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.

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.

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.

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.