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Sökning: db:Swepub > (2010-2011) > Zetterberg Henrik 1973

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51.
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54.
  • Mattsson, Niklas, 1979, et al. (författare)
  • Cerebrospinal Fluid Microglial Markers in Alzheimer's Disease: Elevated Chitotriosidase Activity but Lack of Diagnostic Utility
  • 2011
  • Ingår i: NeuroMolecular Medicine. - : Springer Science and Business Media LLC. - 1535-1084 .- 1559-1174. ; 13:2, s. 151-159
  • Tidskriftsartikel (refereegranskat)abstract
    • Activated microglial cells, which are the resident macrophages of the central nervous system, surround amyloid beta-plaques in Alzheimer's disease (AD) brains. Inflammation including microglial activation may contribute in AD pathogenesis, and biomarkers for this process may thus be of value to study AD pathogenesis and might facilitate development of therapies targeting these cells. We therefore examined cerebrospinal fluid (CSF) biomarkers in patients with AD, other dementias, mild cognitive impairment and in healthy controls. Samples were analyzed for markers with known association to macrophage activity, including chitotriosidase, YKL-40 (CHI3L1, HC gp-39) and chemokine CC motif ligand 2 (CCL2, MCP1). Patients with AD had higher chitotriosidase activity than controls and patients with stable mild cognitive impairment, consistent with the presence of activated microglial cells in AD brains, but with large overlaps between groups. CCL2 and YKL-40 concentrations did not differ among groups. Microglial markers are unlikely to be useful for AD diagnosis, but might be useful for identification of distinct subgroups of patients, and for the development and implementation of drugs targeting microglial pathology.
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55.
  • Mattsson, Niklas, 1979, et al. (författare)
  • Converging molecular pathways in human neural development and degeneration.
  • 2010
  • Ingår i: Neuroscience research. - : Elsevier BV. - 1872-8111 .- 0168-0102. ; 66:3, s. 330-2
  • Tidskriftsartikel (refereegranskat)abstract
    • Animal studies suggest that phosphorylation of microtubule-associated protein tau is a physiological way of destabilizing axons in the developing brain, promoting synaptic plasticity, while in the adult human brain tau phosphorylation is a specific sign of Alzheimer's disease. We here show, for the first time, that newborn human infants have extremely high levels of phosphorylated tau in their cerebrospinal fluid, and that these levels decrease during the first years of life. Tau phosphorylation in Alzheimer's disease may be a physiological response to Alzheimer-associated synaptotoxicity.
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56.
  • Mattsson, Niklas, 1979, et al. (författare)
  • Converging Pathways of Chromogranin and Amyloid Metabolism in the Brain
  • 2010
  • Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 20:4, s. 1039-1048
  • Tidskriftsartikel (refereegranskat)abstract
    • Much is unknown regarding the regulation of Alzheimer-related amyloid-beta protein precursor (A beta PP)-processing in the human central nervous system. It has been hypothesized that amyloidogenic A beta PP-processing preferentially occurs in the regulated secretory pathway of neurons. To test this hypothesis we looked for correlations of A beta PP-derived molecules in cerebrospinal fluid (CSF) with chromogranin (Cg) derived peptides, representing the regulated secretion. Patients with Alzheimer's disease (AD, N = 32), multiple sclerosis (MS, N = 50), and healthy controls (N = 70) were enrolled. CSF was analyzed for the amyloid peptides A beta(1-42), A beta(x-42), A beta(x-40), A beta(x-38), alpha-cleaved soluble A beta PP (sA beta PP alpha), beta-cleaved soluble A beta PP (sA beta PP beta), and peptides derived from CgB and SgII (Secretogranin-II, CgC). We investigated CSF levels of the protease BACE1, which processes A beta PP into A beta, in relation to Cg-levels. Finally, we measured Cg levels in cell media from untreated and BACE1-inhibited SH-SY5Y human neuroblastoma cells. CSF Cg levels correlated to sA beta PP and A beta peptides in AD, MS, and controls, and to CSF BACE1. Cell medium from BACE1-inhibited cells had decreased CgB levels. These results suggest that a large part of A beta PP in the human central nervous system is processed in the regulated secretory pathway of neurons.
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57.
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58.
  • Mattsson, Niklas, 1979, et al. (författare)
  • {gamma}-Secretase-dependent amyloid-{beta} is increased in Niemann-Pick type C: A cross-sectional study.
  • 2011
  • Ingår i: Neurology. - 0028-3878. ; 76:4, s. 366-72
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Niemann-Pick disease type C (NPC) is an inherited disorder characterized by intracellular accumulation of lipids such as cholesterol and glycosphingolipids in endosomes and lysosomes. This accumulation induces progressive degeneration of the nervous system. NPC shows some intriguing similarities with Alzheimer disease (AD), including neurofibrillary tangles, but patients with NPC generally lack amyloid-β (Aβ) plaques. Lipids affect γ-secretase-dependent amyloid precursor protein (APP) metabolism that generates Aβ in vitro, but this has been difficult to prove in vivo. Our aim was to assess the effect of altered lipid constituents in neuronal membranes on amyloidogenic APP processing in humans. METHODS: We examined Aβ in CSF from patients with NPC (n = 38) and controls (n = 14). CSF was analyzed for Aβ(38), Aβ(40), Aβ(42), α-cleaved soluble APP, β-cleaved soluble APP, total-tau, and phospho-tau. RESULTS: Aβ release was markedly increased in NPC, with a shift toward the Aβ(42) isoform. Levels of α- and β-cleaved soluble APP were similar in patients and controls. Patients with NPC had increased total-tau. Patients on treatment with miglustat (n = 18), a glucosylceramide synthase blocker, had lower Aβ(42) and total-tau than untreated patients. CONCLUSION: Increased CSF levels of Aβ(38), Aβ(40), and Aβ(42) and unaltered levels of β-cleaved soluble APP are consistent with increased γ-secretase-dependent Aβ release in the brains of patients with NPC. These results provide the first in vivo evidence that neuronal lipid accumulation facilitates γ-secretase-dependent Aβ production in humans and may be of relevance to AD pathogenesis.
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59.
  • Mattsson, Niklas, 1979, et al. (författare)
  • Growth factors in Parkinson's disease.
  • 2011
  • Ingår i: Biomarkers in medicine. - 1752-0363. ; 5:2, s. 201-2
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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60.
  • Mattsson, Niklas, 1979, et al. (författare)
  • Inter-laboratory variation in cerebrospinal fluid biomarkers for Alzheimer's disease: united we stand, divided we fall.
  • 2010
  • Ingår i: Clinical chemistry and laboratory medicine : CCLM / FESCC. - 1434-6621. ; 48:5, s. 603-7
  • Forskningsöversikt (refereegranskat)abstract
    • Abstract Several drug candidates for Alzheimer's disease are being evaluated in clinical trials, with the goal of finding a drug with disease-modifying effects. When such a drug finally reaches the market, there will be a demand for accurate diagnostic tools useful for early detection of disease and for monitoring biochemical effects. The core cerebrospinal fluid (CSF) biomarkers amyloid peptides (Abeta42), total-tau and phospo-tau are promising in this respect. However, inter-center variation (caused by pre-analytical, analytical and post-analytical factors), and inter-laboratory variation (caused by analytical factors), particularly for CSF Abeta42, lowers their utility in multicenter studies. Here, we discuss the causes of these variations, and present a global quality control program to overcome them.
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