Relationship of Transcobalamin Receptor Antibodies with Baseline Features and Clinical Progression in Parkinson’s Disease
Chadwick Christine1, John Pluvinage1, Peggy Auinger2, Esther Forti3, Lyvin Tat3, Ralph Green3, Michael Wilson1
1University of California San Francisco, 2University of Rochester, 3University of California, Davis
Objective:
To measure the prevalence of serum transcobalamin receptor antibodies (CD320ab) in a large cohort of patients with early Parkinson’s disease (PD) and to assess their relationship with baseline characteristics and clinical progression.
Background:
The transcobalamin receptor (CD320) mediates the entry of holoTC, transporting vitamin B12 (B12) into the central nervous system (CNS). CD320ab have recently been identified which block CNS uptake of holoTC and are associated with “Autoimmune B12 Central Deficiency,” a condition in which neurological symptoms related to B12 deficiency occur despite normal serum B12. Since low B12 levels have been shown to be associated with severity and rate of progression of PD, we sought to determine whether CD320ab are common in PD, and whether they were associated with baseline features or clinical progression.
Design/Methods:
Measurements of baseline CSF and serum B12 and holoTC were available from participants with early untreated PD from the DATATOP study. Serum samples were tested using a Luminex assay to detect CD320ab. Samples were considered seropositive for the CD320 antigen (CD320ab+) using a fold change cutoff of 100. An unpublished study for this assay in a control population without PD showed a prevalence rate of 9.4%.
Results:
The prevalence rate of CD320ab+ was 12.7% (72/566). The mean (SD) CSF holoTC/serum holoTC ratio in males was lower in CD320ab+ than in CD320ab- (0.23 (0.07) vs 0.25 (0.02), p=0.03), but not in females. Baseline clinical features did not differ between CD320ab+ and CD320ab- participants. Mean annualized change in UPDRS and MMSE did not differ between these groups.
Conclusions:
We found a numerically higher prevalence of CD320ab+ in this cohort than in a control population. Baseline features and annualized rates of progression did not differ according to CD320ab status. Further studies are needed to determine whether CD320ab are associated with an elevated risk for PD.
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