Absence of anti-P/Q calcium channel antibody in the sera of patients with anti-Yo antibody-positive paraneoplastic cerebellar degeneration

Tanaka, Kenichi; Motomura, M; Yu, Nan‐Nan; Tanaka, Manabu; Tsuji, Shoutaro

doi:10.1212/wnl.49.3.895

Cited by 6 publications

(3 citation statements)

References 2 publications

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“…Of note, none of 27 patients with PCD and tumours other than SCLC was positive for P/Q-type VGCC antibodies. By contrast, P/Q VGCC antibodies were absent in a smaller series of anti-Yo-positive patients with gynaecological tumours [ 116 ]. Graus et al examined PCD patients with lung cancer with or without anti-Hu antibodies (23 %) but with no symptoms beyond the cerebellum for anti-P/Q-type VGCC, again using a 125 I-ω-conotoxin MVIIC assay, and detected raised levels in 16 (41 %) of 39 patients with positive PCD, 9 of whom did not have clinical or subclinical LEMS (56 %) and 14 of whom were negative for anti-Hu [ 109 ].…”

Section: Anti-vgccmentioning

confidence: 99%

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC

Jarius

Wildemann

2015

J Neuroinflammation

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Serological testing for anti-neural autoantibodies is important in patients presenting with idiopathic cerebellar ataxia, since these autoantibodies may indicate cancer, determine treatment and predict prognosis. While some of them target nuclear antigens present in all or most CNS neurons (e.g. anti-Hu, anti-Ri), others more specifically target antigens present in the cytoplasm or plasma membrane of Purkinje cells (PC). In this series of articles, we provide a detailed review of the clinical and paraclinical features, oncological, therapeutic and prognostic implications, pathogenetic relevance, and differential laboratory diagnosis of the 12 most common PC autoantibodies (often referred to as ‘Medusa head antibodies’ due their characteristic somatodendritic binding pattern when tested by immunohistochemistry). To assist immunologists and neurologists in diagnosing these disorders, typical high-resolution immunohistochemical images of all 12 reactivities are presented, diagnostic pitfalls discussed and all currently available assays reviewed. Of note, most of these antibodies target antigens involved in the mGluR1/calcium pathway essential for PC function and survival. Many of the antigens also play a role in spinocerebellar ataxia. Part 1 focuses on anti-metabotropic glutamate receptor 1-, anti-Homer protein homolog 3-, anti-Sj/inositol 1,4,5-trisphosphate receptor- and anti-carbonic anhydrase-related protein VIII-associated autoimmune cerebellar ataxia (ACA); part 2 covers anti-protein kinase C gamma-, anti-glutamate receptor delta-2-, anti-Ca/RhoGTPase-activating protein 26- and anti-voltage-gated calcium channel-associated ACA; and part 3 reviews the current knowledge on anti-Tr/delta notch-like epidermal growth factor-related receptor-, anti-Nb/AP3B2-, anti-Yo/cerebellar degeneration-related protein 2- and Purkinje cell antibody 2-associated ACA, discusses differential diagnostic aspects, and provides a summary and outlook.

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Section: Anti-vgccmentioning

confidence: 99%

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC

Jarius

Wildemann

2015

J Neuroinflammation

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“…We and others 17 did not find P/Q-type VGCC antibodies in the sera of patients with PCD and tumors other than SCLC, suggesting that it is unlikely that these antibodies simply result from disruption of Purkinje cells, which are rich in VGCCs.…”

Section: Discussionmentioning

confidence: 48%

“…11 These antibodies, however, were not detected in a small series of 11 patients with PCD and gynecological tumors. 17 To better understand the significance of P/Qtype VGCC antibodies in patients with PND-CNS, we examined the sera of 93 patients with these disorders for the presence of P/Q-type VGCC antibodies, and correlated a positive antibody titer with the clinical findings.…”

mentioning

confidence: 99%

P/Q-type voltage-gated calcium channel antibodies in paraneoplastic disorders of the central nervous system

et al. 1999

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Neuronal calcium channel autoantibodies coexisting with type 1 Purkinje cell cytoplasmic autoantibodies (PCA-1 or "anti-Yo")

Lennon¹,

Kryzer²

1998

Neurology

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with po cells, variable mtDNA repopulation of cybrids is functionally inconsequential as long as exogenous mtDNA levels reach 250% the amount of endogenous p+ mtDNA.4 Our dot blots therefore confirmed that both qualitative and quantitative mtDNA repopulation occurred appropriately in our cybrids.Schon et al.'s insistence that cybrid phenotype analysis must limit itself to the study of expanded clones is untenable and illogical and misses the point of using cybrids to screen for mtDNA mutation in candidate diseases. Although past clonal expansion analysis has helped screen for homoplasmic or nearly homoplasmic mtDNA-mutant cybrid cells following fusion of MELASI MERRF fibroblasts/myoblasts with osteosarcoma po cells, the risk of introducing selection bias when screening molecularly uncharacterized candidate diseases for mtDNA mutation outweighs potential benefits. Although some may argue that selection bias (whether due to aneuploidy or any other cause) can be avoided by analyzing an adequate number of clones, there is no better way to ensure this than to assay a mixed population in the first place (increasing the number of clones generates an asymptotic approach toward a "mixed population). Also, heteroplasmic variability can exist even within clone^.^ This phenomenon could further contribute to selection bias. On a practical note, a previous "mixed population" cybrid study showing Parkinson's patient complex I dysfunction persists in cybrids following mitochondrial transfer was recently confirmed using clonal-analysis methodol~gy.~~~ A mixed-population strategy also successfully demonstrated a complex I defect in cybrids generated from patients with Leber's hereditary optic neuropathy.?Drs. Schon, Shoubridge, and Moraes have successfully used cybrid technology to study questions of heteroplasmy in situations primarily involving known mitochondrial tRNA mutations (nine individual human fusions of myoblastdfibroblasts published) using osteosarcoma po cells created and characterized by King and Attardi.* These studies have included very little biochemical characterization-spectrophotometric biochemical analysis of two published cell lines, and no published analyses of oxidative stress. This experience is not generalizable to our completely unrelated work. Based on our experience creating po cells from two unique, neuronally derived human cell lines (neuroblastoma and teratocarcinoma), our generation and characterization of over 100 cybrid cell lines, and our extensive characterization of these cell lines using a number of different biochemical phenotypic markers including spectrophotometric electron transport chain analysis, free radical generation, free radical scavenging enzyme activities, and both static and dynamic calcium homeostasidregulation,1~3~5~g~1z we propose our own criteria for related work in this field: 1) po cell line nuclear background should resemble as closely as possible the nuclear background of the tissue affected in the disease under consideration (neuronal-based cells for neurodegeneration r...

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Absence of anti-P/Q calcium channel antibody in the sera of patients with anti-Yo antibody-positive paraneoplastic cerebellar degeneration

Cited by 6 publications

References 2 publications

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC

P/Q-type voltage-gated calcium channel antibodies in paraneoplastic disorders of the central nervous system

Neuronal calcium channel autoantibodies coexisting with type 1 Purkinje cell cytoplasmic autoantibodies (PCA-1 or "anti-Yo")

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