2026 American Academy of Neurology Autoimmune Abstract Website

Objective:

To examine whether autoimmune diseases (AID) are associated with a distinct clinical phenotype in patients with Parkinson’s disease (PD), including motor and non-motor manifestations, symptoms severity, cognition, and quality of life.

Background:

Epidemiologic studies have shown that AIDs are associated with an increased risk of developing PD. Biologically, growing evidence supports shared genetic pathways (particularly HLA), alpha-synuclein T cell responses, and peripheral immune system activation. However, the clinical phenotypic influence of these autoimmune conditions on PD patients remains under-investigated.

Design/Methods:

We analyzed 495 PD patients from a single-center cohort: 442 without and 53 with AID. 30 had a systemic (i.e. rheumatoid arthritis, inflammatory bowel disease, Sjögren’s syndrome) and 23 had an organ-restricted (i.e., Hashimoto’s thyroiditis, type 1 diabetes) AID. We compared outcomes on the MDS-UPDRS Parts I-IV, REM sleep behavior disorder screening, MoCA, B-SIT, fine motor testing (Purdue pegboard, finger tapping), patient-reported outcomes (PROMIS-29 and Global Health questionnaire), and fall history. All regression models were adjusted for age, sex, PD duration, and levodopa equivalent dose. We compared groups with/without AID and separately considered systemic vs. organ-restricted-AID.

Results:

All groups were similar in age (mean 64.9), sex (63% male), age at PD onset, and age at diagnosis (59 years). AID patients had a shorter disease duration at evaluation (4.6 vs 5.9 years, p = 0.013) reflecting earlier cohort entry. All pre-specified outcomes were non-significant after adjustment (p > 0.05). Among exploratory outcomes, only fear of falling reached uncorrected p < 0.05, consistent with chance expectation. Separating systemic vs. organ-restricted AID did not change the null result.

Conclusions:

In our cohort, AID was not associated with an altered clinical PD phenotype. While limited by modest AID subgroup size and heterogeneity, our findings do not support AID as a major modifier of PD phenotypes. Studies including larger cohorts and allowing for stratification by disease may be warranted.