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Cerebrospinal fluid macrophage biomarkers in amyotrophic lateral sclerosis

Abstract:

Objective: The neurodegenerative disease amyotrophic lateral sclerosis (ALS) is a heterogeneous clinical syndrome involving multiple molecular pathways. The development of biomarkers for use in therapeutic trials is a priority. We sought to use a high-throughput proteomic method to identify novel biomarkers in individual cerebrospinal fluid samples.

Methods: Liquid chromatography-tandem mass spectrometry with label-free quantification was used to identify cerebrospinal fluid proteins using samples from a well-characterised longitudinal cohort comprising patients with ALS (n=43), the upper motor neuron variant primary lateral sclerosis (PLS, n=6), cross-sectional healthy (n=20) and disease controls (Parkinsons’s n=20, ALS mimic disorders n=12).

Results: Three macrophage-derived chitinases showed increased abundance in ALS: chitotriosidase (CHIT1), chitinase-3-like protein 1 (CHI3L1) and chitinase-3-like protein 2 (CHI3L2). Elevated CHI3L1 was common to ALS and PLS, whereas CHIT1 and CHI3L2 levels differed. Chitinase levels correlated with disease progression rate (CHIT1 r=0.56, p<0.001; CHI3L1 r=0.31, p=0.028; CHI3L2 r=0.29, p=0.044). CHIT1, CHI3L1 and CHI3L2 levels correlated with phosphorylated neurofilament heavy chain (pNFH; r=0.62, p<0.001; r=0.49, p<0.001; r=0.41, p<0.001). CHI3L1 levels, but not CHIT1 or CHI3L2, increased over time in those with low initial levels (gradient=0.005 log abundance units/month, p=0.001). High CHIT1 was associated with shortened survival (HR 2.84, p=0.009). Inclusion of pNFH in survival models left only an association of pNFH and survival (HR 1.26, p=0.019).

Interpretation: Neuroinflammatory mechanisms have been consistently implicated through various experimental paradigms. These results support a key role for macrophage activity in ALS pathogenesis, offering novel target engagement and pharmacodynamic biomarkers for neuroinflammation-focused ALS therapy.

Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1002/ana.25143

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Target Discovery Institute
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Target Discovery Institute
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author


Publisher:
Wiley
Journal:
Annals of Neurology More from this journal
Volume:
83
Issue:
2
Pages:
258-268
Publication date:
2018-02-09
Acceptance date:
2018-01-09
DOI:
EISSN:
1531-8249
ISSN:
0364-5134


Keywords:
Pubs id:
pubs:817634
UUID:
uuid:6f15622a-8760-47c8-9c68-381a77d517a6
Local pid:
pubs:817634
Source identifiers:
817634
Deposit date:
2018-01-11
ARK identifier:

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