Antineuronal antibodies in Parkinson's disease.
Antineuronal antibodies (ANAs) have been implicated in the pathophysiology of postinfectious movement disorders, such as Sydenham's chorea. However, their relevance in other movement disorders--in the absence of infectious triggers--remains much disputed. We sought to assess the frequency of ANAs in idiopathic Parkinson's disease (IPD) and to explore whether a specific phenotype is associated with the presence of ANAs. For this purpose, we recruited 76 IPD patients, 9 patients with genetic parkinsonism, and 10 with one of the parkinson-plus syndromes. They were all subjected to a comprehensive clinical review. In addition, 50 patients with non-extrapyramidal neurological disease and 30 healthy blood donors served as control populations. Blood samples were tested for the presence of ANAs with Western blotting, using recombinant proteins of the three putative antigens (aldolase C, neuron-specific enolase, and pyruvate kinase M1). We found these antibodies in 11.8% of the 76 IPD patients, which differed significantly from healthy controls (0%, P = 0.043), but nonsignificantly from patients with genetic parkinsonism (11.1%), with a parkinson-plus syndrome (10%), or from neurological disease controls (4%). With respect to relevant disease characteristics, IPD patients with or without ANAs were indistinguishable, except for atypical disease features (mainly early falls or freezing and marked Pisa syndrome), which were more frequent in the ANA-positive IPD group. We conclude that ANAs do not play a role in the majority of patients with IPD, but might be relevant in the pathogenesis of IPD with atypical features.
van de Warrenburg
Bart P C
BPC
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom.|Department of Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Church
Andrew J
AJ
Department of Neuroimmunology, Institute of Neurology, London, United Kingdom.
Martino
Davide
D
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom.|Department of Neuroimmunology, Institute of Neurology, London, United Kingdom.|Department of Neurological and Psychiatric Sciences, University of Bari, Bari, Italy.
Candler
Paul M
PM
Department of Neuroimmunology, Institute of Neurology, London, United Kingdom.
Bhatia
Kailash P
KP
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom.
Giovannoni
Gavin
G
Institute of Cell and Molecular Science, Queen Mary University London and the Department of Neurology, Barts and The London NHS Trust, London, United Kingdom.
Quinn
Niall P
NP
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom.
D000906:Antibodies / Q000276:immunology*; D000941:Antigens / Q000276:immunology; D001479:Basal Ganglia / Q000276:immunology* / Q000473:pathology*; D015153:Blotting, Western; D002352:Carrier Proteins / Q000378:metabolism; D002531:Cerebellum / Q000201:enzymology / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000276:immunology* / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D008875:Middle Aged; D009474:Neurons / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D010300:Parkinson Disease / Q000150:complications / Q000276:immunology / Q000473:pathology; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013963:Thyroid Hormones / Q000378:metabolism; D000097810:Thyroid Hormone-Binding Proteins
D000906:Antibodies; D000941:Antigens; D002352:Carrier Proteins; D008565:Membrane Proteins; D010751:Phosphopyruvate Hydratase; D013963:Thyroid Hormones; D000097810:Thyroid Hormone-Binding Proteins