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January 2019; 6 (1) ArticleOpen Access

CSF concentrations of soluble TREM2 as a marker of microglial activation in HIV-1 infection

Magnus Gisslén, Amanda Heslegrave, Elena Veleva, Aylin Yilmaz, Lars-Magnus Andersson, Lars Hagberg, Serena Spudich, Dietmar Fuchs, Richard W. Price, Henrik Zetterberg
First published November 7, 2018, DOI: https://doi.org/10.1212/NXI.0000000000000512
Magnus Gisslén
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
MD, PhD
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Amanda Heslegrave
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
PhD
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Elena Veleva
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
BSc
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Aylin Yilmaz
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
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Lars-Magnus Andersson
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
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Lars Hagberg
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
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Serena Spudich
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
MD, MA
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Dietmar Fuchs
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
MSc, PhD
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Richard W. Price
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
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Henrik Zetterberg
From the Department of Infectious Diseases (M.G., A.Y., L.-M.A., L.H.), Institute of Biomedicine, the Sahlgrenska Academy at University of Gothenburg, Sweden; Department of Molecular Neuroscience (A.H., E.V., H.Z.), UCL Institute of Neurology, Queen Square; UK Dementia Research Institute at UCL (A.H., E.V., H.Z.), London, United Kingdom; Department of Neurology and Center for Neuroepidemiology and Clinical Neurological Research (S.S.), Yale University, New Haven, CT; Division of Biological Chemistry (D.F.), Biocenter, Medical University of Innsbruck, Austria; Department of Neurology (R.W.P.), University of California San Francisco; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital; and Department of Psychiatry and Neurochemistry (H.Z.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
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Citation
CSF concentrations of soluble TREM2 as a marker of microglial activation in HIV-1 infection
Magnus Gisslén, Amanda Heslegrave, Elena Veleva, Aylin Yilmaz, Lars-Magnus Andersson, Lars Hagberg, Serena Spudich, Dietmar Fuchs, Richard W. Price, Henrik Zetterberg
Neurol Neuroimmunol Neuroinflamm Jan 2019, 6 (1) e512; DOI: 10.1212/NXI.0000000000000512

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    Figure 1 Concentrations of CSF biomarkers in the 7 participant groups

    The figure shows concentrations of CSF sTREM2 (A), CSF neopterin (B), and age-adjusted CSF NFL (C) in the 7 participant groups. Boxes in all panels depict median and IQR, whiskers show 10–90 percentiles, and “+” designates the mean values. Gray horizontal lines show the upper limit of normal. Statistical comparisons of groups are given in table 2. Measured markers are listed in the title of each panel and findings described in the text.

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    Figure 2 Correlations between CSF biomarkers and age

    The figure shows correlations between CSF sTREM2, neopterin, and NFL (A–C). Regression lines and Pearson correlation coefficient are shown in each panel. Associations between CSF biomarkers and age (D–F). Regression lines and Pearson correlation coefficient are shown in panel D and F. No significant correlation was found between CSF neopterin and age (E). NFL = neurofilament light protein.

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    Figure 3 CSF sTREM2 in HIV-negative controls

    (A) A strong correlation between CSF sTREM2 and CSF NFL was found in HIV-negative controls (n = 11). (B) Both CSF sTREM2 and NFL increase with age in healthy controls. NFL = neurofilament light protein.

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