Poul Henning Jensen

Cerebrospinal fluid α-synuclein contributes to the differential diagnosis of Alzheimer's disease

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • Min Shi, University of Washington, United States
  • Lu Tang, University of Washington, Peking University Third Hospital, United States
  • Jon B Toledo, University of Pennsylvania, United States
  • Carmen Ginghina, University of Washington, United States
  • Hua Wang, Peking University Health Science Centre and Third Hospital, University of Washington, China
  • Patrick Aro, University of Washington, United States
  • Poul Henning Jensen
  • Daniel Weintraub, University of Pennsylvania, United States
  • Alice S Chen-Plotkin, University of Pennsylvania, United States
  • David J Irwin, University of Pennsylvania, United States
  • Murray Grossman, University of Pennsylvania, United States
  • Leo McCluskey, University of Pennsylvania, United States
  • Lauren B Elman, University of Pennsylvania, United States
  • David A Wolk, University of Pennsylvania, United States
  • Edward B Lee, University of Pennsylvania, United States
  • Leslie M Shaw, University of Pennsylvania, United States
  • John Q Trojanowski, University of Pennsylvania, United States
  • Jing Zhang, University of Washington, Peking University Health Science Centre and Third Hospital, China

INTRODUCTION: The ability of Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers (amyloid β peptide 1-42, total tau, and phosphorylated tau) to discriminate AD from related disorders is limited. Biomarkers for other concomitant pathologies (e.g., CSF α-synuclein [α-syn] for Lewy body pathology) may be needed to further improve the differential diagnosis.

METHODS: CSF total α-syn, phosphorylated α-syn at Ser129, and AD CSF biomarkers were evaluated with Luminex immunoassays in 367 participants, followed by validation in 74 different neuropathologically confirmed cases.

RESULTS: CSF total α-syn, when combined with amyloid β peptide 1-42 and either total tau or phosphorylated tau, improved the differential diagnosis of AD versus frontotemporal dementia, Lewy body disorders, or other neurological disorders. The diagnostic accuracy of the combined models attained clinical relevance (area under curve ∼0.9) and was largely validated in neuropathologically confirmed cases.

DISCUSSION: Combining CSF biomarkers representing AD and Lewy body pathologies may have clinical value in the differential diagnosis of AD.

Original languageEnglish
JournalAlzheimer's & Dementia
Volume14
Issue8
Pages (from-to)1052-1062
Number of pages11
ISSN1552-5260
DOIs
Publication statusPublished - 2018

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