
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to analyze the medical history, with regards to previous remote depression, in patients with neuropathologically verified Alzheimer's disease (AD), vascular dementia (VaD) and mixed AD/VaD. The 201 patients included (115 AD, 44 VaD and 42 mixed AD/VaD) had been referred to the Psychogeriatric/Psychiatric Department, Lund University Hospital, for psychogeriatric investigation and were followed-up with clinical records and detailed information on psychiatric history prior to the onset of dementia. Depression was considered to exist when the patient had consulted a psychiatrist or physician and had been diagnosed with a "depressive episode" or "depression" and when anti-depressants and/or other specific treatments had been prescribed. Twenty patients (10%) had suffered from depression earlier in life well before the onset of dementia. Eight of the 9 AD patients with a previous diagnosis of depression had suffered from only one depressive episode and all had responded well to treatment, with complete recovery. In the VaD group, 8 out of 9 patients suffered two or more depressive episodes and only two recovered completely. Events with a possible significant relationship to depression were seen in 8 of the 9 AD patients but in only 1 of the 9 VaD patients. Psychotic symptoms were more common in VaD than in the AD group. The treatment modality of depression was similar in the groups. In conclusion, a history of depression prior to dementia is more common and more therapy-resistant in VaD than in AD.
  • Brunnström, Hans, et al. (författare)
  • Prevalence of dementia subtypes: A 30-year retrospective survey of neuropathological reports.
  • 2009
  • Ingår i: Archives of Gerontology and Geriatrics. - : Elsevier. - 1872-6976. ; Aug 7, s. 146-149
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated the distribution of neuropathologically defined dementia subtypes among individuals with dementia disorder. The neuropathological reports were studied on all patients (n=524; 55.3% females; median age 80, range 39-102 years) with clinically diagnosed dementia disorder who underwent complete autopsy including neuropathological examination within the Department of Pathology at the University Hospital in Lund, Sweden, during the years 1974-2004. The neuropathological diagnosis was Alzheimer's disease (AD) in 42.0% of the cases, vascular dementia (VaD) in 23.7%, dementia of combined Alzheimer and vascular pathology in 21.6%, and frontotemporal dementia in 4.0% of the patients. The remaining 8.8% of the patients had other dementia disorders, including combinations other than combined Alzheimer and vascular pathology. The registered prevalence of dementia subtypes depends on many variables, including referral habits, clinical and neuropathological judgments and diagnostic traditions, all of these variables potentially changing over time. This, however, does not seem to obscure the delineation of the major dementia subgroups. In this material of 30 years from Lund in the south of Sweden, AD by far dominated among dementia subtypes, while cerebrovascular pathology corresponded with the dementia disorder, either entirely or partly, in almost half of the demented patients.
  • Brunnström, Hans, et al. (författare)
  • Response to letter to the editor.
  • 2010
  • Ingår i: The American Journal of Geriatric Psychiatry. - : Elsevier. - 1545-7214. ; 18:1, s. 92-93
  • Tidskriftsartikel (refereegranskat)
  • Brunnström, Hans, et al. (författare)
  • Staging of Lewy-related pathology in dementia
  • 2012
  • Ingår i: Clinical Neuropathology. - : Dustri-Verlag. - 0722-5091. ; 31:4, s. 216-223
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Lewy-related pathology is the characteristic feature of Parkinson's disease with and without dementia and dementia with Lewy bodies (DLB). There are two neuropathological staging systems for Lewy-related pathology commonly employed today: the staging system for Parkinson-related pathology by Braak et al., and the staging system by the Consortium on DLB. There are also several modified systems based on these two scales. Methods: We applied a total of eight different staging systems for Lewy-related pathology to 36 consecutive demented patients with various dementia disorders. Results: The staging systems varied considerably in number of unclassifiable cases (range 0 - 16 out of 36 cases), while the diagnostic agreement between the systems that were able to classify all or the very majority of cases varied only slightly (weighted kappa 0.86 - 0.92 and Spearman's sigma 0.80 - 1.0). Conclusion: The different staging systems for Lewy-related pathology that exist today vary in staging procedure and proportion of unclassifiable cases. The choice of system may affect the stage of Lewy-related pathology and ultimately final diagnosis.
  • Burguillos Garcia, Miguel, et al. (författare)
  • Caspase signalling controls microglia activation and neurotoxicity.
  • 2011
  • Ingår i: Nature. - : Nature Publishing Group. - 0028-0836. ; 472:7343, s. 319-U214
  • Tidskriftsartikel (refereegranskat)abstract
    • Activation of microglia and inflammation-mediated neurotoxicity are suggested to play a decisive role in the pathogenesis of several neurodegenerative disorders. Activated microglia release pro-inflammatory factors that may be neurotoxic. Here we show that the orderly activation of caspase-8 and caspase-3/7, known executioners of apoptotic cell death, regulate microglia activation through a protein kinase C (PKC)-δ-dependent pathway. We find that stimulation of microglia with various inflammogens activates caspase-8 and caspase-3/7 in microglia without triggering cell death in vitro and in vivo. Knockdown or chemical inhibition of each of these caspases hindered microglia activation and consequently reduced neurotoxicity. We observe that these caspases are activated in microglia in the ventral mesencephalon of Parkinson's disease (PD) and the frontal cortex of individuals with Alzheimer's disease (AD). Taken together, we show that caspase-8 and caspase-3/7 are involved in regulating microglia activation. We conclude that inhibition of these caspases could be neuroprotective by targeting the microglia rather than the neurons themselves.
  • Burguillos Garcia, Miguel, et al. (författare)
  • Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation.
  • 2015
  • Ingår i: Cell Reports. - : Cell Press. - 2211-1247. ; 10:9, s. 1626-1638
  • Tidskriftsartikel (refereegranskat)abstract
    • Inflammatory response induced by microglia plays a critical role in the demise of neuronal populations in neuroinflammatory diseases. Although the role of toll-like receptor 4 (TLR4) in microglia's inflammatory response is fully acknowledged, little is known about endogenous ligands that trigger TLR4 activation. Here, we report that galectin-3 (Gal3) released by microglia acts as an endogenous paracrine TLR4 ligand. Gal3-TLR4 interaction was further confirmed in a murine neuroinflammatory model (intranigral lipopolysaccharide [LPS] injection) and in human stroke subjects. Depletion of Gal3 exerted neuroprotective and anti-inflammatory effects following global brain ischemia and in the neuroinflammatory LPS model. These results suggest that Gal3-dependent-TLR4 activation could contribute to sustained microglia activation, prolonging the inflammatory response in the brain.
  • Carlén, Birgitta, et al. (författare)
  • Diagnostic value of electron microscopy in a case of juvenile neuronal ceroid lipofuscinosis
  • 2001
  • Ingår i: Ultrastructural Pathology. - : Taylor & Francis. - 1521-0758. ; 25:4, s. 285-288
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuronal ceroid lipofuscinoses (NCLs) represent a large group of inherited neurodegenerative disorders characterized by an abnormal accumulation of lipopigment in neuronal and extraneuronal cells. The authors present a case of juvenile neuronal ceroid lipofuscinosis in a 7-year-old boy. Ultrastructural examination of a skin biopsy disclosed deposits of curvilinear profiles and fingerprint-like structures in epithelial cells of sweat glands, endothelial cells, peripheral nerve endings, and fibroblasts, These findings allowed specific confirmation of the assumed diagnosis of juvenile neuronal ceroid lipofuscinosis. Due to the genotypic and phenotypic variability within the group of NCLs, the clinical investigation may be long and complicated. With the NCL disorders in mind, an accurate diagnosis based on ultrastructural examination of a skin biopsy may shorten this investigation, thus benefitting the patient.
  • Ceberg, Crister, et al. (författare)
  • Photon activation therapy of RG2 glioma carrying Fischer rats using stable thallium and monochromatic synchrotron radiation.
  • 2012
  • Ingår i: Physics in Medicine and Biology. - : IOP Publishing. - 1361-6560. ; 57:24, s. 8377-8391
  • Tidskriftsartikel (refereegranskat)abstract
    • 75 RG2 glioma-carrying Fischer rats were treated by photon activation therapy (PAT) with monochromatic synchrotron radiation and stable thallium. Three groups were treated with thallium in combination with radiation at different energy; immediately below and above the thallium K-edge, and at 50 keV. Three control groups were given irradiation only, thallium only, or no treatment at all. For animals receiving thallium in combination with radiation to 15 Gy at 50 keV, the median survival time was 30 days, which was 67% longer than for the untreated controls (p = 0.0020) and 36% longer than for the group treated with radiation alone (not significant). Treatment with thallium and radiation at the higher energy levels were not effective at the given absorbed dose and thallium concentration. In the groups treated at 50 keV and above the K-edge, several animals exhibited extensive and sometimes contra-lateral edema, neuronal death and frank tissue necrosis. No such marked changes were seen in the other groups. The results were discussed with reference to Monte Carlo calculated electron energy spectra and dose enhancement factors.
  • Chen, Dongfeng, et al. (författare)
  • Better Prognosis of Patients with Glioma Expressing FGF2-Dependent PDGFRA Irrespective of Morphological Diagnosis.
  • 2013
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Signaling of platelet derived growth factor receptor alpha (PDGFRA) is critically involved in the development of gliomas. However, the clinical relevance of PDGFRA expression in glioma subtypes and the mechanisms of PDGFRA expression in gliomas have been controversial. Under the supervision of morphological diagnosis, analysis of the GSE16011 and the Repository of Molecular Brain Neoplasia Data (Rembrandt) set revealed enriched PDGFRA expression in low-grade gliomas. However, gliomas with the top 25% of PDGFRA expression levels contained nearly all morphological subtypes, which was associated with frequent IDH1 mutation, 1p LOH, 19q LOH, less EGFR amplification, younger age at disease onset and better survival compared to those gliomas with lower levels of PDGFRA expression. SNP analysis in Rembrandt data set and FISH analysis in eleven low passage glioma cell lines showed infrequent amplification of PDGFRA. Using in vitro culture of these low passage glioma cells, we tested the hypothesis of gliogenic factor dependent expression of PDGFRA in glioma cells. Fibroblast growth factor 2 (FGF2) was able to maintain PDGFRA expression in glioma cells. FGF2 also induced PDGFRA expression in glioma cells with low or non-detectable PDGFRA expression. FGF2-dependent maintenance of PDGFRA expression was concordant with the maintenance of a subset of gliogenic genes and higher rates of cell proliferation. Further, concordant expression patterns of FGF2 and PDGFRA were detected in glioma samples by immunohistochemical staining. Our findings suggest a role of FGF2 in regulating PDGFRA expression in the subset of gliomas with younger age at disease onset and longer patient survival regardless of their morphological diagnosis.
  • Chen, Dongfeng, et al. (författare)
  • Glioma Cell Proliferation Controlled by ERK Activity-Dependent Surface Expression of PDGFRA.
  • 2014
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Increased PDGFRA signaling is an essential pathogenic factor in many subtypes of gliomas. In this context the cell surface expression of PDGFRA is an important determinant of ligand sensing in the glioma microenvironment. However, the regulation of spatial distribution of PDGFRA in glioma cells remains poorly characterized. Here, we report that cell surface PDGFRA expression in gliomas is negatively regulated by an ERK-dependent mechanism, resulting in reduced proliferation of glioma cells. Glioma tumor tissues and their corresponding cell lines were isolated from 14 patients and analyzed by single-cell imaging and flow cytometry. In both cell lines and their corresponding tumor samples, glioma cell proliferation correlated with the extent of surface expression of PDGFRA. High levels of surface PDGFRA also correlated to high tubulin expression in glioma tumor tissue in vivo. In glioma cell lines, surface PDGFRA declined following treatment with inhibitors of tubulin, actin and dynamin. Screening of a panel of small molecule compounds identified the MEK inhibitor U0126 as a potent inhibitor of surface PDGFRA expression. Importantly, U0126 inhibited surface expression in a reversible, dose- and time-dependent manner, without affecting general PDGFRA expression. Treatment with U0126 resulted in reduced co-localization between PDGFRA and intracellular trafficking molecules e.g. clathrin, RAB11 and early endosomal antigen-1, in parallel with enhanced co-localization between PDGFRA and the Golgi cisternae maker, Giantin, suggesting a deviation of PDGFRA from the endosomal trafficking and recycling compartment, to the Golgi network. Furthermore, U0126 treatment in glioma cells induced an initial inhibition of ERK1/2 phosphorylation, followed by up-regulated ERK1/2 phosphorylation concomitant with diminished surface expression of PDGFRA. Finally, down-regulation of surface PDGFRA expression by U0126 is concordant with reduced glioma cell proliferation. These findings suggest that manipulation of spatial expression of PDGFRA can potentially be used to combat gliomas.
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