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Soluble TREM2 is elevated in Parkinson's disease subgroups with increased CSF tau.

  • Wilson, Edward N1
  • Swarovski, Michelle S1
  • Linortner, Patricia1
  • Shahid, Marian1
  • Zuckerman, Abigail J1
  • Wang, Qian1
  • Channappa, Divya1, 2
  • Minhas, Paras S1
  • Mhatre, Siddhita D1
  • Plowey, Edward D2
  • Quinn, Joseph F3, 4
  • Zabetian, Cyrus P5, 6
  • Tian, Lu7
  • Longo, Frank M1
  • Cholerton, Brenna2
  • Montine, Thomas J2
  • Poston, Kathleen L1, 8
  • Andreasson, Katrin I1
  • 1 Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.
  • 2 Pathology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.
  • 3 Neurology, Oregon Health and Sciences University, Portland, OR, USA.
  • 4 Neurology, Portland VA Medical Center, Portland, OR, USA.
  • 5 VA Puget Sound Health Care System, Seattle, WA, USA.
  • 6 Neurology, University of Washington, Seattle, WA, USA.
  • 7 Biomedical Data Science and Statistics, Stanford University, Stanford, CA, USA.
  • 8 Neurosurgery, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.
Published Article
Oxford University Press
Publication Date
Mar 01, 2020
DOI: 10.1093/brain/awaa021
PMID: 32065223


Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and affects 1% of the population above 60 years old. Although Parkinson's disease commonly manifests with motor symptoms, a majority of patients with Parkinson's disease subsequently develop cognitive impairment, which often progresses to dementia, a major cause of morbidity and disability. Parkinson's disease is characterized by α-synuclein accumulation that frequently associates with amyloid-β and tau fibrils, the hallmarks of Alzheimer's disease neuropathological changes; this co-occurrence suggests that onset of cognitive decline in Parkinson's disease may be associated with appearance of pathological amyloid-β and/or tau. Recent studies have highlighted the appearance of the soluble form of the triggering receptor expressed on myeloid cells 2 (sTREM2) receptor in CSF during development of Alzheimer's disease. Given the known association of microglial activation with advancing Parkinson's disease, we investigated whether CSF and/or plasma sTREM2 differed between CSF biomarker-defined Parkinson's disease participant subgroups. In this cross-sectional study, we examined 165 participants consisting of 17 cognitively normal elderly subjects, 45 patients with Parkinson's disease with no cognitive impairment, 86 with mild cognitive impairment, and 17 with dementia. Stratification of subjects by CSF amyloid-β and tau levels revealed that CSF sTREM2 concentrations were elevated in Parkinson's disease subgroups with a positive tau CSF biomarker signature, but not in Parkinson's disease subgroups with a positive CSF amyloid-β biomarker signature. These findings indicate that CSF sTREM2 could serve as a surrogate immune biomarker of neuronal injury in Parkinson's disease. © The Author(s) (2020). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For permissions, please email: [email protected]

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