Related Experiment Video
Updated: May 7, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
Elevated titers of anti-thyroperoxidase antibodies in patients with multiple system atrophy: a pilot study
Boris Shihman1, Nir Giladi, Margalit Bleiberg
1Department of Neurology, Rabin Medical Center, Petah-Tiqva, Israel.
Objectives:
Multiple system atrophy (MSA) is a neurodegenerative disease characterized by progressive neuronal loss and alpha-synuclein deposition in oligodendroglial cells in the central nervous system. The cause of MSA remains essentially unknown. A cerebellar syndrome was associated with autoimmune thyroid disease in some cases, apparently not related to MSA and was partially responsive to immunomodulatory therapy.
Patients And Methods:
28 euthyroid patients who fulfilled the diagnostic criteria for probable MSA, 11 with MSA-cerebellar type (MSA-C), 17 with MSA-parkinsonian type (MSA-P), 28 patients with Parkinson's disease (PD) and 26 normal euthyroid controls were tested the for serum levels of anti-thyroperoxidase antibodies (anti-TPO) and anti-thyroglobulin (Anti-TG) antibodies (Ab).
Results:
The laboratory results were statistically similar in all three groups, but 3 MSA-C patients had highly elevated anti-TPO Ab titers.
Conclusion:
We identified the presence of elevated anti-TPO levels in a small subgroup of MSA-C patients but neither in MSA-P or PD patients nor in healthy controls. These findings may suggest an autoimmune etiology in some cases of MSA-C.
More Related Videos
Related Concept Videos
Myasthenia Gravis: Overview and Treatment
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Myasthenia Gravis: Diagnostic Tests
The edrophonium test is a diagnostic tool for myasthenia gravis. It involves...
Myasthenia Gravis ll: Pathophysiology
Graves Disease II: Pathophysiology
Graves' Disease I: Introduction
Hyperthyroidism II: Pathophysiology

