4.0 Article

Contribution of 1425G/A Polymorphism in Protein Kinase C-Eta (PRKCH) Gene and Brain White Matter Lesions to the Risk of Sudden Sensorineural Hearing Loss in a Japanese Nested Case-Control Study

Journal

JOURNAL OF NEUROGENETICS
Volume 25, Issue 3, Pages 82-87

Publisher

INFORMA HEALTHCARE
DOI: 10.3109/01677063.2011.591462

Keywords

brain MRI; polymorphism; protein kinase C-eta; sudden sensorineural hearing loss; white matter lesions

Funding

  1. Research Grant for Longevity Sciences [20shi-2]
  2. Ministry of Health, Labour and Welfare [21A-17]

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Protein kinase C-eta (PRKCH) gene has been recently identified as a susceptible risk locus for cerebral infarction and hemorrhage in the Asian populations. The inner ear artery, a usual branch of anterior inferior cerebellar artery, is an end artery with minimal collaterals, therefore, the inner ear is particularly vulnerable to ischemia. The potential association between the development of stroke and sudden sensorineural hearing loss (SSNHL) has been implied. The authors hypothesized that the PRKCH polymorphism predisposing to stroke is associated with SSNHL risk, in view of brain magnetic resonance imaging (MRI) findings. The authors compared 33 cases of prevalent SSNHL with other cases among 2188 adults aged 40 to 79 years who participated in the Study of Aging, to assess the impact of PRKCH 1425G/A polymorphism in consideration of brain MRI findings. Multiple logistic regression was used to obtain odds ratios (ORs) for SSNHL, with adjustment for other possibly influential factors under additive model of minor allele. The per-allele OR for SSNHL risk was 1.770 (95% confidence interval: 1.024-3.060) after adjustments. The effect of the 1425A-allele varied by white matter lesion (WML) status. A significant impact of the A-allele on SSNHL risk increment was observed in higher-WML group, but not in no-or mild-WML group. The 1425A-allele of PRKCH has probably contributed to the susceptibility to SSNHL, despite the etiological heterogeneity of SSNHL, and the impact of the PRKCH 1425A variation observed in this study may imply underlying vascular pathogenesis of SSNHL.

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