Change in the plasma proteome associated with canine cognitive dysfunction syndrome (CCDS) in Thailand

• Published in: BMC veterinary research Vol. 17; no. 1; p. 60
• Main Authors: Phochantachinda, Sataporn, Chantong, Boonrat, Reamtong, Onrapak, Chatchaisak, Duangthip
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 29.01.2021; BioMed Central; BMC
• Subjects: Aging; Amyloid beta 42; Amyloid beta-protein; Animal cognition; Apolipoproteins; Biomarkers; Brain; Canine cognitive dysfunction syndrome; Coagulation; Cognition disorders; Cognitive ability; Cytokines; Degeneration; Development and progression; Disease; Diseases; Dogs; Glycoproteins; Health aspects; Identification and classification; Immunoglobulins; Inflammation; LC-MS/MS; Lipid metabolism; Measurement; Nervous system; Neurodegenerative diseases; Pathology; Plasma; Plasma proteins; Population studies; Protein expression; Proteins; Proteomes; Proteomics; Questionnaires; Tumor necrosis factor-TNF; Thailand; Amyloid beta 42; Canine cognitive dysfunction syndrome; LC-MS/MS
• ISSN: 1746-6148; 1746-6148
• DOI: 10.1186/s12917-021-02744-w

Canine cognitive dysfunction syndrome (CCDS) is a progressive neurodegenerative disorder found in senior dogs. Due to the lack of biological markers, CCDS is commonly underdiagnosed. The aim of this study was to identify potential plasma biomarkers using proteomics techniques and to increase our understanding of the pathogenic mechanism of the disease. Plasma amyloid beta 42 (Aβ ) has been seen to be a controversial biomarker for CCDS. Proteomics analysis was performed for protein identification and quantification. Within CCDS, ageing, and adult dogs, 87 proteins were identified specific to Canis spp. in the plasma samples. Of 87 proteins, 48 and 41 proteins were changed in the ageing and adult groups, respectively. Several distinctly expressed plasma proteins identified in CCDS were involved in complement and coagulation cascades and the apolipoprotein metabolism pathway. Plasma Aβ levels considerably overlapped within the CCDS and ageing groups. In the adult group, the Aβ level was low compared with that in the other groups. Nevertheless, plasma Aβ did not show a correlation with the Canine Cognitive Dysfunction Rating scale (CCDR) score in the CCDS group (p = 0.131, R  = 0.261). Our present findings suggest that plasma Aβ does not show potential for use as a diagnostic biomarker in CCDS. The nano-LC-MS/MS data revealed that the predictive underlying mechanism of CCDS was the co-occurrence of inflammation-mediated acute phase response proteins and complement and coagulation cascades that partly functioned by apolipoproteins and lipid metabolism. Some of the differentially expressed proteins may serve as potential predictor biomarkers along with Aβ in plasma for improved CCDS diagnosis. Further study in larger population-based cohort study is required in validation to define the correlation between protein expression and the pathogenesis of CCDS.