Biomarkers of neurodegeneration and glial activation validated in Alzheimer’s disease assessed in longitudinal cerebrospinal fluid samples of Parkinson’s disease | Zendy

Michael Bartl | Zendy; Mohammed Dakna | Zendy; Douglas Galasko | Zendy; Samantha J. Hutten | Zendy; Tatiana Foroud | Zendy; Marian Quan | Zendy; Kenneth Marek | Zendy; Andrew Siderowf | Zendy; Jonas Franz | Zendy; Claudia Trenkwalder | Zendy; Brit Mollenhauer | Zendy

Open Access

Biomarkers of neurodegeneration and glial activation validated in Alzheimer’s disease assessed in longitudinal cerebrospinal fluid samples of Parkinson’s disease

Author(s) -

Michael Bartl,

Mohammed Dakna,

Douglas Galasko,

Samantha J. Hutten,

Tatiana Foroud,

Marian Quan,

Kenneth Marek,

Andrew Siderowf,

Jonas Franz,

Claudia Trenkwalder,

Brit Mollenhauer

Publication year - 2021

Publication title -

plos one

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.99

H-Index - 332

ISSN - 1932-6203

DOI - 10.1371/journal.pone.0257372

Subject(s) - biomarker , cerebrospinal fluid , glial fibrillary acidic protein , medicine , neurodegeneration , gastroenterology , area under the curve , pathology , alzheimer's disease , neuroinflammation , oncology , disease , biology , immunohistochemistry , biochemistry

Aim Several pathophysiological processes are involved in Parkinson’s disease (PD) and could inform in vivo biomarkers. We assessed an established biomarker panel, validated in Alzheimer’s Disease, in a PD cohort. Methods Longitudinal cerebrospinal fluid (CSF) samples from PPMI (252 PD, 115 healthy controls, HC) were analyzed at six timepoints (baseline, 6, 12, 24, 36, and 48 months follow-up) using Elecsys® electrochemiluminescence immunoassays to quantify neurofilament light chain (NfL), soluble TREM2 receptor (sTREM2), chitinase-3-like protein 1 (YKL40), glial fibrillary acidic protein (GFAP), interleukin-6 (IL-6), S100, and total α-synuclein (αSyn). Results αSyn was significantly lower in PD (mean 103 pg/ml vs. HC: 127 pg/ml, p<0.01; area under the curve [AUC]: 0.64), while all other biomarkers were not significantly different (AUC NfL: 0.49, sTREM2: 0.54, YKL40: 0.57, GFAP: 0.55, IL-6: 0.53, S100: 0.54, p>0.05) and none showed a significant difference longitudinally. We found significantly higher levels of all these markers between PD patients who developed cognitive decline during follow-up, except for αSyn and IL-6. Conclusion Except for αSyn, the additional biomarkers did not differentiate PD and HC, and none showed longitudinal differences, but most markers predict cognitive decline in PD during follow-up.

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