Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Expert Rev Mol Diagn. 2014 Jun;14(5):593-603. doi: 10.1586/14737159.2014.922880.
CADASIL is an autosomal dominant inherited disease, characterized by mid-adult onset of cerebrovascular disease and dementia. CADASIL is caused by mutations in the NOTCH3 gene, which encodes the NOTCH3 protein. Pathogenic mutations in CADASIL are highly distinctive in the sense that they lead to the loss or gain of a cysteine residue in 1 of the 34 EGFr domains of the NOTCH3 protein. The majority are missense mutations, but small deletions, insertions and splice-site mutations have been reported, which typically also lead to a numerical cysteine alteration. Whether numerical cysteine-altering mutations are a rule in CADASIL remains subject of debate, as there are reports suggesting pathogenicity of other types of mutations. However, for most of these the association with CADASIL was later revoked or is questionable. Here, we discuss and provide recommendations for the interpretation of NOTCH3 mutations in the diagnosis of CADASIL.
CADASIL 是一种常染色体显性遗传疾病,其特征是成年中期发生脑血管疾病和痴呆。CADASIL 是由 NOTCH3 基因突变引起的,该基因编码 NOTCH3 蛋白。CADASIL 中的致病性突变非常独特,因为它们导致 NOTCH3 蛋白的 34 个 EGFr 结构域中的 1 个中的半胱氨酸残基丢失或获得。大多数是错义突变,但也有报道小的缺失、插入和剪接位点突变,这些突变通常也会导致数目的半胱氨酸改变。数值性半胱氨酸改变是否是 CADASIL 的规则仍存在争议,因为有报道表明其他类型的突变也具有致病性。然而,对于大多数这些突变,与 CADASIL 的关联后来被撤销或存在疑问。在这里,我们讨论并为 NOTCH3 突变在 CADASIL 诊断中的解释提供建议。