Glycoprotein pathways altered in frontotemporal dementia with autoimmune disease

Fiona Bright, Jared S. Katzeff, John R. Hodges, Olivier Piguet, Jillian J. Kril, Glenda M. Halliday, Woojin Scott Kim*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)
41 Downloads (Pure)

Abstract

Behavioral variant frontotemporal dementia (bvFTD) is a younger onset form of neurodegeneration initiated in the frontal and/or temporal lobes with a slow clinical onset but rapid progression. bvFTD is highly complex biologically with different pathological signatures and genetic variants that can exhibit a spectrum of overlapping clinical manifestations. Although the role of innate immunity has been extensively investigated in bvFTD, the involvement of adaptive immunity in bvFTD pathogenesis is poorly understood. We analyzed blood serum proteomics to identify proteins that are associated with autoimmune disease in bvFTD. Eleven proteins (increased: ATP5B, CALML5, COLEC11, FCGBP, PLEK, PLXND1; decreased: APOB, ATP8B1, FAM20C, LOXL3, TIMD4) were significantly altered in bvFTD with autoimmune disease compared to those without autoimmune disease. The majority of these proteins were enriched for glycoprotein-associated proteins and pathways, suggesting that the glycome is targeted in bvFTD with autoimmune disease.

Original languageEnglish
Article number736260
Pages (from-to)1-9
Number of pages9
JournalFrontiers in Immunology
Volume12
DOIs
Publication statusPublished - 1 Sept 2021
Externally publishedYes

Bibliographical note

Copyright the Author(s) 2021. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • autoimmune disease
  • biomarker
  • frontotemporal dementia
  • glycome
  • glycoprotein
  • proteomics
  • serum
  • thyroid

Fingerprint

Dive into the research topics of 'Glycoprotein pathways altered in frontotemporal dementia with autoimmune disease'. Together they form a unique fingerprint.

Cite this